[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 100 of about 354
1. dos Santos VM, Cintra Osterne EM, de Castro RA, Marques HV Jr: Bilateral male breast cancer: too many concerns? Asian Pac J Cancer Prev; 2007 Oct-Dec;8(4):640-1
MedlinePlus Health Information. consumer health - Prostate Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Bilateral male breast cancer: too many concerns?
  • The male breast cancer accounts for nearly 1% of all breast cancer cases and bilateral involvement occurs in less than 2% of the cases.
  • Estrogen treatment for prostate cancer is a risk factor for primary breast cancer.
  • Bilateral breast carcinomas were found in a 79-year-old Brazilian black man, following prostate cancer treatment with estrogen.
  • Prostate cancer metastases could be found in breast tissue, and might be indistinguishable from primary breast tumours on histological evaluation without immunohistochemistry.
  • Coexistence of prostate cancer with breast cancer increases future-longevity concerns.
  • [MeSH-major] Breast Neoplasms, Male / chemically induced. Estrogens / adverse effects. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Aged. Brazil. Humans. Immunoenzyme Techniques. Male

  • Genetic Alliance. consumer health - Breast Cancer.
  • Genetic Alliance. consumer health - Breast Cancer, Male.
  • MedlinePlus Health Information. consumer health - Male Breast Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18260745.001).
  • [ISSN] 2476-762X
  • [Journal-full-title] Asian Pacific journal of cancer prevention : APJCP
  • [ISO-abbreviation] Asian Pac. J. Cancer Prev.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] Thailand
  • [Chemical-registry-number] 0 / Estrogens
  •  go-up   go-down


2. Gu GL, Wang SL, Wei XM, Ren L, Zou FX: Axillary metastasis as the first manifestation of male breast cancer: a case report. Cases J; 2008;1(1):285
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Axillary metastasis as the first manifestation of male breast cancer: a case report.
  • BACKGROUND: Breast cancer is very rare in men, and the occurrence of occult breast cancer which present axillary metastasis as the first manifestation is even rarer in men.
  • CASE PRESENTATION: We report a 72-year-old male Han-Chinese patient who presented axillary metastasis as the first manifestation of breast cancer and got correctly diagnoses by histological examination.
  • The histopathologic examination showed that no tumor focus was found in his breast tissue, but two out of fifteen of axillary lymph nodes were invaded by infiltrating ductal carcinoma.
  • The IHC stain showed that estrogen receptor (ER) and progestin receptor (PR) were negative, Human epidermal receptor (HER-2) oncoprotein (+++), P53 protein expressed (+++), Bcl-2 oncoprotein (+++), nm23 protein (++), proliferating cell nuclear antigen (PCNA) (+++) and multidrug-resistance protein (MRP) (++).
  • After operation, he did not receive endocrine therapy, chemotherapy and radiotherapy because of his senility.
  • He is alive without any residual or metastasis disease 29 months after being diagnosed.
  • CONCLUSION: This is the first case in our hospital that presents axillary metastases as the first manifestation of male breast cancer.


3. DeYoung MP, Tress M, Narayanan R: Identification of Down's syndrome critical locus gene SIM2-s as a drug therapy target for solid tumors. Proc Natl Acad Sci U S A; 2003 Apr 15;100(8):4760-5
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification of Down's syndrome critical locus gene SIM2-s as a drug therapy target for solid tumors.
  • We report here a cancer drug therapy use of a gene involved in Down's syndrome.
  • Using bioinformatics approaches, we recently predicted Single Minded 2 gene (SIM2) from Down's syndrome critical region to be specific to certain solid tumors.
  • Involvement of SIM2 in solid tumors has not previously been reported.
  • Intrigued by a possible association between a Down's syndrome gene and solid tumors, we monitored SIM2 expression in solid tumors.
  • Isoform-specific expression of SIM2 short-form (SIM2-s) was seen selectively in colon, prostate, and pancreatic carcinomas but not in breast, lung, or ovarian carcinomas nor in most normal tissues.
  • In colon tumors, SIM2-s expression was seen in early stages.
  • Antisense inhibition of SIM2-s expression in a colon cancer cell line caused inhibition of gene expression, growth inhibition, and apoptosis.
  • The administration of the antisense, but not the control, oligonucleotides caused a pronounced inhibition of tumor growth in nude mice with no major toxicity.
  • Our findings provide a strong rationale for the genes-to-drugs paradigm, establish SIM2-s as a molecular target for cancer therapeutics, and may further understanding of the cancer risk of Down's syndrome patients.
  • [MeSH-major] DNA-Binding Proteins / genetics. Down Syndrome / genetics. Neoplasms / drug therapy. Neoplasms / genetics. Nuclear Proteins / genetics
  • [MeSH-minor] Animals. Base Sequence. Basic Helix-Loop-Helix Transcription Factors. Colonic Neoplasms / drug therapy. Colonic Neoplasms / genetics. Colonic Neoplasms / pathology. DNA, Complementary / genetics. DNA, Neoplasm / genetics. Drosophila Proteins. Female. Gene Expression. Humans. Male. Mice. Mice, Nude. Oligodeoxyribonucleotides, Antisense / genetics. Oligodeoxyribonucleotides, Antisense / therapeutic use. Oncogenes. Protein Isoforms / genetics. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Neoplasm / genetics. RNA, Neoplasm / metabolism. Tumor Cells, Cultured

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • MedlinePlus Health Information. consumer health - Down Syndrome.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Science. 1987 Oct 9;238(4824):193-7 [2889267.001]
  • [Cites] Mol Cell Biol. 1999 Aug;19(8):5811-22 [10409767.001]
  • [Cites] Genomics. 1989 Aug;5(2):325-31 [2529205.001]
  • [Cites] J Gastroenterol Hepatol. 1991 Jan-Feb;6(1):81-9 [1653058.001]
  • [Cites] Cell. 1991 Dec 20;67(6):1157-67 [1760843.001]
  • [Cites] Pharmacogenetics. 1993 Oct;3(5):213-30 [8287061.001]
  • [Cites] Antisense Res Dev. 1993 Winter;3(4):309-22 [8155973.001]
  • [Cites] Annu Rev Pharmacol Toxicol. 1995;35:307-40 [7598497.001]
  • [Cites] J Biol Chem. 1995 Nov 3;270(44):26292-302 [7592839.001]
  • [Cites] Bioessays. 1995 Dec;17(12):1055-63 [8634067.001]
  • [Cites] Cancer Res. 1999 Nov 1;59(21):5403-7 [10554005.001]
  • [Cites] Nucleic Acids Res. 2000 Jan 1;28(1):10-4 [10592169.001]
  • [Cites] Biochem Pharmacol. 2000 Jan 1;59(1):65-85 [10605936.001]
  • [Cites] Mol Med Today. 2000 Feb;6(2):72-81 [10652480.001]
  • [Cites] Lancet. 2000 Jan 15;355(9199):165-9 [10675114.001]
  • [Cites] Med Res Rev. 2000 May;20(3):189-96 [10797463.001]
  • [Cites] Cancer Res. 2000 Aug 1;60(15):4037-43 [10945605.001]
  • [Cites] Hum Mol Genet. 2001 Apr;10(7):663-7 [11257097.001]
  • [Cites] Breast Cancer Res. 2001;3(3):158-75 [11305951.001]
  • [Cites] JAMA. 2001 Nov 14;286(18):2296-307 [11710896.001]
  • [Cites] Cancer Invest. 2002;20(1):82-101 [11855380.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Mar 19;99(6):3712-6 [11880605.001]
  • [Cites] In Vivo. 2002 Jul-Aug;16(4):239-48 [12224133.001]
  • [Cites] Anticancer Res. 2002 Nov-Dec;22(6A):3149-57 [12530058.001]
  • [Cites] Clin Gastroenterol. 1981 Sep;10(3):755-71 [7032764.001]
  • [Cites] J Biol Chem. 1995 Dec 29;270(52):31353-7 [8537407.001]
  • [Cites] Genes Dev. 1996 Jan 1;10(1):103-17 [8557189.001]
  • [Cites] Cell. 1997 Feb 7;88(3):333-46 [9039260.001]
  • [Cites] Nat Genet. 1997 Apr;15 Spec No:415-6 [9140408.001]
  • [Cites] Science. 1997 May 23;276(5316):1268-72 [9157888.001]
  • [Cites] Genome Res. 1997 Jun;7(6):615-24 [9199934.001]
  • [Cites] Hum Mol Genet. 1997;6(10):1713-27 [9300664.001]
  • [Cites] Cancer. 1997 Sep 1;80(5):929-35 [9307193.001]
  • [Cites] Curr Opin Genet Dev. 1998 Jun;8(3):316-21 [9690992.001]
  • [Cites] Br J Surg. 1998 Nov;85(11):1460-7 [9823903.001]
  • [Cites] J Pediatr Hematol Oncol. 1999 Mar-Apr;21(2):149-51 [10206462.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Jun 8;96(12):6745-50 [10359783.001]
  • [Cites] Cell. 1988 Jan 15;52(1):133-41 [3345559.001]
  • (PMID = 12676991.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / DNA, Complementary; 0 / DNA, Neoplasm; 0 / DNA-Binding Proteins; 0 / Drosophila Proteins; 0 / Nuclear Proteins; 0 / Oligodeoxyribonucleotides, Antisense; 0 / Protein Isoforms; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / SIM2 protein, human; 0 / sim protein, Drosophila
  • [Other-IDs] NLM/ PMC153629
  •  go-up   go-down


Advertisement
4. Skourou C, Hoopes PJ, Paulsen KD: Tissue permittivity: a monitor for progressive tissue fibrosis as observed in bystander tissues following experimental high dose rate irradiation. Cancer Biol Ther; 2009 Dec;8(23):2223-9
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tissue permittivity: a monitor for progressive tissue fibrosis as observed in bystander tissues following experimental high dose rate irradiation.
  • Fibrosis is a pathological condition resulting from radiation injury which often limits the prescription of higher (or boost) doses of radiation, risking inadequate tumor control in patients.
  • Recent studies have documented reduction in fibrotic lesions after administration of pentoxyfilline and tocopherol combinations to breast cancer patients receiving adjuvant radiation therapy.
  • Despite the promise of these findings, no techniques or markers are available which can be used to identify the onset or progression of fibrosis in such patients at stages early enough to allow maximum benefit from these types of pharmacological agents.
  • Relative permittivity of skeletal muscle has been investigated in an animal model utilizing high dose rate radiation both at the treatment site as well as on the contralateral site, and was found to be directly related to the formation and progression of fibrotic lesions.
  • A cubic increase in the quantified fibrotic fraction of the tissue (2.7%-13.9% over 11 w post irradiation) was reflected in a linear increase in the tissue's relative permittivity (epsilon(r) = 6.3-8.8 over 11 w post irradiation).
  • These findings mandate further investigation of the relationship between tissue's relative permittivity and subcellular injury leading to fibrosis using electrical impedance spectroscopy (EIS).
  • [MeSH-major] Hindlimb / radiation effects. Muscles / pathology. Muscles / radiation effects. Radiation Injuries, Experimental / diagnosis
  • [MeSH-minor] Animals. Electric Impedance. Fibrosis. Male. Radiotherapy Dosage. Rats

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Health Phys. 2003 Jul;85(1):31-5 [12852468.001]
  • [Cites] J Radiat Res. 2009 Jan;50(1):1-9 [18838844.001]
  • [Cites] Hum Exp Toxicol. 2004 Feb;23(2):81-6 [15070065.001]
  • [Cites] Phys Med Biol. 2004 Mar 7;49(5):665-83 [15070195.001]
  • [Cites] Cancer Res. 1993 Sep 1;53(17):3880-6 [8358713.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1995 Aug 30;33(1):99-109 [7642437.001]
  • [Cites] Phys Med Biol. 1996 Nov;41(11):2231-49 [8938024.001]
  • [Cites] Biol Pharm Bull. 2002 Sep;25(9):1192-6 [12230116.001]
  • [Cites] Pacing Clin Electrophysiol. 2000 Aug;23(8):1283-7 [10962753.001]
  • [Cites] Phys Med Biol. 1996 Nov;41(11):2251-69 [8938025.001]
  • [Cites] Radiat Res. 1999 Jul;152(1):41-50 [10381839.001]
  • [Cites] J Clin Oncol. 2005 Dec 1;23(34):8570-9 [16260695.001]
  • [Cites] Mutat Res. 2006 May 11;597(1-2):98-112 [16414093.001]
  • [Cites] Nutrition. 2007 Jan;23(1):96 [17070015.001]
  • [Cites] Phys Med Biol. 2007 Jan 21;52(2):347-63 [17202619.001]
  • [Cites] Semin Radiat Oncol. 2007 Apr;17(2):99-107 [17395040.001]
  • [Cites] Semin Radiat Oncol. 2007 Apr;17(2):149-55 [17395045.001]
  • [Cites] Acta Oncol. 2007;46(4):525-33 [17497320.001]
  • [Cites] Mutat Res. 2008 Mar 1;639(1-2):35-44 [18082226.001]
  • [Cites] Cancer Radiother. 2008 Nov;12(6-7):565-70 [18760649.001]
  • [Cites] Curr Cancer Drug Targets. 2004 Feb;4(1):53-64 [14965267.001]
  • (PMID = 19823045.001).
  • [ISSN] 1555-8576
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Grant] United States / NIBIB NIH HHS / EB / R01 EB001982
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC3819449
  •  go-up   go-down


5. Aloysius MM, Zaitoun AM, Bates TE, Ilyas M, Constantin-Teodosiu D, Rowlands BJ, Lobo DN: Immunohistochemical expression of mitochondrial membrane complexes (MMCs) I, III, IV and V in malignant and benign periampullary epithelium: a potential target for drug therapy of periampullary cancer? BMC Cancer; 2010;10:80
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunohistochemical expression of mitochondrial membrane complexes (MMCs) I, III, IV and V in malignant and benign periampullary epithelium: a potential target for drug therapy of periampullary cancer?
  • No published data are available on the relative abundance of MMCs in different periampullary cancers.
  • Therefore, we studied the expression profile of MMCs I, III, IV and V in periampullary cancers, reactive pancreatitis, normal pancreas and chronic pancreatitis.
  • METHODS: This was a retrospective study on tissue microarrays constructed from formalin-fixed paraffin-embedded tissue from 126 consecutive patients (cancer = 104, chronic pancreatitis = 22) undergoing pancreatic resections between June 2001 and June 2006.
  • 78 specimens of chronic pancreatitis tissue were obtained adjacent to areas of cancer.
  • Normal pancreatic tissue was obtained from the resection specimens in a total of 30 patients.
  • Metastatic tumours in 61 regional lymph nodes from 61 patients were also studied.
  • RESULTS: MMCs I, III, IV and V were highly expressed (p < 0.05) in all primary periampullary cancers compared with metastatic lymph nodes and adjacent benign pancreas.
  • MMCs III, IV and V were highly expressed in all cancers regardless of type compared with chronic pancreatitis (p < 0.05).
  • Higher expression of MMCs I and V was associated with better survival and may, in part, relate to lower expression of these MMCs in poorly differentiated tumours compared with well and moderately differentiated tumours.
  • CONCLUSIONS: Differential expression of MMCs III, IV and V in primary periampullary cancers compared with adjacent benign periampullary tissue and chronic pancreatitis is a novel finding, which may render them attractive anticancer targets.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Immunohistochemistry / methods. Mitochondria / metabolism. Pancreatic Neoplasms / metabolism
  • [MeSH-minor] Adult. Aged. Cell Proliferation. Epithelium / drug effects. Female. Humans. Lymphatic Metastasis. Male. Middle Aged. Neoplasm Metastasis. Oxidative Stress. Pancreas / pathology. Pancreatitis / pathology. Phosphorylation. Retrospective Studies

  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Science. 2000 Aug 18;289(5482):1150-1 [10970229.001]
  • [Cites] Cell. 2000 Jan 7;100(1):57-70 [10647931.001]
  • [Cites] Breast Cancer Res Treat. 2001 Jul;68(1):9-19 [11678313.001]
  • [Cites] Toxicol Appl Pharmacol. 2001 Nov 1;176(3):145-52 [11714246.001]
  • [Cites] Cell. 2003 Feb 21;112(4):481-90 [12600312.001]
  • [Cites] Am J Physiol Lung Cell Mol Physiol. 2003 Jul;285(1):L189-98 [12665464.001]
  • [Cites] Trends Mol Med. 2004 Aug;10(8):372-8 [15310457.001]
  • [Cites] BMJ. 2004 Sep 18;329(7467):668-73 [15374918.001]
  • [Cites] Cancer. 1993 Dec 15;72(12):3641-7 [8252480.001]
  • [Cites] Science. 1998 Aug 28;281(5381):1309-12 [9721092.001]
  • [Cites] Biochem Biophys Res Commun. 2005 Mar 11;328(2):623-32 [15694394.001]
  • [Cites] Gastroenterology. 2005 May;128(6):1606-25 [15887154.001]
  • [Cites] Biochem Pharmacol. 2005 Jul 1;70(1):1-12 [15907809.001]
  • [Cites] Cell Metab. 2005 Jun;1(6):401-8 [16054089.001]
  • [Cites] Nat Rev Cancer. 2005 Nov;5(11):857-66 [16327764.001]
  • [Cites] Oncogene. 2006 Aug 7;25(34):4787-97 [16892091.001]
  • [Cites] Oncogene. 2006 Aug 7;25(34):4812-30 [16892093.001]
  • [Cites] Exp Physiol. 2006 Sep;91(5):807-19 [16857720.001]
  • [Cites] FEBS Lett. 2006 Oct 2;580(22):5125-9 [16979626.001]
  • [Cites] Biochem Biophys Res Commun. 2007 Mar 2;354(1):50-5 [17214968.001]
  • [Cites] J Bioenerg Biomembr. 2007 Feb;39(1):65-72 [17294131.001]
  • [Cites] Am J Physiol Cell Physiol. 2007 Jul;293(1):C12-21 [17475665.001]
  • [Cites] Gut. 2007 Aug;56(8):1134-52 [17625148.001]
  • [Cites] Biochem Biophys Res Commun. 2007 Dec 7;364(1):131-7 [17931597.001]
  • [Cites] Clin Cancer Res. 2009 Mar 1;15(5):1593-600 [19223492.001]
  • [Cites] BMC Cancer. 2009;9:327 [19754967.001]
  • [Cites] Oral Oncol. 2001 Jan;37(1):72-6 [11120486.001]
  • (PMID = 20202214.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Other-IDs] NLM/ PMC2841142
  •  go-up   go-down


6. Skubitz KM, Pambuccian S, Manivel JC, Skubitz AP: Identification of heterogeneity among soft tissue sarcomas by gene expression profiles from different tumors. J Transl Med; 2008 May 06;6:23
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification of heterogeneity among soft tissue sarcomas by gene expression profiles from different tumors.
  • The heterogeneity that soft tissue sarcomas (STS) exhibit in their clinical behavior, even within histological subtypes, complicates patient care.
  • Morphologic features are generally good predictors of biologic behavior, however, metastatic propensity, tumor growth, and response to chemotherapy may be determined by gene expression patterns that do not correlate well with morphology.
  • One approach to identify heterogeneity is to search for genetic markers that correlate with differences in tumor behavior.
  • In this study, gene expression in 53 samples of STS and AF [including 16 malignant fibrous histiocytoma (MFH), 9 leiomyosarcoma, 12 liposarcoma, 4 synovial sarcoma, and 12 samples of AF] was determined at Gene Logic Inc. (Gaithersburg, MD) using Affymetrix GeneChip U_133 arrays containing approximately 40,000 genes/ESTs.
  • In addition, several genes that are targets of some anti-tumor drugs were found to be differentially expressed in particular subsets of STS.

  • MedlinePlus Health Information. consumer health - Soft Tissue Sarcoma.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cancer. 1984 Feb 1;53(3):530-41 [6692258.001]
  • [Cites] J Lab Clin Med. 2004 Aug;144(2):78-91 [15322502.001]
  • [Cites] Cancer. 1986 Jul 15;58(2):306-9 [3719523.001]
  • [Cites] Cancer. 1988 Feb 15;61(4):817-23 [3338039.001]
  • [Cites] Cancer. 1988 Sep 1;62(5):994-8 [3409180.001]
  • [Cites] Am J Physiol. 1992 Dec;263(6 Pt 1):L627-33 [1476204.001]
  • [Cites] Ann N Y Acad Sci. 1992 Dec 4;667:101-11 [1309029.001]
  • [Cites] Mod Pathol. 1995 Sep;8(7):705-10 [8539226.001]
  • [Cites] J Clin Oncol. 1997 Jan;15(1):350-62 [8996162.001]
  • [Cites] Am J Pathol. 1997 Aug;151(2):329-34 [9250146.001]
  • [Cites] J Surg Oncol. 1999 Oct;72(2):77-82 [10518103.001]
  • [Cites] Cancer Immun. 2005 Feb 1;5:2 [15683221.001]
  • [Cites] Cancer Invest. 2005;23(2):105-18 [15813502.001]
  • [Cites] N Engl J Med. 2005 Aug 18;353(7):701-11 [16107623.001]
  • [Cites] Cancer Res. 2005 Oct 15;65(20):9226-35 [16230383.001]
  • [Cites] Histopathology. 2006 Jan;48(1):22-31 [16359534.001]
  • [Cites] Histopathology. 2006 Jan;48(1):51-62 [16359537.001]
  • [Cites] J Clin Oncol. 2006 Mar 1;24(7):1195-203 [16505440.001]
  • [Cites] J Lab Clin Med. 2006 May;147(5):250-67 [16697773.001]
  • [Cites] Transl Res. 2006 Nov;148(5):223-48 [17145569.001]
  • [Cites] J Natl Compr Canc Netw. 2007 Apr;5(4):364-99 [17442230.001]
  • [Cites] Mayo Clin Proc. 2007 Nov;82(11):1409-32 [17976362.001]
  • [Cites] Annu Rev Pathol. 2006;1:119-50 [18039110.001]
  • [Cites] Cancer Cell. 2007 Dec;12(6):514-27 [18068629.001]
  • [Cites] Oncogene. 1999 Nov 11;18(47):6615-20 [10597266.001]
  • [Cites] J Clin Pathol. 1999 Sep;52(9):695-6 [10655994.001]
  • [Cites] Nature. 2000 Feb 3;403(6769):503-11 [10676951.001]
  • [Cites] Nature. 2000 Aug 17;406(6797):747-52 [10963602.001]
  • [Cites] Int J Cancer. 2001 Mar 20;95(2):102-7 [11241320.001]
  • [Cites] Nat Med. 2001 Jun;7(6):673-9 [11385503.001]
  • [Cites] Breast Cancer Res. 2001;3(6):365-72 [11737887.001]
  • [Cites] Lab Invest. 2002 Jan;82(1):97-103 [11796830.001]
  • [Cites] Hum Pathol. 2002 Jan;33(1):39-46 [11823972.001]
  • [Cites] Lancet. 2002 Apr 13;359(9314):1301-7 [11965276.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 May 14;99(10):6973-8 [11983872.001]
  • [Cites] J Lab Clin Med. 2003 May;141(5):297-308 [12761473.001]
  • [Cites] Clin Cancer Res. 2003 Jun;9(6):1941-56 [12796356.001]
  • [Cites] Am J Pathol. 2003 Aug;163(2):691-700 [12875988.001]
  • [Cites] Cancer. 2003 Sep 1;98(5):1029-38 [12942572.001]
  • [Cites] J Lab Clin Med. 2004 Feb;143(2):89-98 [14966464.001]
  • [Cites] Clin Cancer Res. 2004 Jul 15;10(14):4776-83 [15269152.001]
  • [Cites] Cancer Immun. 2004 Aug 9;4:7 [15298487.001]
  • [Cites] J Clin Invest. 1985 Jan;75(1):11-8 [3965498.001]
  • (PMID = 18460215.001).
  • [ISSN] 1479-5876
  • [Journal-full-title] Journal of translational medicine
  • [ISO-abbreviation] J Transl Med
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA106878-03; United States / NCI NIH HHS / CA / R01 CA106878; United States / NCI NIH HHS / CA / R01 CA106878-03; United States / NCI NIH HHS / CA / R01CA106878
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / RNA, Neoplasm
  • [Other-IDs] NLM/ PMC2412854
  •  go-up   go-down


7. Karamanakos P, Mitsiades CS, Lembessis P, Kontos M, Trafalis D, Koutsilieris M: Male breast adenocarcinoma in a prostate cancer patient following prolonged anti-androgen monotherapy. Anticancer Res; 2004 Mar-Apr;24(2C):1077-81
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Male breast adenocarcinoma in a prostate cancer patient following prolonged anti-androgen monotherapy.
  • We report the case of an 82-year-old male patient with a > 8-year history of prostate cancer (PrCa), who developed breast adenocarcinoma (BrCa) (Ki-67+ and negative for ER, PR, PSA and HER2/neu) after prolonged (approximately 7-year) anti-androgen (flutamide) monotherapy for locally advanced PrCa.
  • Biochemical and molecular analyses showed hyperestrogenemia (serum estradiol = 266 pg/ml, with normal range < 74 pg/ml), germline BRCA-1 mutation (T to C at nucleotide 3232, in exon 11, causing Glu to Gly change at codon 1038) and chromosome 9 inversion (karyotype of 46,XY with inv(9) (p11q21)).
  • Following bilateral mastectomy without adjuvant systemic therapy, the patient has been disease-free (from both BrCa and PrCa) for > 3 years.
  • In contrast to LHRH-based hormonal therapies for PrCa, anti-androgen monotherapy causes hyper-estrogenemia due to the suppressed negative feedback loop of androgens on LHRH and LH production, stimulation of testicular androgen production and their intracrine transformation to estrogens in peripheral target tissues.
  • This case report illustrates that PrCa patients receiving anti-androgen monotherapy may be at risk of BrCa, in the event of the concomitant presence of other genetically-determined predisposing factors, and indicates the importance of exercising caution against indiscriminate and prolonged use of anti-androgen monotherapy in patients with risk factors for male BrCa.
  • [MeSH-major] Adenocarcinoma / chemically induced. Androgen Antagonists / adverse effects. Breast Neoplasms, Male / chemically induced. Flutamide / adverse effects. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Aged. Antineoplastic Agents, Hormonal / adverse effects. Antineoplastic Agents, Hormonal / therapeutic use. Humans. Male


8. Kanhai RC, Hage JJ, van Diest PJ, Bloemena E, Mulder JW: Short-term and long-term histologic effects of castration and estrogen treatment on breast tissue of 14 male-to-female transsexuals in comparison with two chemically castrated men. Am J Surg Pathol; 2000 Jan;24(1):74-80
Hazardous Substances Data Bank. BICALUTAMIDE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Short-term and long-term histologic effects of castration and estrogen treatment on breast tissue of 14 male-to-female transsexuals in comparison with two chemically castrated men.
  • The histologic changes induced in the mammary gland of male-to-female transsexuals have not yet been reported in the literature.
  • We studied the histologic changes induced by chemical and surgical castration and estrogen therapy in the breasts of 14 such patients, with particular reference to acinar and lobular formation.
  • To objectify the influence of cross-sex treatment, the histologic findings were compared with those in two men treated hormonally for prostate cancer.
  • The slight increase in the plasma estrogen-to-androgen ratio seen in idiopathic gynecomastia usually does not induce acinar and lobular formation in the male breast.
  • In men treated with nonprogestative antiandrogens for prostate cancer, only moderate acinar and lobular formation occurs.
  • Only in male-to-female transsexuals in whom progestative chemical castration is combined with feminizing estrogen therapy will full acinar and lobular formation occur with hormonally stimulated nuclei and pseudolactational changes.
  • Hence, combined progestative antiandrogens and estrogens are necessary for genetically male breast tissue to mimic the natural histology of the female breast.
  • Apocrine metaplasia may occur in breasts of male-to-female transsexuals, but so far, only four cases of breast cancer in male-to-female transsexuals have been documented.
  • [MeSH-major] Androgen Antagonists / administration & dosage. Breast / anatomy & histology. Breast / pathology. Castration / methods. Estradiol Congeners / administration & dosage. Ethinyl Estradiol / administration & dosage. Gynecomastia / pathology. Orchiectomy. Transsexualism / drug therapy. Transsexualism / surgery
  • [MeSH-minor] Adult. Aged. Anilides / administration & dosage. Cyproterone Acetate / administration & dosage. Female. Flutamide / therapeutic use. Follow-Up Studies. Humans. Male. Mastectomy, Subcutaneous. Metaplasia. Nitriles. Time Factors. Tosyl Compounds

  • Hazardous Substances Data Bank. CYPROTERONE ACETATE .
  • Hazardous Substances Data Bank. ETHINYLESTRADIOL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 10632490.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Anilides; 0 / Estradiol Congeners; 0 / Nitriles; 0 / Tosyl Compounds; 423D2T571U / Ethinyl Estradiol; 4KM2BN5JHF / Cyproterone Acetate; 76W6J0943E / Flutamide; A0Z3NAU9DP / bicalutamide
  •  go-up   go-down


9. Petrocca S, La Torre M, Cosenza G, Bocchetti T, Cavallini M, Di Stefano D, Sammartino F, Ziparo V: Male breast cancer: a case report and review of the literature. Chir Ital; 2005 May-Jun;57(3):365-71
MedlinePlus Health Information. consumer health - Male Breast Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Male breast cancer: a case report and review of the literature.
  • Breast cancer in men is an uncommon disease.
  • Because of its rarity little is known about its aetiology, clinical behaviour and treatment.
  • Retrospective studies show that when age- and stage-matched breast cancer in men and women are compared, there is no difference in survival between the two groups.
  • Nevertheless, because of the absence of screening protocols and the limited amount of mammary tissue in men, allowing rapid local infiltration, a late diagnosis is often made, with a poor survival rate.
  • Most of our current knowledge about the biology, natural history, surgical therapeutic strategies, adjuvant radiotherapy and chemotherapy protocols of male breast carcinoma has been extrapolated from its female counterpart.
  • The Authors report the case of a male patient with breast cancer and pagetoid diffusion in the nipple region, and, on the basis of a review of the literature, summarise what is currently known about this rare neoplasm in terms of prognostic factors, therapy and survival.
  • [MeSH-major] Breast Neoplasms, Male / pathology. Breast Neoplasms, Male / surgery. Carcinoma, Ductal, Breast / pathology. Carcinoma, Ductal, Breast / surgery
  • [MeSH-minor] Aged. Humans. Male. Mastectomy, Radical / methods. Neoadjuvant Therapy / methods. Neoplasm Staging. Prognosis

  • Genetic Alliance. consumer health - Breast Cancer.
  • Genetic Alliance. consumer health - Breast Cancer, Male.
  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16231827.001).
  • [ISSN] 0009-4773
  • [Journal-full-title] Chirurgia italiana
  • [ISO-abbreviation] Chir Ital
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Italy
  • [Number-of-references] 39
  •  go-up   go-down


10. Liukkonen S, Saarto T, Mäenpää H, Sjöström-Mattson J: Male breast cancer: a survey at the Helsinki University Central Hospital during 1981-2006. Acta Oncol; 2010 Apr;49(3):322-7
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Male breast cancer: a survey at the Helsinki University Central Hospital during 1981-2006.
  • BACKGROUND: The purpose was to analyze the behavior of male breast cancer.
  • METHODS: Fifty-eight male breast cancer patients were treated at the HUCH during 1981-2006.
  • Data on risk factors, tumor characteristics, clinical presentation, treatment and survival were obtained by chart review.
  • The median size of the primary tumor was 1.8 cm and 14% were T4 tumors.
  • Forty-seven percent had lymph node metastases and 4% distant metastases at diagnosis.
  • Ductal carcinoma was the most common tumor type.
  • All tumors with known receptor status were positive for estrogen receptor (ER) and 79% for progesterone receptor (PgR).
  • A family history of breast cancer, obesity, high alcohol intake and liver cirrhosis were the most often seen risk factors.
  • Nineteen percent had one or two other malignancies, the most common second malignancy being prostate cancer in 7%.
  • Sixty percent of the patients received radiotherapy, 64% adjuvant hormonal treatment, 20% adjuvant chemotherapy, and 2% adjuvant trastuzumab.
  • Fourteen patients (25%) experienced a relapse of which 60% were distant, bone being the most common site.
  • During follow-up 21 patients (37%) died, of whom nine of breast cancer and 12 due to other causes.
  • CONCLUSIONS: Male breast cancer behaves and is today treated in many respects like postmenopausal breast cancer.
  • However, due to rudimentary breast tissue the symptoms, diagnosis and especially a higher amount of T4 tumors differ from that of females.
  • [MeSH-major] Breast Neoplasms, Male / epidemiology. Breast Neoplasms, Male / etiology. Neoplasm Recurrence, Local / epidemiology. Neoplasms, Second Primary / epidemiology. Prostatic Neoplasms / epidemiology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Alcohol Drinking / adverse effects. Axilla. Biomarkers, Tumor / analysis. Bone Neoplasms / epidemiology. Bone Neoplasms / mortality. Bone Neoplasms / secondary. Bone Neoplasms / therapy. Chemotherapy, Adjuvant. Disease-Free Survival. Finland / epidemiology. Humans. Lymph Node Excision / statistics & numerical data. Male. Mastectomy / methods. Mastectomy / statistics & numerical data. Middle Aged. Neoplasm Staging. Obesity / complications. Radiotherapy, Adjuvant. Receptors, Estrogen / analysis. Receptors, Progesterone / analysis. Risk Factors. Sentinel Lymph Node Biopsy. Survival Analysis


11. Kanoh T, Iino Y, Horiguchi J, Takei H, Maemura M, Yokoe T, Morishita Y: A case report of advanced male breast cancer with an objective response to tamoxifen treatment. Breast Cancer; 2000;7(3):256-60
Hazardous Substances Data Bank. TAMOXIFEN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A case report of advanced male breast cancer with an objective response to tamoxifen treatment.
  • A 70-year-old man presented with a firm tumor in his right breast first noticed eight years ago.
  • The tumor had enlarged gradually and had produced an ulcer with bleeding.
  • On physical examination, a huge tumor entirely occupied the right breast and extensively had infiltrated the chest wall.
  • Invasive ductal carcinoma of the breast was diagnosed by incisional biopsy,confirming advanced breast cancer with lung metastases and bilateral pleural effusion(T4cN2M1, Stage IV).
  • Because ER and PgR levels were 110 fmol/mg and 190 fmol/mg, respectively, and because his general condition was poor, we selected medical treatment with tamoxifen(TAM).
  • Thirty-two weeks later, the tumor had showed pronounced reduction with scarring.
  • The patient underwent local excision of the scar tissue.
  • The tumor in the chest wall recurred two months after the end of TAM treatment, possibly because the patient did not accept continuous TAM therapy.
  • The patient died from complications of brain metastasis 32 months after the start of TAM treatment.
  • We report a rare case of advanced male breast cancer and on the effectiveness of continuous TAM treatment.
  • [MeSH-major] Antineoplastic Agents, Hormonal / therapeutic use. Brain Neoplasms / secondary. Breast Neoplasms, Male / drug therapy. Breast Neoplasms, Male / pathology. Carcinoma, Ductal, Breast / secondary. Lung Neoplasms / secondary. Tamoxifen / therapeutic use
  • [MeSH-minor] Aged. Biopsy. Fatal Outcome. Humans. Male. Neoplasm Staging. Quality of Life. Tomography, X-Ray Computed. Treatment Outcome


12. Bentz EK, Pils D, Bilban M, Kaufmann U, Hefler LA, Reinthaller A, Singer CF, Huber JC, Horvat R, Tempfer CB: Gene expression signatures of breast tissue before and after cross-sex hormone therapy in female-to-male transsexuals. Fertil Steril; 2010 Dec;94(7):2688-96
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gene expression signatures of breast tissue before and after cross-sex hormone therapy in female-to-male transsexuals.
  • OBJECTIVE: To evaluate gene expression signatures of breast tissue in female-to-male (FtM) transsexuals under cross-sex hormone therapy (HT).
  • INTERVENTION(S): Breast tissue biopsy before and after 2 years of intramuscular testosterone undecanoate (1,000 mg every 12 wk) and oral lynestrenole (5 mg daily), and gene signature analysis by global gene expression array covering 28,869 genes.
  • We identified eight breast cancer-associated gene expression signatures significantly overlapping with differentially regulated probe sets after cross-sex HT.
  • CONCLUSION(S): Cross-sex HT in FtM transsexuals leads to the up-regulation and down-regulation of 243 and 2,007 distinct genes, respectively, and is associated with breast cancer-related gene expression signatures.
  • [MeSH-major] Breast / metabolism. Gene Expression Profiling. Gonadal Steroid Hormones / therapeutic use. Transsexualism / drug therapy. Transsexualism / genetics
  • [MeSH-minor] Administration, Oral. Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. Breast Neoplasms / genetics. Carcinoma / genetics. Carcinoma / metabolism. Chemotaxis, Leukocyte / physiology. Female. Gene Expression / drug effects. Genes, Neoplasm. Humans. Injections, Intramuscular. Lynestrenol / administration & dosage. Lynestrenol / pharmacology. Male. Microarray Analysis. Sex Reassignment Procedures. Testosterone / administration & dosage. Testosterone / analogs & derivatives. Testosterone / pharmacology. Validation Studies as Topic

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. Lynestrenol .
  • Hazardous Substances Data Bank. TESTOSTERONE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright © 2010 American Society for Reproductive Medicine. Published by Elsevier Inc. All rights reserved.
  • (PMID = 20537635.001).
  • [ISSN] 1556-5653
  • [Journal-full-title] Fertility and sterility
  • [ISO-abbreviation] Fertil. Steril.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Gonadal Steroid Hormones; 3XMK78S47O / Testosterone; H16A5VCT9C / testosterone undecanoate; N2Z8ALG4U5 / Lynestrenol
  •  go-up   go-down


13. Kusama M, Imamura Y: Impact of radiofrequency ablation therapy for breast cancer in nipple-areolar complex. J Clin Oncol; 2009 May 20;27(15_suppl):e11511

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Impact of radiofrequency ablation therapy for breast cancer in nipple-areolar complex.
  • : e11511 Background: Preservation of the safety surgical margin is difficult in BCT of a breast cancer in the vicinity of the nipple-areola complex, and mastectomy is required even for tiny tumors, with consequent poor cosmetic efects.
  • Radiofrequency ablation (RFA) is an advanced, minimally invasive technique for breast cancer.
  • Its application for the tumor in the nipple-areola region has recieved considerable interest.
  • METHODS: RFA of 32 malignant lesion was performed in 30 patients with nipple-areolar breast cancer (Tis: 4, T1: 18; T2: 8).
  • One of the patients had received preoperative chemotherapy.
  • And one patient was male breast cancer(T2).Surgery was performed on an outpatient basis.A 19-gauge cooled-tip needle was used in all cases.
  • About 10-20ml of 5% glucose solutions was injected between the nipple-areola and the tumor before RFA to maintain a space to avoid heat damage that can occur due to diffusion of RF waves.
  • RFA was continued until the moisture of the tumor was vaporized.
  • Irradiation of radiofrequency with a boost was conducted in 23 patients.
  • RESULTS: In one patient, who had undergone preoperative chemotherapy was observed a recurrence in the nipple on 9 months later, but disappeared after a second ablation of RF.
  • Cosmetic features were maintained after surgery, except in the case that received preoperative chemotherapy, in which a mild deformity in the nipple was evident.
  • There has been no recurrence in the 29 primary cases over a relatively short observation period.
  • CONCLUSIONS: RFA enables treatment of breast cancer in the nipple-areolar region without damage to the surrounding tissues and degradation of cosmetic features.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27964636.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


14. Syed SK, Beeram M, Takimoto CH, Jakubowitz J, Kimura M, Ducharme M, Gadgeel S, De Jager R, Rowinsky E, Lorusso P: Phase I and Pharmacokinetics (PK) of DJ-927, an oral taxane, in patients (Pts) with advanced cancers. J Clin Oncol; 2004 Jul 15;22(14_suppl):2028

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase I and Pharmacokinetics (PK) of DJ-927, an oral taxane, in patients (Pts) with advanced cancers.
  • : 2028 Background: DJ-927, a novel semi-synthetic taxane and a poor substrate of P-glycoprotein (Pgp), is orally bioavailable and possesses potent anti-tumor activity against Pgp expressing human cancers.
  • Pts were stratified based on prior therapy into minimally (MP) and heavily (HP) pretreated cohorts.
  • Demographics: 23 male / 17 female; median [range] age- 57 [31-81]; PS 0 [7], PS 1 [31], and PS 2 [2].
  • Primary tumors are colorectal [15], breast [4], pancreas [5], renal cell [3], soft tissue sarcoma [3] and others [10].
  • Minimal drug-related toxicities were observed at doses 5 days duration [7] and grade 3 thrombocytopenia [4] were the predominant hematological toxicities observed at 40 and 35 mg/m<sup>2</sup> doses.
  • Minor responses were seen in taxane-refractory breast carcinoma [1] and transitional cell carcinoma of the bladder [1].
  • Disease stabilization for >3 months was noted in 8 pts.
  • CONCLUSIONS: DJ-927 generates predictable systemic drug exposures and has been well tolerated when orally administered.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 28015577.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


15. Gewurz BE, Dezube BJ, Pantanowitz L: HIV and the breast. AIDS Read; 2005 Aug;15(8):392-6, 399-402
MedlinePlus Health Information. consumer health - HIV/AIDS Medicines.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] HIV and the breast.
  • HIV infection and antiretroviral therapy may alter the spectrum and frequency of diseases that affect the breast.
  • The differential diagnosis of conditions of the breast that a practitioner may encounter in HIV-infected persons includes infection, morphologic alterations, and malignancy.
  • Atypical infections may involve the breast as CD4+ T-cell counts wane.
  • True gynecomastia, resulting from proliferation of male breast ducts and periductal stroma, might be differentiated from lipomastia--a manifestation of lipodystrophy, characterized by the deposition of adipose tissue in the breast.
  • In the era of HAART, HIV-infected patients with malignancy--particularly those who have robust CD4+ T-cell counts and well-controlled HIV viral loads--should be treated similarly to their HIV-negative counterparts.
  • [MeSH-major] Anti-HIV Agents / adverse effects. Breast Diseases / diagnosis. Breast Neoplasms. Gynecomastia. HIV Infections / drug therapy
  • [MeSH-minor] Diagnosis, Differential. Female. Humans. Male


16. Sánchez-Serrano M, Crespo J, Mirabet V, Cobo AC, Escribá MJ, Simón C, Pellicer A: Twins born after transplantation of ovarian cortical tissue and oocyte vitrification. Fertil Steril; 2010 Jan;93(1):268.e11-3
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Twins born after transplantation of ovarian cortical tissue and oocyte vitrification.
  • OBJECTIVE: To present a combination of ovarian tissue and oocyte cryopreservation as an effective strategy for achieving pregnancy in a breast cancer patient.
  • SETTING: Tertiary care university-affiliated hospital, tissue bank, and infertility clinic.
  • PATIENT(S): A 36-year-old patient diagnosed with atypical medullar breast cancer and negative for estrogen, P, and HER2 receptors underwent ovarian tissue cryopreservation before receiving chemotherapy and radiotherapy.
  • INTERVENTION(S): Laparoscopic ovarian cortex extraction, ovarian tissue cryopreservation, ovarian tissue thawing and transplantation, controlled ovarian stimulation (COS), oocyte retrieval, vitrification and IVF, and embryo culture and replacement.
  • CONCLUSION(S): Ovarian tissue cryopreservation and grafting preserves fertility.
  • Simultaneous oocyte vitrification increases the success of assisted reproductive technology in poor-prognosis patients and avoids the consequences of the short lifespan of the transplanted tissue.
  • [MeSH-major] Breast Neoplasms / therapy. Cryopreservation. Fertility. Oocytes. Ovary / transplantation. Twins
  • [MeSH-minor] Adult. Embryo Culture Techniques. Embryo Transfer. Female. Fertilization in Vitro. Gestational Age. Humans. Infant, Newborn. Male. Oocyte Retrieval. Ovulation Induction. Pregnancy. Treatment Outcome

  • Genetic Alliance. consumer health - Transplantation.
  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2010 American Society for Reproductive Medicine. Published by Elsevier Inc. All rights reserved.
  • (PMID = 19880105.001).
  • [ISSN] 1556-5653
  • [Journal-full-title] Fertility and sterility
  • [ISO-abbreviation] Fertil. Steril.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


17. Oktay K, Buyuk E, Veeck L, Zaninovic N, Xu K, Takeuchi T, Opsahl M, Rosenwaks Z: Embryo development after heterotopic transplantation of cryopreserved ovarian tissue. Lancet; 2004 Mar 13;363(9412):837-40
Hazardous Substances Data Bank. MENOTROPINS .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Embryo development after heterotopic transplantation of cryopreserved ovarian tissue.
  • BACKGROUND: Cancer treatments, including chemotherapy, radiotherapy, and radical surgery, can induce premature menopause and infertility in hundreds of thousands of women of reproductive age every year.
  • One of the ways to possibly preserve fertility before these treatments is to cryopreserve ovarian tissue for later transplantation.
  • We aimed to restore fertility by cryopreservation and transplantation of ovarian tissue.
  • METHODS: Ovarian tissue was cryopreserved from a 30-year-old woman with breast cancer before chemotherapy-induced menopause, and this tissue was transplanted beneath the skin of her abdomen 6 years later.
  • Of the eight oocytes suitable for in-vitro fertilisation, one fertilised normally and developed into a four-cell embryo.
  • INTERPRETATION: Fertility and ovarian endocrine function can be preserved in women by long-term ovarian tissue banking.
  • [MeSH-minor] Abdominal Wall / surgery. Adolescent. Antineoplastic Agents / adverse effects. Bone Marrow Transplantation. Breast Neoplasms / drug therapy. Breast Neoplasms / surgery. Estradiol / blood. Female. Follicle Stimulating Hormone / blood. Humans. Infertility, Female / blood. Infertility, Female / chemically induced. Infertility, Female / etiology. Male. Menopause, Premature / drug effects. Menopause, Premature / physiology. Oocytes / growth & development. Oocytes / physiology. Ovarian Follicle / growth & development. Sperm Injections, Intracytoplasmic

  • Genetic Alliance. consumer health - Transplantation.
  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • Hazardous Substances Data Bank. ESTRADIOL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Lancet. 2004 Mar 13;363(9412):832-3 [15031021.001]
  • [CommentIn] Lancet. 2004 May 29;363(9423):1830 [15172795.001]
  • [CommentIn] Lancet. 2004 May 29;363(9423):1829-30 [15172792.001]
  • (PMID = 15031026.001).
  • [ISSN] 1474-547X
  • [Journal-full-title] Lancet (London, England)
  • [ISO-abbreviation] Lancet
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 4TI98Z838E / Estradiol; 9002-68-0 / Follicle Stimulating Hormone
  •  go-up   go-down


18. Thaller C, Shalev M, Frolov A, Eichele G, Thompson TC, Williams RH, Dillioglugil O, Kadmon D: Fenretinide therapy in prostate cancer: effects on tissue and serum retinoid concentration. J Clin Oncol; 2000 Nov 15;18(22):3804-8
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Fenretinide therapy in prostate cancer: effects on tissue and serum retinoid concentration.
  • PURPOSE: To examine the feasibility of using fenretinide (4-HPR) for the prevention and treatment of prostate cancer.
  • MATERIALS AND METHODS: We measured the impact of 4-HPR therapy on retinoid concentrations in vivo, in a mouse model of prostate cancer and clinically, in patients with prostate cancer who were given oral 4-HPR (200 mg/d) or placebo for 4 weeks before undergoing a radical prostatectomy.
  • RESULTS: Prostate tumors in mice treated with 4-HPR contained high levels of 4-HPR and of all-trans-retinoic acid (RA) and reduced levels of retinol (ROH).
  • Patients given 4-HPR were found to have significantly higher concentrations of 4-HPR in the cancerous prostate as compared with the serum levels (463 nmol/L v 326 nmol/L; P =.049), but they were only 1/10 the levels found in mice and were far below the concentrations reported in human breast tissue.
  • Serum and tissue ROH levels were reduced to less than half the concentrations found in untreated controls.
  • RA concentrations in human serum and in cancerous prostates were not significantly affected by 4-HPR treatment, in contrast with the findings in mice.
  • CONCLUSION: The standard oral dose of 4-HPR proposed for breast cancer (200 mg/d) achieved only modest drug levels in the prostate and is unlikely to be effective for prostate cancer prevention or treatment.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Fenretinide / therapeutic use. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / metabolism. Tretinoin / metabolism. Vitamin A / metabolism
  • [MeSH-minor] Aged. Animals. Double-Blind Method. Humans. Male. Mice. Mice, Inbred C57BL. Middle Aged. Placebos. Prostatectomy

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • MedlinePlus Health Information. consumer health - Vitamin A.
  • Hazardous Substances Data Bank. ALL-TRANS-RETINOIC ACID .
  • Hazardous Substances Data Bank. VITAMIN A .
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11078493.001).
  • [ISSN] 0732-183X
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / MOI RR-00188; United States / PHS HHS / / P50-58204
  • [Publication-type] Clinical Trial; Journal Article; Randomized Controlled Trial; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Placebos; 11103-57-4 / Vitamin A; 187EJ7QEXL / Fenretinide; 5688UTC01R / Tretinoin
  •  go-up   go-down


19. Sumiyoshi K, Shibayama Y, Akashi S, Nohara T, Iwamoto M, Kobayashi T, Nishimura H, Yoshinaka R, Harada T, Tanigawa N: Detection of human epidermal growth factor receptor 2 protein and gene in fine needle aspiration cytology specimens and tissue sections from invasive breast cancer: can cytology specimens take the place of tissue sections? Oncol Rep; 2006 Apr;15(4):803-8
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Detection of human epidermal growth factor receptor 2 protein and gene in fine needle aspiration cytology specimens and tissue sections from invasive breast cancer: can cytology specimens take the place of tissue sections?
  • Overexpression of HER2 protein and HER2 gene amplification in breast cancer are prognostic factors for the response to specific medical treatments such as trastuzumab, endocrine therapy, and chemotherapy.
  • Whereas HER2 expression and gene amplification are generally examined in tissue sections, we investigated whether specimens from fine needle aspiration cytology (FNAC) are adequate for these analyses.
  • HER2 protein overexpression and HER2 gene amplification were assessed in both FNAC specimens and tissue sections from 58 cases of invasive breast cancer.
  • Immunohistochemistry assay for HER2 protein expression was performed according to the HercepTest protocol, and HER2 gene amplification was examined with the Spot-light CISH (chromogenic in situ hybridization) Detection kit.
  • There was a significant positive correlation between assessments of HER2 protein status in the cytology specimens and tissue sections.
  • The sensitivity, specificity, and accuracy of HER2 gene amplification detection in cytology specimens in relation to those in tissue sections were 84.0% (21/25 cases), 87.9% (29/33 cases), and 86.2% (50/58 cases), respectively.
  • FNAC specimens are suitable for detection of HER2 overexpression and HER2 gene amplification in invasive breast cancer.
  • [MeSH-major] Breast Neoplasms / pathology. Receptor, Epidermal Growth Factor / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biopsy, Fine-Needle / methods. Carcinoma, Ductal / genetics. Carcinoma, Ductal / metabolism. Carcinoma, Ductal / pathology. Chromosomes, Human, Pair 17 / genetics. Female. Gene Amplification. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. In Situ Hybridization / methods. Male. Microtomy / methods. Middle Aged. Neoplasm Invasiveness. Receptor, ErbB-2 / analysis. Receptor, ErbB-2 / genetics. Reproducibility of Results. Tissue Fixation

  • Genetic Alliance. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16525662.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] EC 2.7.10.1 / ERBB2 protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptor, ErbB-2
  •  go-up   go-down


20. Tani T, Okada K, Takahashi S, Suzuki N, Shimada Y, Itoi E: Doxorubicin-loaded calcium phosphate cement in the management of bone and soft tissue tumors. In Vivo; 2006 Jan-Feb;20(1):55-60
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Doxorubicin-loaded calcium phosphate cement in the management of bone and soft tissue tumors.
  • Several materials have been used as drug delivery systems to maintain a high concentration of anticancer drugs at localized sites.
  • The feasibility of using doxorubicin-loaded calcium phosphate cement (CPC) as a new material, which can release the drug as well as fill a postoperative bony defect, was investigated.
  • Culture medium incubated with doxorubicin-loaded CPC from 1 to 7 days suppressed the proliferation of RMT-1 E4 rat breast cancer cells.
  • Doxorubicin-loaded CPC markedly inhibited the proliferation of sarcoma 180 cells in the mouse air-pouch model.
  • These results indicate that doxorubicin-loaded CPC may be useful in the local treatment of malignant bone and soft tissue tumors.
  • [MeSH-major] Bone Neoplasms / drug therapy. Calcium Phosphates / chemistry. Doxorubicin / administration & dosage. Soft Tissue Neoplasms / drug therapy
  • [MeSH-minor] Animals. Biomechanical Phenomena. Cell Line, Tumor. Male. Rabbits. Rats

  • MedlinePlus Health Information. consumer health - Bone Cancer.
  • Hazardous Substances Data Bank. DOXORUBICIN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16433029.001).
  • [ISSN] 0258-851X
  • [Journal-full-title] In vivo (Athens, Greece)
  • [ISO-abbreviation] In Vivo
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Calcium Phosphates; 80168379AG / Doxorubicin; 97Z1WI3NDX / calcium phosphate
  •  go-up   go-down


21. Fang Z, Matsumoto S, Ae K, Kawaguchi N, Yoshikawa H, Ueda T, Ishii T, Araki N, Kito M: Postradiation soft tissue sarcoma: a multiinstitutional analysis of 14 cases in Japan. J Orthop Sci; 2004;9(3):242-6
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Postradiation soft tissue sarcoma: a multiinstitutional analysis of 14 cases in Japan.
  • Radiation therapy (RT) is commonly used to treat malignant tumors, but it leads to side effects and complications.
  • Postradiation sarcomas developing from a previously irradiated area are especially vicious to deal with, though their occurrence is rare.
  • This article focuses on the clinical manifestations, pathological characteristics, and therapeutic effects concerning postradiation soft tissue sarcomas (PRSTSs).
  • Their histological types were malignant fibrous histiocytoma (eight cases), extraskeletal osteosarcoma (four cases), fibrosarcoma (one case), and leiomyosarcoma (one case).
  • The primary diagnoses, RT history, latent period, and outcome of treatment were studied retrospectively.
  • The original tumors included uterine cancer (seven cases), breast cancer (four cases), synovial sarcoma (one case), squamous cell carcinoma (one case), and Hodgkin's disease (one case).
  • There were 13 women and 1 man, with ages ranging from 23 to 77 years (mean 58 years) at the time of the appearance of the PRSTS.
  • RT doses ranged from 48 to 91 Gy (mean 62 Gy).
  • Of the 10 patients whose tumors were removed with a wide margin, one had a local recurrence; 3 cases were performed with a marginal margin and all 3 had a local recurrence.
  • One of three who underwent RT and one of five who underwent chemotherapy (CT) responded.
  • Of the 14 patients, 6 (42.9 %) survived continuously disease free, 2 (14.3%) died from other causes, 2 (14.3%) has an unknown outcome, and 4 (28.6 %) died of the disease during the follow-up period of 16-36 months (mean 24 months).
  • The deaths due to other causes included an esophageal cancer and a wound infection.
  • The prognosis of the PRSTS patients was not poor if the tumor could be removed with a wide surgical margin.
  • Because adjuvant therapies including RT and CT had a poor effect on PRSTSs, the primary treatment of PRSTSs should be radical resection with a wide margin.
  • [MeSH-major] Neoplasms, Second Primary / surgery. Sarcoma / surgery. Soft Tissue Neoplasms / surgery
  • [MeSH-minor] Adult. Aged. Breast Neoplasms / radiotherapy. Female. Histiocytoma, Benign Fibrous / etiology. Histiocytoma, Benign Fibrous / surgery. Humans. Japan. Male. Middle Aged. Neoplasm Recurrence, Local. Radiotherapy / adverse effects. Radiotherapy Dosage. Uterine Neoplasms / radiotherapy

  • Genetic Alliance. consumer health - Soft tissue sarcoma.
  • MedlinePlus Health Information. consumer health - Soft Tissue Sarcoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] The Japanese Orthopaedic Association
  • (PMID = 15168177.001).
  • [ISSN] 0949-2658
  • [Journal-full-title] Journal of orthopaedic science : official journal of the Japanese Orthopaedic Association
  • [ISO-abbreviation] J Orthop Sci
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] Japan
  •  go-up   go-down


22. Marchettini P, Stuart OA, Mohamed F, Yoo D, Sugarbaker PH: Docetaxel: pharmacokinetics and tissue levels after intraperitoneal and intravenous administration in a rat model. Cancer Chemother Pharmacol; 2002 Jun;49(6):499-503
Hazardous Substances Data Bank. TAXOL .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Docetaxel: pharmacokinetics and tissue levels after intraperitoneal and intravenous administration in a rat model.
  • PURPOSE: Docetaxel (Taxotere) has been shown to possess a broad spectrum of antitumor activity against various malignancies such as breast and lung cancers, but also against intraabdominal malignancies such as mesothelioma and ovarian cancer.
  • For cancers occurring within the abdominal cavity, the advantage of intraperitoneal chemotherapy is the prolonged high drug concentration that can be achieved locally with low systemic toxicity.
  • Using a rat model, this study was designed to compare the pharmacokinetics and tissue distribution of intraperitoneal versus intravenous docetaxel.
  • At the end of the procedure the rats were killed and docetaxel concentrations in peritoneal fluid, plasma and selected tissue samples were determined by high-performance liquid chromatography (HPLC).
  • RESULTS: When docetaxel was delivered at 15 mg/kg the area under the curve (AUC) of the peritoneal fluid was significantly higher with intraperitoneal administration (110.6 microg/ml.min) as compared to intravenous administration (0.043 microg/ml.min; P=0.0079).
  • This represents more than a 2500-fold increase in exposure for tissues at peritoneal surfaces after intraperitoneal administration.
  • Also, high concentrations of drug were observed in the abdominal wall and in the colon after intraperitoneal delivery.
  • [MeSH-minor] Absorption. Animals. Area Under Curve. Dose-Response Relationship, Drug. Injections, Intraperitoneal. Injections, Intravenous. Male. Models, Animal. Neoplasms / drug therapy. Rats. Rats, Sprague-Dawley. Tissue Distribution

  • Hazardous Substances Data Bank. DOCETAXEL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12107555.001).
  • [ISSN] 0344-5704
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Taxoids; 15H5577CQD / docetaxel; P88XT4IS4D / Paclitaxel
  •  go-up   go-down


23. Sheldon DG, James TA, Kraybill WG: Palliative surgery of soft tissue sarcoma. Surg Oncol Clin N Am; 2004 Jul;13(3):531-41, ix
MedlinePlus Health Information. consumer health - Soft Tissue Sarcoma.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Palliative surgery of soft tissue sarcoma.
  • Despite an increasing trend towards early diagnosis of breast cancer,patients still present with locally advanced disease.
  • Also, in some patients chemotherapy will fail, and local and regional recurrence will occur.
  • [MeSH-major] Palliative Care / methods. Peritoneal Neoplasms / surgery. Quality of Life. Sarcoma / surgery. Soft Tissue Neoplasms / surgery
  • [MeSH-minor] Amputation / methods. Female. Humans. Male. Pain, Intractable / diagnosis. Pain, Intractable / therapy. Patient Selection. Randomized Controlled Trials as Topic. Risk Assessment. Survival Analysis. Terminally Ill. Treatment Outcome

  • Genetic Alliance. consumer health - Soft tissue sarcoma.
  • MedlinePlus Health Information. consumer health - Palliative Care.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15236734.001).
  • [ISSN] 1055-3207
  • [Journal-full-title] Surgical oncology clinics of North America
  • [ISO-abbreviation] Surg. Oncol. Clin. N. Am.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 34
  •  go-up   go-down


24. Dubois V, Dasnois L, Lebtahi K, Collot F, Heylen N, Havaux N, Fernandez AM, Lobl TJ, Oliyai C, Nieder M, Shochat D, Yarranton GT, Trouet A: CPI-0004Na, a new extracellularly tumor-activated prodrug of doxorubicin: in vivo toxicity, activity, and tissue distribution confirm tumor cell selectivity. Cancer Res; 2002 Apr 15;62(8):2327-31
Hazardous Substances Data Bank. DOXORUBICIN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] CPI-0004Na, a new extracellularly tumor-activated prodrug of doxorubicin: in vivo toxicity, activity, and tissue distribution confirm tumor cell selectivity.
  • The search for cancer therapies that are more selective for tumor cells and spare normal sensitive cells has been very active for at least 20 years.
  • The extracellularly tumor-activated peptidic prodrug of doxorubicin (Dox) CPI-0004Na (N-succinyl-beta-alanyl-L-leucyl-L-alanyl-L-leucyl-Dox) is potentially such a treatment.
  • Here, we report the results of lethality studies performed with this compound in the mouse, showing that it is up to 4.6 times less toxic than Dox.HCl by the i.v. route and up to 16.2 times after i.p. administration.
  • Pharmacokinetics and tissue distribution data indicate that this reduced toxicity is attributable to a lower uptake of Dox in normal tissues after treatment with CPI-0004Na than after the administration of an equimolar dose of Dox.HCl.
  • Because of this reduced toxicity, higher doses of CPI-0004Na than of the parent drug could be used to treat nude mice bearing s.c. human breast (MCF-7/6) and colon (LS-174-T and CXF-280/10) tumors.
  • Particularly, LS-174-T tumors that do not respond to Dox were inhibited by 68% after treatment with CPI-0004Na.
  • Tissue distribution studies performed with MCF-7/6 tumor-bearing nude mice and comparing CPI-0004Na and Dox.HCl confirmed that the improved activity of the prodrug is actually the result of selective generation and uptake of Dox at the tumor site.
  • Dox levels in tumor tissue were 2-fold higher after treatment with CPI-0004Na than after treatment with an equimolar dose of Dox.HCl, whereas normal tissue levels were reduced 1.4-29-fold.
  • [MeSH-minor] Animals. Breast Neoplasms / drug therapy. Breast Neoplasms / metabolism. Female. Humans. Male. Mice. Mice, Inbred BALB C. Mice, Nude. Tissue Distribution. Xenograft Model Antitumor Assays

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11956091.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / N-(succinyl-beta-alanyl-L-leucyl-L-alanyl-L-leucyl)doxorubicin; 0 / Oligopeptides; 0 / Prodrugs; 80168379AG / Doxorubicin
  •  go-up   go-down


25. Choi YH, Ahn JH, Kim SB, Jung KH, Gong GY, Kim MJ, Son BH, Ahn SH, Kim WK: Tissue microarray-based study of patients with lymph node-negative breast cancer shows that HER2/neu overexpression is an important predictive marker of poor prognosis. Ann Oncol; 2009 Aug;20(8):1337-43
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tissue microarray-based study of patients with lymph node-negative breast cancer shows that HER2/neu overexpression is an important predictive marker of poor prognosis.
  • BACKGROUND: Despite good prognosis in most cases of lymph node (LN)-negative breast cancer, individual patients may have markedly different clinical outcomes.
  • Here, we investigated the prognostic significance of HER2/neu overexpression in these tumors.
  • MATERIALS AND METHODS: We employed a tissue microarray to examine HER2/neu overexpression by immunohistochemical staining in 359 consecutive patients diagnosed with LN-negative breast cancer, who underwent surgery from January 1993 to December 1998.
  • The 10-year disease-free survival (DFS) values (81.2% versus 61.8%, P value 0.000) and overall survival (OS) rates (85.7% versus 63.9%, P value 0.000) were significantly different between cases with HER2/neu-negative or HER2/neu-positive tumors.
  • After multivariate analysis, HER2/neu status and tumor size were identified as independent prognostic factors for 10-year OS.
  • Moreover, HER2/neu overexpression was significantly associated with poorer clinical outcomes in an intermediate-risk group identified by the St Gallen classification (10-year DFS, 79.6% versus 61.8%, P value 0.000; 10-year OS, 84.7% versus 63.9%, P value 0.000).
  • CONCLUSIONS: Our results show that HER2/neu overexpression is an important independent prognostic factor for LN-negative breast cancer cases and support the theory that more intensive adjuvant chemotherapy is required in the population with HER2/neu overexpression.

  • Genetic Alliance. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19221151.001).
  • [ISSN] 1569-8041
  • [Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology
  • [ISO-abbreviation] Ann. Oncol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 2.7.10.1 / Receptor, ErbB-2
  •  go-up   go-down


26. Virtanen A, Pukkala E, Auvinen A: Incidence of bone and soft tissue sarcoma after radiotherapy: a cohort study of 295,712 Finnish cancer patients. Int J Cancer; 2006 Feb 15;118(4):1017-21
MedlinePlus Health Information. consumer health - Soft Tissue Sarcoma.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Incidence of bone and soft tissue sarcoma after radiotherapy: a cohort study of 295,712 Finnish cancer patients.
  • Radiotherapy is commonly used for treatment of malignant disease.
  • As a consequence of radiotherapy, an increased risk of developing a second malignant neoplasm has been shown.
  • The aim of this study was to examine the risk of developing a bone or soft tissue sarcoma after radiotherapy for a first primary cancer.
  • The study population included all the patients with primary cancers of breast, cervix uteri, corpus uteri, lung, ovary, prostate, rectum and lymphoma diagnosed during 1953-2000 and identified from the Finnish Cancer Registry.
  • Compared to the national incidence rates, after 10 years of follow-up sarcoma risk was increased among patients who had received neither radiotherapy nor chemotherapy (standardised incidence ratio (SIR) 2.0, 95% CI 1.3-3.0), radiotherapy without chemotherapy (SIR 3.2, 95% CI 2.3-4.3), chemotherapy without radiotherapy (SIR 4.9, 95% CI 1.0-14.4), as well as combined radiotherapy and chemotherapy (SIR 3.4, 95% CI 0.4-12.5).
  • In conclusion, radiotherapy appears to be associated with an increased risk of developing sarcoma especially among younger patients.
  • [MeSH-major] Bone Neoplasms / epidemiology. Bone Neoplasms / etiology. Neoplasms, Radiation-Induced / epidemiology. Osteosarcoma / epidemiology. Osteosarcoma / etiology. Sarcoma / epidemiology. Sarcoma / etiology
  • [MeSH-minor] Adult. Aged. Cohort Studies. Female. Finland / epidemiology. Humans. Incidence. Male. Middle Aged. Neoplasms / radiotherapy. Registries / statistics & numerical data. Risk Factors


27. Molina JR, Kaufmann SH, Reid JM, Rubin SD, Gálvez-Peralta M, Friedman R, Flatten KS, Koch KM, Gilmer TM, Mullin RJ, Jewell RC, Felten SJ, Mandrekar S, Adjei AA, Erlichman C: Evaluation of lapatinib and topotecan combination therapy: tissue culture, murine xenograft, and phase I clinical trial data. Clin Cancer Res; 2008 Dec 1;14(23):7900-8
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Evaluation of lapatinib and topotecan combination therapy: tissue culture, murine xenograft, and phase I clinical trial data.
  • PURPOSE: Topotecan resistance can result from drug efflux by P-glycoprotein (Pgp) and breast cancer resistance protein (BCRP) as well as survival signals initiated by epidermal growth factor receptor family members.
  • The present studies were done to determine the effect of combining topotecan and the dual epidermal growth factor receptor/HER2 inhibitor lapatinib in tissue culture, a murine xenograft model, and a phase I clinical trial.
  • Antiproliferative effects of the combination were assessed in mice bearing HER2+ BT474 breast cancer xenografts.
  • Based on tolerability in this preclinical model, 37 patients with advanced-stage cancers received escalating doses of lapatinib and topotecan in a phase I trial.
  • Pharmacokinetic analyses showed that combined drug administration resulted in decreased topotecan clearance consistent with transporter-mediated interactions.
  • Seventeen (46%) patients had disease stabilization.

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. Topotecan .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Natl Compr Canc Netw. 2007 Mar;5(3):314-23 [17439759.001]
  • [Cites] Pharmacol Ther. 2007 Feb;113(2):429-41 [17208306.001]
  • [Cites] Cell Prolif. 2007 Aug;40(4):580-94 [17635524.001]
  • [Cites] J Pharmacol Exp Ther. 2007 Sep;322(3):1246-52 [17556638.001]
  • [Cites] Expert Rev Anticancer Ther. 2007 Sep;7(9):1183-92 [17892419.001]
  • [Cites] Clin Cancer Res. 2007 Nov 1;13(21):6440-9 [17975156.001]
  • [Cites] Kidney Int. 2008 Jan;73(2):220-5 [17978814.001]
  • [Cites] Cancer Res. 2008 Jan 15;68(2):571-9 [18199554.001]
  • [Cites] Drug Metab Dispos. 2008 Apr;36(4):695-701 [18216274.001]
  • [Cites] Cancer Res. 1999 Dec 1;59(23):5938-46 [10606239.001]
  • [Cites] J Natl Cancer Inst. 2000 Feb 2;92(3):205-16 [10655437.001]
  • [Cites] Clin Cancer Res. 2000 May;6(5):2053-63 [10815932.001]
  • [Cites] J Natl Cancer Inst. 2000 Oct 18;92(20):1651-6 [11036110.001]
  • [Cites] Cancer Res. 2001 Jan 15;61(2):739-48 [11212277.001]
  • [Cites] Cancer Res. 2001 Apr 15;61(8):3458-64 [11309308.001]
  • [Cites] Clin Cancer Res. 2001 Apr;7(4):935-41 [11309344.001]
  • [Cites] Cancer Res. 2002 Mar 15;62(6):1676-81 [11912139.001]
  • [Cites] J Pathol. 2002 Oct;198(2):213-9 [12237881.001]
  • [Cites] J Biol Chem. 2002 Nov 15;277(46):44236-43 [12218061.001]
  • [Cites] Mol Cancer Ther. 2001 Dec;1(2):85-94 [12467226.001]
  • [Cites] Anticancer Drug Des. 1998 Jun;13(4):279-89 [9627668.001]
  • [Cites] Clin Cancer Res. 1999 Apr;5(4):909-16 [10213228.001]
  • [Cites] Cancer Res. 1999 Sep 15;59(18):4559-63 [10493507.001]
  • [Cites] Biochem J. 1953 Aug;55(1):170-1 [13093635.001]
  • [Cites] Cancer Res. 2005 Feb 15;65(4):1541-6 [15735043.001]
  • [Cites] Cancer Res. 2006 Feb 1;66(3):1630-9 [16452222.001]
  • [Cites] Nat Rev Drug Discov. 2006 Mar;5(3):219-34 [16518375.001]
  • [Cites] Curr Opin Investig Drugs. 2002 Nov;3(11):1652-9 [12476969.001]
  • [Cites] Oncogene. 2003 May 22;22(21):3205-12 [12761490.001]
  • [Cites] Oncogene. 2003 Oct 20;22(47):7340-58 [14576842.001]
  • [Cites] Oncogene. 2003 Oct 20;22(47):7537-52 [14576857.001]
  • [Cites] Rapid Commun Mass Spectrom. 2004;18(3):285-92 [14755613.001]
  • [Cites] Br J Cancer. 2004 Aug 16;91(4):795-802 [15280923.001]
  • [Cites] Nature. 1985 Aug 29-Sep 4;316(6031):817-9 [2863759.001]
  • [Cites] J Natl Cancer Inst. 1989 Jan 18;81(2):116-24 [2562856.001]
  • [Cites] Cancer Res. 1991 Nov 15;51(22):6039-44 [1682041.001]
  • [Cites] Cancer Res. 1992 Apr 15;52(8):2268-78 [1348448.001]
  • [Cites] J Natl Cancer Inst. 1993 Oct 20;85(20):1637-43 [8411243.001]
  • [Cites] Cancer Chemother Pharmacol. 1997;40 Suppl:S3-8 [9272126.001]
  • [Cites] Cancer Res. 2006 May 1;66(9):4802-7 [16651435.001]
  • [Cites] Oncology (Williston Park). 2006 Apr;20(5 Suppl 2):15-25 [16736979.001]
  • [Cites] Oncologist. 2006 Nov-Dec;11(10):1047-57 [17110623.001]
  • [Cites] Cancer Res. 2006 Dec 1;66(23):11305-13 [17145877.001]
  • [Cites] Nat Rev Drug Discov. 2007 Jun;6(6):431-2 [17633789.001]
  • (PMID = 19047120.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA090628-08; United States / NCI NIH HHS / CA / K12 CA090628-08; United States / NCI NIH HHS / CA / R01 CA073709; United States / NCI NIH HHS / CA / K12 CA090628; United States / NCI NIH HHS / CA / R01 CA73709; United States / NCI NIH HHS / CA / P30 CA015083; United States / NCI NIH HHS / CA / P30 CA15083
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Quinazolines; 0VUA21238F / lapatinib; 7M7YKX2N15 / Topotecan
  • [Other-IDs] NLM/ NIHMS121727; NLM/ PMC2725396
  •  go-up   go-down


28. Lotrionte M, Palazzoni G, Natali R, Comerci G, Abbate A, Loperfido F, Biondi-Zoccai G: Assessment of left ventricular systolic dysfunction by tissue Doppler imaging to detect subclinical cardiomyopathy early after anthracycline therapy. Minerva Cardioangiol; 2007 Dec;55(6):711-20
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Assessment of left ventricular systolic dysfunction by tissue Doppler imaging to detect subclinical cardiomyopathy early after anthracycline therapy.
  • AIM: Anthracycline (ANT) chemotherapy for breast cancer, while associated with high response rates, is fraught by risks of irreversible cardiotoxicity.
  • We evaluated the role of systolic tissue Doppler imaging (TDI) in appraising postchemotherapy left ventricular (LV) remodelling.
  • METHODS: Patients undergoing ANT-chemotherapy for breast cancer were enrolled, and underwent baseline and >6-months echocardiography (standard and TDI).
  • Follow-up overall analysis showed significant deterioration in LVEF, end-diastolic diameter (EDD) end-systolic diameter (ESD), and TDI-systolic parameters (all P<0.05).
  • CONCLUSION: Subclinical systolic dysfunction occurs in almost 50% of patients early after chemotherapy for breast cancer, with a more adverse by LV-TDI remodelling implying a more pronounced deterioration of standard echocardiographic parameters.
  • [MeSH-major] Anthracyclines / adverse effects. Breast Neoplasms / drug therapy. Cardiomyopathies / chemically induced. Echocardiography. Ventricular Dysfunction, Left / diagnosis
  • [MeSH-minor] Adult. Data Interpretation, Statistical. Diastole. Female. Follow-Up Studies. Humans. Male. Middle Aged. Systole. Time Factors

  • Genetic Alliance. consumer health - Cardiomyopathy.
  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Cardiomyopathy.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18091640.001).
  • [ISSN] 0026-4725
  • [Journal-full-title] Minerva cardioangiologica
  • [ISO-abbreviation] Minerva Cardioangiol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Anthracyclines
  •  go-up   go-down


29. Kluger HM, DiVito K, Berger AJ, Halaban R, Ariyan S, Camp RL, Rimm DL: Her2/neu is not a commonly expressed therapeutic target in melanoma -- a large cohort tissue microarray study. Melanoma Res; 2004 Jun;14(3):207-10
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Her2/neu is not a commonly expressed therapeutic target in melanoma -- a large cohort tissue microarray study.
  • Melanoma is among the most chemotherapy-resistant malignancies.
  • Numerous new agents have been developed that target specific molecules on cancer cells, including the monoclonal antibody trastuzumab, which targets Her2/neu and has been very beneficial in the treatment of breast cancer.
  • We therefore examined Her2/neu expression in a very large cohort of melanoma specimens in order to determine the value of exploring trastuzumab therapy for melanoma patients.
  • Immunohistochemical staining was performed on two tissue microarrays, together containing 600 intact specimens.
  • Expression was evaluated semi-quantitatively and correlated with tumour stage and other clinicopathological data.
  • Among the primary cutaneous specimens (n=269), 7% had positive Her2/neu staining, while 3.6% of the recurrent or metastatic specimens (n=331) had positive Her2/neu staining (P=0.06).
  • Among the primary lesions there was no significant correlation between Her2/neu expression, Clark level and ulceration; however, Her2/neu expression was associated with lesions with a Breslow depth of < 2 mm (P=0.05).
  • Using this very large cohort of melanoma specimens, we found only a few cases with aberrant Her2/neu expression, many of them being primary cutaneous lesions rather than recurrent or metastatic lesions.
  • Our findings suggest that drugs that specifically target Her2/neu are not likely to be useful for the treatment of metastatic melanoma or as adjuvant therapy for melanoma patients at high risk for recurrence.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Melanoma / genetics. Melanoma / therapy. Oligonucleotide Array Sequence Analysis. Receptor, ErbB-2 / genetics
  • [MeSH-minor] Cohort Studies. Female. Humans. Immunohistochemistry. Male. Neoplasm Staging

  • MedlinePlus Health Information. consumer health - Melanoma.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15179190.001).
  • [ISSN] 0960-8931
  • [Journal-full-title] Melanoma research
  • [ISO-abbreviation] Melanoma Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA44542; United States / NIGMS NIH HHS / GM / GM07205; United States / NIEHS NIH HHS / ES / K08 ES11571; United States / NCI NIH HHS / CA / R21 CA100825-01
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.1 / Receptor, ErbB-2
  •  go-up   go-down


30. Hayashi M, Tsuchiya H, Yamamoto N, Karita M, Shirai T, Nishida H, Takeuchi A, Tomita K: Caffeine-potentiated chemotherapy for metastatic carcinoma and lymphoma of bone and soft tissue. Anticancer Res; 2005 May-Jun;25(3c):2399-405
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Caffeine-potentiated chemotherapy for metastatic carcinoma and lymphoma of bone and soft tissue.
  • BACKGROUND: We previously reported that caffeine-potentiated chemotherapy induced significantly good response in patients with musculoskeletal sarcomas.
  • In that series, patients with metastatic carcinoma or lymphoma were treated with caffeine-potentiated chemotherapy.
  • PATIENTS AND METHODS: Five patients with metastatic carcinoma or lymphoma were treated with caffeine-potentiated chemotherapy.
  • RESULTS: Primary tumors were diagnosed as breast cancer, adenocarcinoma of the lung, clear cell adenocarcinoma of the vagina, diffuse large B-cell lymphoma and gastric cancer.
  • Good responses (gross tumor shrinkage >30%, or histologically >90% necrosis) to chemotherapy were seen in all five patients.
  • Survival time was >1 year in all patients, and three out of five patients presented no evidence of local recurrence or metastasis at the final follow-up.
  • CONCLUSION: Caffeine-potentiated chemotherapy may be of benefit for malignant tumors other than musculoskeletal sarcoma.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bone Neoplasms / drug therapy. Caffeine / pharmacology. Carcinoma / drug therapy. Lymphoma, B-Cell / drug therapy. Lymphoma, Large B-Cell, Diffuse / drug therapy. Soft Tissue Neoplasms / drug therapy
  • [MeSH-minor] Aged. Breast Neoplasms / drug therapy. Breast Neoplasms / pathology. Drug Synergism. Female. Humans. Lung Neoplasms / drug therapy. Lung Neoplasms / pathology. Male. Middle Aged. Stomach Neoplasms / drug therapy. Stomach Neoplasms / pathology. Vaginal Neoplasms / drug therapy. Vaginal Neoplasms / pathology

  • MedlinePlus Health Information. consumer health - Bone Cancer.
  • MedlinePlus Health Information. consumer health - Caffeine.
  • Hazardous Substances Data Bank. CAFFEINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16080466.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 3G6A5W338E / Caffeine
  •  go-up   go-down


31. Pentheroudakis G, Greco FA, Pavlidis N: Molecular assignment of tissue of origin in cancer of unknown primary may not predict response to therapy or outcome: a systematic literature review. Cancer Treat Rev; 2009 May;35(3):221-7
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular assignment of tissue of origin in cancer of unknown primary may not predict response to therapy or outcome: a systematic literature review.
  • BACKGROUND: Gene expression profiling platforms were recently shown to accurately assign cancer of unknown primary (CUP) to a primary tissue of origin, with unknown impact on patient outcome.
  • We examined chemotherapy activity and outcome in CUP trials and in metastatic solid tumour trials in order to screen for a distinct biological behaviour of CUP.
  • Chemotherapy activity and patient survival data were narratively compared to data from phase III chemotherapy trials on patients with metastatic breast, lung, pancreatic and colon cancer, to which CUP is most commonly classified by molecular profiling.
  • RESULTS: Lung and pancreatic tumours were the primaries most commonly found in CUP autopsy series, whereas microarray platforms assigned CUP to breast, colon in a third and pancreatic, lung primaries in <25% of cases.
  • 14 phase II trials managed 918 CUP patients with platinum-based chemotherapy resulting in objective response rate (ORR) of 32%.
  • Six trials administered anthracycline-containing or gastrointestinal-type chemotherapy in 401 CUP patients, reporting ORR of 22%.
  • The median of quoted median survival times was nine months for platinum and seven for anthracycline or GI-type regimens.
  • Though tumour shrinkage and median survival in CUP patients were similar to those of patients with metastatic lung and pancreatic cancer, they were vastly inferior to response rates of 40-70% and median survival of 15-24 months seen in patients with metastatic breast and bowel cancer.
  • CONCLUSION: This systematic review hints that CUP, though accurately classified by molecular methods, may harbour molecular/genetic traits distinct from tumours of known primaries.
  • These should be sought and the impact of molecularly classified primary site-directed therapy on patient outcome prospectively validated in trials.
  • [MeSH-major] Gene Expression Profiling. Neoplasms, Unknown Primary / pathology
  • [MeSH-minor] Anthracyclines / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Autopsy. Clinical Trials as Topic / statistics & numerical data. DNA, Neoplasm / analysis. Female. Gastrointestinal Neoplasms / drug therapy. Humans. Male. Neoplasm Metastasis / drug therapy. Neoplasm Metastasis / pathology. Neoplasm Proteins / analysis. Organ Specificity. Organoplatinum Compounds / administration & dosage. Prognosis. RNA, Neoplasm / analysis. Survival Analysis. Treatment Outcome

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19046817.001).
  • [ISSN] 1532-1967
  • [Journal-full-title] Cancer treatment reviews
  • [ISO-abbreviation] Cancer Treat. Rev.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Anthracyclines; 0 / DNA, Neoplasm; 0 / Neoplasm Proteins; 0 / Organoplatinum Compounds; 0 / RNA, Neoplasm
  • [Number-of-references] 67
  •  go-up   go-down


32. Schöffski P, Blay JY, De Greve J, Brain E, Machiels JP, Soria JC, Sleijfer S, Wolter P, Ray-Coquard I, Fontaine C, Munzert G, Fritsch H, Hanft G, Aerts C, Rapion J, Allgeier A, Bogaerts J, Lacombe D: Multicentric parallel phase II trial of the polo-like kinase 1 inhibitor BI 2536 in patients with advanced head and neck cancer, breast cancer, ovarian cancer, soft tissue sarcoma and melanoma. The first protocol of the European Organization for Research and Treatment of Cancer (EORTC) Network Of Core Institutes (NOCI). Eur J Cancer; 2010 Aug;46(12):2206-15
ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Multicentric parallel phase II trial of the polo-like kinase 1 inhibitor BI 2536 in patients with advanced head and neck cancer, breast cancer, ovarian cancer, soft tissue sarcoma and melanoma. The first protocol of the European Organization for Research and Treatment of Cancer (EORTC) Network Of Core Institutes (NOCI).
  • We performed a multi-centre, multi-tumour phase II trial to investigate the efficacy, safety and pharmacokinetics of BI 2536 in five solid tumour types.
  • PATIENTS AND METHODS: Patients with advanced head and neck, breast and ovarian cancer, soft tissue sarcoma and melanoma were selected according to protocol-defined general and tumour-specific criteria.
  • They were 18years old, had a good performance status, adequate bone marrow, renal and liver function, measurable progressive disease and had completed other relevant systemic treatments >4weeks ago.
  • The rate of objective responses (RECIST criteria) was chosen as primary end-point.
  • RESULTS: Seventy six patients were included, 71 started treatment and received a median number of two cycles (four in ovarian cancer).
  • CONCLUSIONS: BI 2536 showed limited antitumour activity according to the design of this trial in five different tumour types.
  • Derivatives of BI 2536 with a more favourable pharmacological profile are currently explored further in prospective studies.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Neoplasms / drug therapy. Pteridines / administration & dosage
  • [MeSH-minor] Adult. Aged. Breast Neoplasms / drug therapy. Breast Neoplasms / metabolism. Feasibility Studies. Female. Head and Neck Neoplasms / drug therapy. Head and Neck Neoplasms / metabolism. Humans. Infusions, Intravenous. Male. Melanoma / drug therapy. Melanoma / metabolism. Middle Aged. Ovarian Neoplasms / drug therapy. Ovarian Neoplasms / metabolism. Patient Compliance. Sarcoma / drug therapy. Sarcoma / metabolism. Treatment Outcome. Young Adult

  • Genetic Alliance. consumer health - Ovarian cancer.
  • Genetic Alliance. consumer health - Soft tissue sarcoma.
  • Genetic Alliance. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20471824.001).
  • [ISSN] 1879-0852
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / BI 2536; 0 / Pteridines
  •  go-up   go-down


33. Tanaka Y, Slitt AL, Leazer TM, Maher JM, Klaassen CD: Tissue distribution and hormonal regulation of the breast cancer resistance protein (Bcrp/Abcg2) in rats and mice. Biochem Biophys Res Commun; 2005 Jan 07;326(1):181-7
Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tissue distribution and hormonal regulation of the breast cancer resistance protein (Bcrp/Abcg2) in rats and mice.
  • Breast cancer resistance protein (Bcrp/Abcg2) is a member of the ABC transporter family.
  • The purpose of this study was to quantify Bcrp mRNA in rat and mouse tissues, and to determine whether there are gender differences in Bcrp mRNA expression.
  • Rat Bcrp mRNA levels were high in intestine and male kidney, and intermediate in testes.
  • Male-predominant expression of Bcrp was observed in rat kidney and mouse liver.
  • Furthermore, gonadectomy and hypophysectomy experiments were conducted to determine whether sex steroids and/or growth hormone are responsible for Bcrp gender-divergent expression patterns.
  • Male-predominant expression of Bcrp in rat kidney appears to be due to the suppressive effect of estradiol, and male-predominant expression of Bcrp in mouse liver appears to be due to the inductive effect of testosterone.
  • [MeSH-minor] ATP Binding Cassette Transporter, Sub-Family G, Member 2. Animals. Castration. Female. Hormone Replacement Therapy / methods. Hypophysectomy. Male. Mice. Mice, Inbred C57BL. Organ Specificity / drug effects. Ovariectomy. Rats. Rats, Sprague-Dawley. Sex Factors. Species Specificity. Tissue Distribution / drug effects

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. ESTRADIOL .
  • Hazardous Substances Data Bank. TESTOSTERONE .
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15567169.001).
  • [ISSN] 0006-291X
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Grant] United States / NIEHS NIH HHS / ES / ES-09714; United States / NIEHS NIH HHS / ES / F32 ES011239; United States / NIEHS NIH HHS / ES / F32 ES011239-01; United States / NIEHS NIH HHS / ES / ES-07079; United States / NIEHS NIH HHS / ES / F32 ES011239-02
  • [Publication-type] Comparative Study; Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ATP Binding Cassette Transporter, Sub-Family G, Member 2; 0 / ATP-Binding Cassette Transporters; 0 / Abcg2 protein, rat; 3XMK78S47O / Testosterone; 4TI98Z838E / Estradiol
  •  go-up   go-down


34. Dicker AP: The safety and tolerability of low-dose irradiation for the management of gynaecomastia caused by antiandrogen monotherapy. Lancet Oncol; 2003 Jan;4(1):30-6
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Gynaecomastia--a benign and often painful enlargement of the male breast--is a common side-effect of some therapies for prostate cancer, including non-steroidal antiandrogen monotherapy.
  • Although gynaecomastia and breast pain are not harmful to the overall health of the patient, they can be serious enough to influence treatment decisions in the management of prostate cancer.
  • Prophylactic low-dose irradiation can be effective in reducing the incidence and severity of both gynaecomastia and breast pain.
  • In addition, irradiation may be effective in treating breast pain due to the development of gynaecomastia.
  • Low-dose electron irradiation confers advantageous tissue dosing, is well tolerated, and has manageable side-effects, the most common of which is reversible skin erythema.
  • Irradiation is likely to be an effective management option with an acceptable low risk of long-term complications for gynaecomastia associated with hormone therapy for prostate cancer.
  • [MeSH-minor] Breast Neoplasms / etiology. Breast Neoplasms, Male / etiology. Female. Humans. Male. Neoplasms, Radiation-Induced. Prostatic Neoplasms / drug therapy. Radiotherapy Dosage. Risk Factors

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12517537.001).
  • [ISSN] 1470-2045
  • [Journal-full-title] The Lancet. Oncology
  • [ISO-abbreviation] Lancet Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Androgen Antagonists
  • [Number-of-references] 54
  •  go-up   go-down


35. Beyrouti MI, Beyrouti R, Beyrouti R, Ben Amar M, Affes N, Frikha F, Abid M, Mnif H, Ayadi L, Ghorbel A: [Breast cancer in men]. Presse Med; 2007 Dec;36(12 Pt 3):1919-24
MedlinePlus Health Information. consumer health - Male Breast Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Breast cancer in men].
  • [Transliterated title] Cancer du sein chez l'homme.
  • Breast cancer in men is rare and most often occurs at or after the age of 60 years.
  • Prognosis is poor when it is discovered at a late stage, as it often is in men, although it should be easier to detect because men have so little breast tissue.
  • A family history of breast cancer is found in 5-10% of cases.
  • Infiltrating ductal carcinoma accounts for most cases (70-90%) of male breast cancers.
  • Immunohistochemical analysis shows that tumors are positive for progesterone and estrogen receptors more frequently in men than women.
  • Diagnosis is based on clinical examination, ultrasonography, and mammography.
  • Aspiration cytology often makes it possible to confirm the malignancy.
  • Excisional biopsy with an immediate intraoperative pathology examination confirms malignancy and makes wider excision possible during the same procedure.
  • A modified radical mastectomy with removal of some lymph nodes (Patey's mastectomy) is the standard basic treatment.
  • Hormone therapy is also a first-line treatment.
  • Chemotherapy is reserved for young men with substantial lymph node invasion and negative for hormonal receptors.
  • The prognosis of breast cancer in men remains uncertain because of the frequently late diagnosis, unpredictable course, and high potential for metastasis.
  • [MeSH-major] Breast Neoplasms, Male
  • [MeSH-minor] Adolescent. Adult. Age Factors. Aged. Aged, 80 and over. Biopsy. Breast / pathology. Carcinoma, Ductal, Breast / epidemiology. Child. Female. Humans. Incidence. Male. Mammography. Mastectomy, Modified Radical. Middle Aged. Prognosis. Ultrasonography, Mammary

  • Genetic Alliance. consumer health - Breast Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17448628.001).
  • [ISSN] 0755-4982
  • [Journal-full-title] Presse medicale (Paris, France : 1983)
  • [ISO-abbreviation] Presse Med
  • [Language] fre
  • [Publication-type] Comparative Study; Journal Article; Review
  • [Publication-country] France
  • [Number-of-references] 59
  •  go-up   go-down


36. Ford CE, Faedo M, Crouch R, Lawson JS, Rawlinson WD: Progression from normal breast pathology to breast cancer is associated with increasing prevalence of mouse mammary tumor virus-like sequences in men and women. Cancer Res; 2004 Jul 15;64(14):4755-9
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Progression from normal breast pathology to breast cancer is associated with increasing prevalence of mouse mammary tumor virus-like sequences in men and women.
  • Mouse mammary tumor virus (MMTV)-like sequences have been found in up to 40% of breast cancer samples but in <2% of normal breast tissue samples from Australian women studied by our group.
  • Screening of a larger and more diverse cohort of female breast cancer samples has now shown a correlation of MMTV-like sequences with the severity (grade) of breast cancer.
  • Thirty-two percent (43 of 136) of female breast cancer samples were positive for MMTV-like sequences when screened using PCR.
  • A significant gradient of MMTV positivity was observed with increasing severity of cancer from 23% of infiltrating ductal carcinoma (IDC) grade I tumors to 34% of IDC grade II tumors (P = 0.00034) and 38% of IDC grade III tumors (P = 0.00002).
  • We also report for the first time the detection of MMTV-like sequences in 62% (8 of 13) of male breast cancer samples and 19% (10 of 52) of male gynecomastia samples screened.
  • MMTV-like sequences were demonstrated in various premalignant breast lesions of females, including fibroadenoma (20%) and fibrocystic disease (28%) samples, at a significantly higher prevalence than that seen in normal breast tissue (1.8%; P = 0.00001).
  • Study of a longitudinal cohort of female breast cancer patients indicated that MMTV was co-incident with tumor but was not present when tumor was absent on histology.
  • These results support the association of MMTV-like sequences with development of breast tumors in men and women and suggest association of MMTV with increasing severity of cancer.
  • [MeSH-major] Breast Neoplasms / virology. Breast Neoplasms, Male / virology. Cell Transformation, Viral / genetics. Mammary Tumor Virus, Mouse / genetics. Precancerous Conditions / virology
  • [MeSH-minor] Adult. Aged. Animals. Breast / cytology. Carcinoma in Situ / genetics. Carcinoma in Situ / virology. Carcinoma, Ductal / genetics. Carcinoma, Ductal / virology. Cohort Studies. Disease Progression. Female. Humans. Longitudinal Studies. Male. Mice. Middle Aged. NIH 3T3 Cells. Sex Factors

  • Genetic Alliance. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Male Breast Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15256443.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  •  go-up   go-down


37. Leibovitch I, Gillatt D, Hopwood P, Iversen P, Mansel RE, McLeod D, Vela-Navarrete R, Richaud P, See W, Tyrrell C, Wirth M: Management options for gynaecomastia and breast pain associated with nonsteroidal antiandrogen therapy : case report series. Clin Drug Investig; 2003;23(3):205-15

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Management options for gynaecomastia and breast pain associated with nonsteroidal antiandrogen therapy : case report series.
  • OBJECTIVE: To present management options for gynaecomastia and mastodynia associated with nonsteroidal antiandrogen therapy, supported by relevant data and case studies.
  • BACKGROUND: Gynaecomastia (male breast enlargement) and breast pain/ sensitivity (mastodynia or mastalgia) are pharmacologically expected adverse effects of nonsteroidal antiandrogen therapy for prostate cancer.
  • They are caused by proliferation of glandular tissue in response to an increase in the ratio of estrogen to androgen.
  • Gynaecomastia and mastodynia are benign conditions, and many patients choose to tolerate them as acceptable, usually mild or moderate, adverse effects of therapy.
  • Recent data show that nonsteroidal antiandrogen monotherapy significantly reduces disease progression in localised and locally advanced prostate cancer, a finding that may result in wider and more long-term use of this treatment.
  • (1) risk reduction using pretreatment breast irradiation;.
  • (2) stopping antiandrogen therapy;.
  • (3) acceptance of gynaecomastia and/or mastodynia in the context of the significant clinical benefit of antiandrogen treatment;.
  • (4) prompt treatment (liposuction/breast tissue excision, hormonal manipulation or pain control with irradiation or analgesics); and (5) later treatment (liposuction/breast tissue excision, hormonal manipulation or pain control with irradiation or analgesics).
  • CONCLUSIONS: The risk of developing gynaecomastia is lessened by prophylactic breast irradiation.
  • Following the development of gynaecomastia, treatment options include readjustment of the estrogen-to-androgen ratio using antiestrogens, surgery in the form of liposuction or, for more advanced cases, breast tissue excision.
  • Mastodynia may be controlled by post-treatment irradiation or analgesics.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Urol. 1965 Nov;94(5):604-6 [5846201.001]
  • [Cites] J Urol. 1969 Nov;102(5):607-9 [5347770.001]
  • [Cites] J Urol. 2002 Aug;168(2):429-35 [12131282.001]
  • [Cites] Endocr Relat Cancer. 1999 Jun;6(2):315-24 [10731125.001]
  • [Cites] Eur Urol. 1998;33(5):447-56 [9643663.001]
  • [Cites] Lancet Oncol. 2003 Jan;4(1):30-6 [12517537.001]
  • [Cites] N Engl J Med. 1993 Feb 18;328(7):490-5 [8421478.001]
  • [Cites] Am J Roentgenol Radium Ther Nucl Med. 1973 Mar;117(3):662-3 [4693024.001]
  • [Cites] J Urol. 1979 Feb;121(2):182-4 [423330.001]
  • [Cites] Oncologist. 1997;2(1):18-27 [10388026.001]
  • [Cites] J Urol. 1969 Sep;102(3):336-7 [5808889.001]
  • [Cites] J Urol. 1998 Apr;159(4):1309 [9507867.001]
  • [Cites] J Clin Oncol. 1999 Jul;17(7):2027-38 [10561254.001]
  • [Cites] Urology. 1997 Dec;50(6):929-33 [9426725.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1988 Sep;15(3):749-51 [2458332.001]
  • [Cites] Urology. 1974 Jan;3(1):51-3 [4812899.001]
  • [Cites] Clin Oncol. 1979 Sep;5(3):257-60 [498617.001]
  • [Cites] J Urol. 2000 Nov;164(5):1579-82 [11025708.001]
  • [Cites] Metabolism. 1986 Aug;35(8):705-8 [3526085.001]
  • [Cites] Urology. 2001 Aug;58(2):146-51 [11489683.001]
  • [Cites] Urology. 2000 Nov 1;56(5):713-20 [11068286.001]
  • [Cites] Pediatr Clin North Am. 1990 Dec;37(6):1389-404 [2259545.001]
  • [Cites] J Urol. 1972 Apr;107(4):624-5 [5014373.001]
  • [Cites] Scand J Urol Nephrol. 1969;3(3):183-7 [5375746.001]
  • [Cites] South Med J. 1990 Nov;83(11):1283-5 [2237557.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1986 Mar;12(3):407-8 [3957739.001]
  • [Cites] Eur Urol. 1999;36 Suppl 2:20-6 [10529562.001]
  • [Cites] J Clin Endocrinol Metab. 1979 Feb;48(2):338-40 [429488.001]
  • [Cites] Am J Roentgenol Radium Ther Nucl Med. 1969 Aug;106(4):839-40 [5806013.001]
  • [Cites] Prostate Cancer Prostatic Dis. 1999 Jul;2(4):167-171 [12496773.001]
  • (PMID = 23340926.001).
  • [ISSN] 1173-2563
  • [Journal-full-title] Clinical drug investigation
  • [ISO-abbreviation] Clin Drug Investig
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] New Zealand
  •  go-up   go-down


38. Prezioso D, Piccirillo G, Galasso R, Altieri V, Mirone V, Lotti T: Gynecomastia due to hormone therapy for advanced prostate cancer: a report of ten surgically treated cases and a review of treatment options. Tumori; 2004 Jul-Aug;90(4):410-5
MedlinePlus Health Information. consumer health - Prostate Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gynecomastia due to hormone therapy for advanced prostate cancer: a report of ten surgically treated cases and a review of treatment options.
  • AIMS AND BACKGROUND: Gynecomastia is an abnormal increase in the volume of the male breast that is generally considered to be due to an increased estrogen/androgen ratio.
  • Pathological causes of gynecomastia include organic diseases and therapy, such as the administration of estrogens and antiandrogens, which alter the ratio of circulating hormones.
  • Hormone therapy for prostate cancer is generally well tolerated but often accompanied by the occurrence of gynecomastia and breast pain or tenderness.
  • Treatments are available to alleviate or prevent the development of gynecomastia, including medical treatment with antiestrogens and aromatase inhibitors.
  • Alternatively, mastectomy with excision of the gland, liposuction or an association of the two techniques have proved to be effective.
  • Radiation therapy may provide effective relief from the breast pain associated with gynecomastia.
  • In this paper we show the good results of mastectomy performed with a lower semicircular periareolar incision in men suffering from gynecomastia due to antiandrogen therapy for inoperable prostate cancer.
  • In addition, we present a review of the various techniques used for the treatment of gynecomastia.
  • METHODS AND STUDY DESIGN: During the period from September 1998 to May 2001, 10 patients receiving hormone treatment for metastatic or inoperable prostatic cancer were selected for the study if they had breast pain and bilateral gynecomastia.
  • Five of these patients had been offered prophylactic radiotherapy before treatment but refused, while the remaining five patients had refused radiotherapy after hormone treatment.
  • These patients were therefore given the option of surgical treatment.
  • Before surgery all patients underwent clinical and ultrasound examination of the breast.
  • Moreover, breast pain disappeared about one week after surgery.
  • Histological examination of the excised glands showed fibrosclerotic tissue and a small amount of fat.
  • CONCLUSION: Surgical liposuction can be considered an effective treatment for gynecomastia, in particular in the very early stages because the breast becomes irreversibly fibrous as the disease progresses.
  • [MeSH-major] Androgen Antagonists / adverse effects. Antineoplastic Agents, Hormonal / adverse effects. Gynecomastia / chemically induced. Gynecomastia / surgery. Lipectomy. Mastectomy. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Humans. Male. Middle Aged. Neoplasm Staging. Retrospective Studies. Treatment Outcome

  • Genetic Alliance. consumer health - TEN.
  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Mastectomy.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15510985.001).
  • [ISSN] 0300-8916
  • [Journal-full-title] Tumori
  • [ISO-abbreviation] Tumori
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Antineoplastic Agents, Hormonal
  •  go-up   go-down


39. Ortiz R, Au JL, Lu Z, Gan Y, Wientjes MG: Biodegradable intraprostatic doxorubicin implants. AAPS J; 2007 Jun 29;9(2):E241-50
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Systemic chemotherapy is not effective in the treatment of prostate-confined cancer.
  • We developed biodegradable, doxorubicin-loaded cylinders for intraprostatic implantation and evaluated the feasibility of using regional intraprostatic drug therapy to treat prostate-confined cancer.
  • The in vitro and in vivo drug release, intraprostatic pharmacokinetics, and histopathology in dogs implanted with the cylinders were studied.
  • The doxorubicin-loaded cylinders made of PLG polymers of 7.9 to 54 kDa molecular weight (MW) had a diameter of ~800 mum, drug loading of 10% to 30% (wt/wt), and even distribution of crystalline drug throughout the matrix.
  • Decreasing polymer MW and increasing drug loading were associated with higher initial burst release and overall release rates.
  • The in vivo drug release from cylinders (33-kDa PLG, 30% drug loading) in dog prostates was rapid (approximately 80% in 48 hours).
  • Spatial drug distribution, visualized using confocal fluorescence microscopy, showed high concentrations confined to the lobule containing the implant (referred to as the implanted lobule), with steep concentration gradients over the septa separating the lobules.
  • Concentrations in the implanted lobule were about 8 times higher than concentrations delivered by an intravenous injection.
  • These results indicate the feasibility of using biodegradable PLG cylinders as intraprostatic implants to selectively deliver high drug concentrations to prostate tissue.

  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. DOXORUBICIN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Surg Oncol. 1997 Sep;66(1):65-75 [9290696.001]
  • [Cites] J Urol. 1992 Nov;148(5):1457-60 [1279212.001]
  • [Cites] Eur J Surg Oncol. 1997 Oct;23(5):409-14 [9393568.001]
  • [Cites] Hepatogastroenterology. 1997 Nov-Dec;44(18):1541-6 [9427019.001]
  • [Cites] Clin Cancer Res. 1998 Feb;4(2):277-82 [9516911.001]
  • [Cites] Eur J Surg Oncol. 2000 Feb;26(1):73-9 [10718184.001]
  • [Cites] Int J Pharm. 2001 Feb 1;213(1-2):103-16 [11165098.001]
  • [Cites] J Control Release. 2001 Jul 6;74(1-3):31-46 [11489481.001]
  • [Cites] CA Cancer J Clin. 2003 Jan-Feb;53(1):5-26 [12568441.001]
  • [Cites] Ann Oncol. 2003;14 Suppl 3:iii26-30 [12821535.001]
  • [Cites] Breast Cancer Res Treat. 1986;7(3):129-45 [3096402.001]
  • [Cites] Urol Res. 1989;17(1):43-6 [2493705.001]
  • [Cites] Eur J Cancer Clin Oncol. 1989 Mar;25(3):505-11 [2703005.001]
  • [Cites] Gynecol Oncol. 1990 Jan;36(1):1-6 [2403957.001]
  • [Cites] Vet Pathol. 1990 Sep;27(5):347-53 [1700534.001]
  • [Cites] Biomaterials. 1990 Nov;11(9):699-701 [2090306.001]
  • [Cites] J Pharm Biomed Anal. 1991;9(10-12):995-1002 [1822225.001]
  • [Cites] J Cancer Res Clin Oncol. 1993;119(8):457-62 [8509436.001]
  • [Cites] Pharm Res. 1993 Jul;10(7):1093-5 [8378254.001]
  • [Cites] J Biomater Sci Polym Ed. 1995;6(9):775-95 [7772566.001]
  • [Cites] Ann Surg Oncol. 1996 Jan;3(1):44-50 [8770301.001]
  • [Cites] Pharm Res. 1996 May;13(5):671-82 [8860421.001]
  • [Cites] Drugs. 1997 Mar;53(3):358-88 [9074840.001]
  • [Cites] Lancet. 1997 Mar 29;349(9056):906-10 [9093251.001]
  • [Cites] Gynecol Oncol. 1998 Mar;68(3):267-73 [9570979.001]
  • [Cites] Cancer Res. 1998 Jul 1;58(13):2777-83 [9661891.001]
  • [Cites] Hepatogastroenterology. 1998 May-Jun;45(21):638-43 [9684109.001]
  • [Cites] J Clin Oncol. 1998 Sep;16(9):3000-6 [9738568.001]
  • [Cites] Hepatogastroenterology. 1998 Jul-Aug;45(22):1125-9 [9756018.001]
  • [Cites] J Control Release. 1998 Nov 13;55(2-3):281-95 [9795083.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1998 Dec 1;42(5):1063-7 [9869230.001]
  • [Cites] Cancer. 1999 Feb 15;85(4):980-7 [10091778.001]
  • [Cites] Gan To Kagaku Ryoho. 1999 Mar;26(4):509-14 [10097748.001]
  • [Cites] N Engl J Med. 2005 May 12;352(19):1977-84 [15888698.001]
  • [Cites] Clin Cancer Res. 2005 Jun 1;11(11):4204-11 [15930358.001]
  • [Cites] CA Cancer J Clin. 2005 Sep-Oct;55(5):300-18; quiz 323-5 [16166075.001]
  • [Cites] Expert Opin Drug Deliv. 2005 Mar;2(2):363-76 [16296760.001]
  • [Cites] Anticancer Res. 2005 Nov-Dec;25(6B):3825-31 [16312042.001]
  • [Cites] Crit Rev Oncol Hematol. 2005 Dec;56(3):379-96 [16310371.001]
  • [Cites] Urology. 2006 Sep;68(3):463-9 [17010721.001]
  • [Cites] Neurosurgery. 2006 Dec;59(6):1296-302; discussion 1302-3 [17277693.001]
  • [Cites] Clin Cancer Res. 2007 Feb 15;13(4):1278-87 [17317840.001]
  • [Cites] Pharm Res. 1997 Oct;14(10):1406-14 [9358554.001]
  • (PMID = 17907765.001).
  • [ISSN] 1550-7416
  • [Journal-full-title] The AAPS journal
  • [ISO-abbreviation] AAPS J
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01CA74179
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 80168379AG / Doxorubicin
  • [Other-IDs] NLM/ PMC2751414
  •  go-up   go-down


40. Ross JS, Fletcher JA, Linette GP, Stec J, Clark E, Ayers M, Symmans WF, Pusztai L, Bloom KJ: The Her-2/neu gene and protein in breast cancer 2003: biomarker and target of therapy. Oncologist; 2003;8(4):307-25
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The Her-2/neu gene and protein in breast cancer 2003: biomarker and target of therapy.
  • The HER-2/neu oncogene encodes a transmembrane tyrosine kinase receptor with extensive homology to the epidermal growth factor receptor.
  • In this review, the association of HER-2/neu gene and protein abnormalities with prognosis and response to therapy with trastuzumab and to other therapies in breast cancer is presented.
  • By considering a series of 80 published studies encompassing more than 25,000 patients, the relative advantages and disadvantages of Southern blotting, polymerase chain reaction amplification, and fluorescence in situ hybridization assays designed to detect HER-2/neu gene amplification are compared with HER-2/neu protein overexpression assays performed by immunohistochemical techniques applied to frozen and paraffin-embedded tissues and enzyme immunoassays performed on tumor cytosols.
  • The significance of HER-2/neu overexpression in ductal carcinoma in situ and the HER-2/neu status in uncommon female breast conditions and male breast cancer are also considered.
  • The role of HER-2/neu testing for the prediction of response to trastuzumab therapy in breast cancer is presented as well as its potential impact on responses to standard and newer hormonal therapies, cytotoxic chemotherapy, and radiation.
  • The review also evaluates the status of serum-based testing for circulating HER-2/neu receptor protein and its ability to predict disease outcome and therapy response.
  • [MeSH-major] Breast Neoplasms / genetics. Breast Neoplasms / therapy. Gene Expression Regulation, Neoplastic. Genes, erbB-2 / genetics. Genetic Predisposition to Disease
  • [MeSH-minor] Adult. Age Distribution. Aged. Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Humanized. Biomarkers, Tumor / analysis. Breast Neoplasms, Male / genetics. Breast Neoplasms, Male / mortality. Breast Neoplasms, Male / pathology. Breast Neoplasms, Male / therapy. Combined Modality Therapy. Education, Medical, Continuing. Female. Humans. Incidence. Male. Middle Aged. Neoplasm Staging. Prognosis. Risk Assessment. Sensitivity and Specificity. Survival Analysis. Trastuzumab. Treatment Outcome


41. Ross JS, Fletcher JA, Bloom KJ, Linette GP, Stec J, Symmans WF, Pusztai L, Hortobagyi GN: Targeted therapy in breast cancer: the HER-2/neu gene and protein. Mol Cell Proteomics; 2004 Apr;3(4):379-98
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Targeted therapy in breast cancer: the HER-2/neu gene and protein.
  • The HER-2/neu oncogene, a member of the epidermal growth factor receptor or erb gene family, encodes a transmembrane tyrosine kinase receptor that has been linked to prognosis and response to therapy with the anti-HER-2-humanized monoclonal antibody, trastuzumab (Herceptin, Genentech, South San Francisco, CA) in patients with advanced metastatic breast cancer.
  • HER-2/neu status has also been tested for its ability to predict the response of breast cancer to other therapies including hormonal therapies, topoisomerase inhibitors, and anthracyclines.
  • This review includes an analysis of 80 published studies encompassing more than 25,000 patients designed to consider the relative advantages and disadvantages of the various methods of measuring HER-2/neu in clinical breast cancer specimens.
  • Southern blotting, PCR amplification detection, and fluorescence in situ hybridization assays designed to detect HER-2/neu gene amplification are compared with HER-2/neu protein overexpression assays performed by immunohistochemical techniques applied to frozen and paraffin-embedded tissues and enzyme immunoassays performed on tumor cytosols.
  • The significance of HER-2/neu overexpression in ductal carcinoma in situ and the HER-2/neu status in uncommon female breast conditions and male breast cancer are also considered.
  • The role of HER-2/neu testing for the prediction of response to trastuzumab therapy in breast cancer is reviewed along with the current studies designed to test whether HER-2/neu status can predict the response to standard and newer hormonal therapies, cytotoxic chemotherapy, and radiation.
  • The review will also evaluate the status of serum-based testing for circulating HER-2/neu receptor protein and its ability to predict disease outcome and therapy response.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Biomarkers, Tumor / metabolism. Breast Neoplasms. Receptor, ErbB-2 / analysis. Receptor, ErbB-2 / physiology
  • [MeSH-minor] Female. Humans. Male. Predictive Value of Tests


42. Ross JS, Gray GS: Targeted therapy for cancer: the HER-2/neu and Herceptin story. Clin Leadersh Manag Rev; 2003 Nov-Dec;17(6):333-40
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Targeted therapy for cancer: the HER-2/neu and Herceptin story.
  • The HER-2/neu oncogene encodes a transmembrane tyrosine kinase receptor with extensive homology to the epidermal growth factor receptor.
  • In this article, the association of HER-2/neu gene and protein abnormalities with prognosis and response to therapy with Herceptin and other therapies in breast cancer is presented.
  • By considering a series of 80 published studies encompassing more than 25,000 patients, the relative advantages and disadvantages of Southern blotting, polymerase chain reaction amplification, and fluorescence in situ hybridization assays designed to detect HER-2/neu gene amplification are compared with HER-2/neu protein overexpression assays performed by immunohistochemical techniques applied to frozen and paraffin-embedded tissues and enzyme immunoassays performed on tumor cytosols.
  • The significance of HER-2/neu overexpression in ductal carcinoma in situ and the HER-2/neu status in uncommon female breast conditions and male breast cancer also are considered.
  • The role of HER-2/neu testing for the prediction of response to Herceptin therapy in breast cancer is presented as well as its potential impact on responses to standard and newer hormonal therapies, cytotoxic chemotherapy, and radiation.
  • The review also will evaluate the status of serum-based testing for circulating HER-2/neu receptor protein and its ability to predict disease outcome and therapy response.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Breast Neoplasms / drug therapy. Breast Neoplasms / genetics. Genes, erbB-2 / genetics. Receptor, ErbB-2 / analysis
  • [MeSH-minor] Antibodies, Monoclonal, Humanized. Biomarkers, Tumor. Combined Modality Therapy. Drug Delivery Systems. Female. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Trastuzumab

  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • Hazardous Substances Data Bank. Trastuzumab .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 14692077.001).
  • [ISSN] 1527-3954
  • [Journal-full-title] Clinical leadership & management review : the journal of CLMA
  • [ISO-abbreviation] Clin Leadersh Manag Rev
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; EC 2.7.10.1 / Receptor, ErbB-2; P188ANX8CK / Trastuzumab
  • [Number-of-references] 70
  •  go-up   go-down


43. Janssens JP, Russo J, Russo I, Michiels L, Donders G, Verjans M, Riphagen I, Van den Bossche T, Deleu M, Sieprath P: Human chorionic gonadotropin (hCG) and prevention of breast cancer. Mol Cell Endocrinol; 2007 Apr 15;269(1-2):93-8
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Human chorionic gonadotropin (hCG) and prevention of breast cancer.
  • Animal and 'in vitro' experiences learned that human chorionic gonadotropin (hCG) is capable to protect from breast cancer.
  • Receptors for hCG/luteinizing hormone (LH) are present on human female and male breast cancer cells. hCG decreases proliferation and invasion of breast cancer MCF-7 cells by inhibiting NF-kappa B, AP-1 activation and other genes.
  • All these pieces of evidence suggest that hCG is active in human breast cancer.
  • We performed a pilot study phase I trial for testing the inhibitory effects or recombinant hCG (rhCG) on primary breast cancer.
  • Twenty-five postmenopausal women with newly diagnosed breast cancers of more than 1.5 cm were biopsied before randomization to receive either 500 microg rhCG (n=20) or placebo.
  • After 2 weeks, surgery was done and tissues were analysed with regard to morphological, immunohistochemical and biochemical changes in tissues and plasma. rhCG reduces significantly the proliferative index and the expression of both the oestrogen receptor and progesterone receptor. rhCG does not modify the hormonal level of estradiol, progesterone, inhibin and follicle stimulating hormone (FSH) but increases significantly the level of LH.
  • In a second pilot study, we tested the clinical efficacy through an open-label single centre study in 13 postmenopausal women with metastatic breast cancer.
  • A 500 microg rhCG once every 2 days shows activity in postmenopausal metastatic breast cancer.
  • The time to progression is relatively short.
  • Response to previous hormonal treatment is indicative for rhCG activity.
  • Given the data in primary and metastatic breast cancer rhCG further large scale investigation is highly warranted. rhCG can be an realistic option in (chemo-) prevention trials.
  • [MeSH-major] Breast Neoplasms / prevention & control. Carcinoma / drug therapy. Chorionic Gonadotropin / therapeutic use
  • [MeSH-minor] Antineoplastic Agents, Hormonal / therapeutic use. Female. Humans. Neoplasm Metastasis / drug therapy. Postmenopause

  • Genetic Alliance. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17386970.001).
  • [ISSN] 0303-7207
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Chorionic Gonadotropin
  • [Number-of-references] 31
  •  go-up   go-down


44. Rafajlovski S, Tatić V, Ilić S, Kanjuh V: [Frequency of metastatic tumors in the heart]. Vojnosanit Pregl; 2005 Dec;62(12):915-20

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Frequency of metastatic tumors in the heart].
  • INTRODUCTION: Secondary or metastatic tumors in the heart occur more frequently than primary ones, and, according to the published series, their frequency found in autopsic material ranges from 1.6% to 20.6%.
  • Metastatic tumors in the heart are rarely clinically symptomatic, and, therefore, they are rarely diagnosed within the lifetime.
  • The aim of this study was to analyze the frequency of metastatic tumors of the heart, their primary localization, as well as the localization of the metastases found in the autopsic material within the period 1972-2004.
  • METHODS: During the autopsy of the patients died of metastatic tumors, we microscopically and macroscopically analyzed all the organs and tissues to determine the metastases of primary tumors in other organs, especially in the heart and pericardium.
  • In 2 928 (25.6%) out of 11 403 autopsies, the presence of malignant tumor was diagnosed, and in 79 (2.7%) of these cases, metastasis of the heart was found out.
  • The most frequent metastases in the heart were caused by pulmonary carcinoma (18 cases), leukemia and malignant lymphoma (8 cases, each), then pancreatic and breast carcinoma, while the metastases of other carcinomas were rather rare.
  • CONCLUSION: Metastatic tumors of the heart are rather rare, and rarely clinically symptomatic, and, thus, rarely diagnosed during life.
  • The methods of choice for the diagnosis of the metastasis in the heart are echocardiography, computerized tomography, magnetic resonance imaging, cytological analysis of the pericardial effusion and biopsy.
  • The treatment includes surgery, chemotherapy and radiotherapy.
  • [MeSH-major] Heart Neoplasms / secondary
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Humans. Male. Middle Aged

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16375220.001).
  • [ISSN] 0042-8450
  • [Journal-full-title] Vojnosanitetski pregled
  • [ISO-abbreviation] Vojnosanit Pregl
  • [Language] srp
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Serbia and Montenegro
  •  go-up   go-down


45. Singer CF, Hudelist G, Lamm W, Mueller R, Handl C, Kubista E, Czerwenka K: Active (p)CrkL is overexpressed in human malignancies: potential role as a surrogate parameter for therapeutic tyrosine kinase inhibition. Oncol Rep; 2006 Feb;15(2):353-9
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Active (p)CrkL is overexpressed in human malignancies: potential role as a surrogate parameter for therapeutic tyrosine kinase inhibition.
  • CrkL is a nuclear adaptor and transcriptional activator in Bcr-Abl expressing cells and constitutes the major tyrosine phosphorylated protein in CML, but the expression and biological function of CrkL in other malignancies is largely unknown.
  • Using immunohistochemistry, we have analyzed the protein expression of activated (p)CrkL in normal and malignant tissues.
  • We then treated K562 leukemia cells with imatinib to analyze the effect of tyrosine kinase inhibition on CrkL activation. pCrkL expression was predominantly epithelial and detected in the majority of non-malignant prostate (79%), 49% of colon biopsies, 36% of skin biopsies, and 41% of samples obtained from normal brain.
  • Protein expression was, however, considerably less frequent in normal breast (18%), lung (16%) and ovarian (12%) tissues.
  • In contrast to their corresponding benign tissues, pCrkL expression was significantly more common in breast cancer samples (49%, p<0.0001; Fisher's exact test), lung carcinomas (55%, p=0.0002), lymphatic tissues (80% vs. 10%, p=0.012), skin cancer (67%, p=0.020), ovarian malignomas (50%, p<0.0001) and colon carcinomas (63%, p<0.03).
  • By contrast, activated CrkL was significantly less frequent in prostate carcinoma samples when compared to corresponding non-malignant prostatic tissues (14% vs. 79%, p<0.0001).
  • pCrkL expression was abrogated in K562 cells with the addition of the tyrosine kinase inhibitor imatinib, which indicates that phosphorylation of CrkL is mediated through targets of therapeutic TK inhibition.
  • We hypothesize that pCrkL is selectively up-regulated in a number of malignant tumor entities and involved in malignant transformation.
  • We further suggest that pCrkL might serve as a potential surrogate parameter for the efficacy of therapeutic TK inhibition.
  • [MeSH-major] Adaptor Proteins, Signal Transducing / biosynthesis. Biomarkers, Tumor / analysis. Neoplasms / drug therapy. Neoplasms / metabolism. Nuclear Proteins / biosynthesis. Protein Kinase Inhibitors / therapeutic use. Protein-Tyrosine Kinases / drug effects
  • [MeSH-minor] Benzamides. Blotting, Western. Cell Line, Tumor. Enzyme Activation / drug effects. Female. Humans. Imatinib Mesylate. Immunohistochemistry. Male. Piperazines / therapeutic use. Pyrimidines / therapeutic use. Up-Regulation

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • Hazardous Substances Data Bank. IMATINIB MESYLATE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16391854.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Benzamides; 0 / Biomarkers, Tumor; 0 / CRKL protein; 0 / Nuclear Proteins; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases
  •  go-up   go-down


46. Omura Y: Beneficial effects and side effects of DHEA: true anti-aging and age-promoting effects, as well as anti-cancer and cancer-promoting effects of DHEA evaluated from the effects on the normal and cancer cell telomeres and other parameters. Acupunct Electrother Res; 2005;30(3-4):219-61
MedlinePlus Health Information. consumer health - Seniors' Health.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Beneficial effects and side effects of DHEA: true anti-aging and age-promoting effects, as well as anti-cancer and cancer-promoting effects of DHEA evaluated from the effects on the normal and cancer cell telomeres and other parameters.
  • The author evaluated the effects of DHEA (Dehydroepiandrosterone) on the amount of telomeres of normal cells and cancer cells and found the following: Contrary to the literature, which often recommended 25-50 mg of DHEA daily for the average adult human being, the author found that, depending on the individual, the maximum increase of normal cell telomere was obtained by a single optimal dose of 1.25-12.5 mg.
  • This was examined in 50 people, both males and females, between the ages of 20-80 years old.
  • When one optimal dose was given to each individual, the average telomere amount in normal tissues, measured in Bi-Digital O-Ring Test units, often increased from anywhere between 25-300 ng to between 500-530 ng.
  • Cancer cell telomere reduced from higher than 1100 ng to less than 1 yg (=10(-24) g) with equally significant normalization of abnormal cancer parameters (such as Integrin alpha5beta1, Oncogen C-fosAb2, Acetylcholine, etc.).
  • Circulatory improvement and an increase in grasping force of up to 25% were also detected, along with the changing of a few white hairs to black hairs.
  • The beneficial effects of one optimal dose of DHEA generally lasted between 1 to 4 months, though in some individuals it lasted for a much shorter period of time due to a number of negative factors such as excessive stress/work, excessive exposure to low temperatures and toxic substances, or use of common pain medicines.
  • On the other hand, if a patient took an excessive dose of DHEA, the amount of normal cell telomere decreased, while there was an increase in cancer cell telomere.
  • It was found that those who took an overdose of 25-50 mg daily for more than 3 months had a high incidence of cancer of the prostate gland, breast, colon, lung, and stomach.
  • Also, when the average normal cell telomere levels were less than 110 ng, compared with a normal value of 120-130 ng, and when DHEA in different parts of the body was also extremely low (less than 1-2 ng), one could suspect the possible presence of a malignant tumor somewhere in the body.
  • When normal cell telomere was less than 110 ng, most individuals felt very weary with marked tiredness in the eyes, and grasping force was often reduced.
  • [MeSH-major] Aging / drug effects. Dehydroepiandrosterone / administration & dosage. Dehydroepiandrosterone / adverse effects. Neoplasms / chemically induced. Neoplasms / drug therapy. Telomere / drug effects. Telomere / genetics
  • [MeSH-minor] Adjuvants, Immunologic / administration & dosage. Adjuvants, Immunologic / adverse effects. Adult. Aged. Aged, 80 and over. Antineoplastic Agents / administration & dosage. Antineoplastic Agents / adverse effects. Chromosome Aberrations. Dose-Response Relationship, Drug. Female. Humans. Male. Middle Aged. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16617690.001).
  • [ISSN] 0360-1293
  • [Journal-full-title] Acupuncture & electro-therapeutics research
  • [ISO-abbreviation] Acupunct Electrother Res
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / Antineoplastic Agents; 459AG36T1B / Dehydroepiandrosterone
  •  go-up   go-down


47. Sidorenko IuS, Orlovskaia LA, Soldatkina NV, Emel'ianova LE, Kas'ianenko VN: [Method of surgical chemotherapy on organism automedia during surgical procedures for breast and colon cancer]. Khirurgiia (Mosk); 2006;(10):27-9
MedlinePlus Health Information. consumer health - Mastectomy.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Method of surgical chemotherapy on organism automedia during surgical procedures for breast and colon cancer].
  • Method of surgical chemotherapy on organism automedia during surgical procedures for breast and colon malignant tumors has been developed.
  • The method consists in intravenous autohemochemotherapy and local autoplasmochemotherapy (into residuary mammary tissue or regional arterial mesenteric vessel).
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Blood Transfusion, Autologous / methods. Breast Neoplasms / drug therapy. Colectomy / methods. Colonic Neoplasms / drug therapy. Mastectomy / methods
  • [MeSH-minor] Chemotherapy, Adjuvant. Follow-Up Studies. Humans. Injections, Intravenous. Intraoperative Period. Male. Middle Aged. Neoplasm Staging. Treatment Outcome

  • Genetic Alliance. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17159863.001).
  • [ISSN] 0023-1207
  • [Journal-full-title] Khirurgiia
  • [ISO-abbreviation] Khirurgiia (Mosk)
  • [Language] rus
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  •  go-up   go-down


48. Hubarieva HO, Kindzel's'kyĭ LP, Ponomar'ova OV, Udatova TV, Shpil'ova SI, Smolanka II, Korovin SI, Ivankin VS: [Systemic enzymotherapy as a method of prophylaxis of postradiation complications in oncological patients]. Lik Sprava; 2000 Oct-Dec;(7-8):94-100
Hazardous Substances Data Bank. CHYMOTRYPSIN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Set out in the paper are results of treatment of those patients with carcinoma of the lung, uterine cervix, hysterocarcinoma, breast cancer, malignant thymomas, malignant non-Hodgkin's lymphomas, and lymphogranulematosis having been administered combined, chemoradiation or radiation treatments against the background of a complex of accompanying therapy involving systemic enzymotherapy.
  • Polyenzymic drugs were found to be capable of improving results of treatment of acute radiation reactions and preventing postradiation fibrous changes in the lungs, skin, fatty tissue, soft tissue, liver, kidneys.
  • Thus, systemic enzymotherapy is capable of improving the quality of life and results of treatment of oncological patients.

  • MedlinePlus Health Information. consumer health - Radiation Therapy.
  • Hazardous Substances Data Bank. BROMELAINS .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16786662.001).
  • [ISSN] 1019-5297
  • [Journal-full-title] Likars'ka sprava
  • [ISO-abbreviation] Lik. Sprava
  • [Language] UKR
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Ukraine
  • [Chemical-registry-number] 0 / Drug Combinations; 0 / Phlogenzym; 5G06TVY3R7 / Rutin; 60098-82-0 / chymotrypsin, papain, trypsin drug combination; 72506-65-1 / Wobenzym; 9001-00-7 / Bromelains; EC 3.- / Hydrolases; EC 3.4.21.1 / Chymotrypsin; EC 3.4.21.4 / Trypsin; EC 3.4.22.2 / Papain
  •  go-up   go-down


49. Hollmén M, Määttä JA, Bald L, Sliwkowski MX, Elenius K: Suppression of breast cancer cell growth by a monoclonal antibody targeting cleavable ErbB4 isoforms. Oncogene; 2009 Mar 12;28(10):1309-19
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Suppression of breast cancer cell growth by a monoclonal antibody targeting cleavable ErbB4 isoforms.
  • ErbB4 isoforms mediate different cellular activities depending on their susceptibility to proteolytic cleavage.
  • Here, we describe characterization of a monoclonal antibody (mAb 1479) that selectively recognizes the ectodomain of cleavable ErbB4 JM-a isoforms both in vitro and in vivo. mAb 1479 was used to analyse ErbB4 JM-a expression and ectodomain shedding in a series of 17 matched breast cancer/histologically normal peripheral breast tissue pairs.
  • ErbB4 ectodomain was observed in 75% of tumors expressing ErbB4 but only in 18% of normal breast tissue samples expressing ErbB4.
  • Difference in the relative quantity of ErbB4 ectodomain between normal and tumor tissue pairs was statistically significant (P=0.015).
  • Treatment with mAb 1479 suppressed ErbB4 function by inhibiting ErbB4 tyrosine phosphorylation and ectodomain shedding, and by stimulating ErbB4 downregulation and ubiquitination. mAb 1479 suppressed both anchorage-dependent and -independent growth of human breast cancer cell lines that naturally express cleavable ErbB4 JM-a.
  • These findings indicate that ErbB4 ectodomain shedding is enhanced in breast cancer tissue in vivo, and that mAb 1479 represents a potential drug candidate that suppresses breast cancer cell growth by selectively binding cleavable ErbB4 isoforms.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Breast Neoplasms / drug therapy. Receptor, Epidermal Growth Factor / antagonists & inhibitors
  • [MeSH-minor] Animals. Antibodies, Monoclonal, Humanized. Cell Proliferation / drug effects. Child, Preschool. Female. Humans. Male. Mice. Mice, Inbred BALB C. Phosphorylation. Protein Isoforms. Receptor, ErbB-4. Trastuzumab

  • Genetic Alliance. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. Trastuzumab .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19151766.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Protein Isoforms; EC 2.7.10.1 / ERBB4 protein, human; EC 2.7.10.1 / Erbb4 protein, mouse; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptor, ErbB-4; P188ANX8CK / Trastuzumab
  •  go-up   go-down


50. Zhang W, Shannon WD, Duncan J, Scheffer GL, Scheper RJ, McLeod HL: Expression of drug pathway proteins is independent of tumour type. J Pathol; 2006 Jun;209(2):213-9
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of drug pathway proteins is independent of tumour type.
  • Current clinicopathological staging systems have the advantage of standardized criteria for assessing tumour stage, and a relationship between advancing tumour stage and poor prognosis has been established for most cancers.
  • However, these tools have not led to clear criteria for therapy selection in individual patients.
  • Indeed, the concept of therapy based on anatomical location seems quaint.
  • Therefore, a representative drug pathway (irinotecan) was evaluated across common tumour types to test the hypothesis that pharmacological proteins are expressed independent of anatomical location.
  • Many enzymes are involved in controlling the disposition of irinotecan, including the cellular target (TOP1), metabolism enzymes (CES2, UGT1A1, CYP3A4, CYP3A5), and cellular transporters of the anti-cancer agent (ABCB1, ABCC1, ABCC2, ABCC3, ABCC5, ABCG2).
  • These 11 proteins were evaluated in tissue microarrays containing colon, breast, prostate, ovary, and lung cancers; brain tumours; melanoma; lymphoma; and selected normal tissues.
  • A total of 255 tumours and 37 normal tissue samples were evaluable for all proteins.
  • Linear discriminant analysis designed to predict the tissue type from the protein expression levels revealed a 49.6% misclassification rate, indicating that protein expression of this drug pathway is not associated with tissue type.
  • Cluster analysis identified a variety of tumours with the same pharmacological profile.
  • The anatomy independence of drug pathways stimulates efforts to move away from our traditional approaches to the selection of cancer therapy.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / analysis. Camptothecin / analogs & derivatives. Neoplasm Proteins / analysis. Neoplasms / chemistry
  • [MeSH-minor] Adenocarcinoma / chemistry. Adenocarcinoma / enzymology. Brain Neoplasms / chemistry. Brain Neoplasms / enzymology. Breast Neoplasms / chemistry. Breast Neoplasms / enzymology. Colonic Neoplasms / chemistry. Colonic Neoplasms / enzymology. Cytochrome P-450 Enzyme System / analysis. Drug Resistance, Neoplasm. Enzyme Inhibitors / analysis. Female. Humans. Immunohistochemistry / methods. Lung Neoplasms / chemistry. Lung Neoplasms / enzymology. Lymphoma / chemistry. Lymphoma / enzymology. Male. Melanoma / chemistry. Melanoma / enzymology. Multidrug Resistance-Associated Proteins / analysis. Ovarian Neoplasms / chemistry. Ovarian Neoplasms / enzymology. Prostatic Neoplasms / chemistry. Prostatic Neoplasms / enzymology. Tissue Array Analysis / methods

  • COS Scholar Universe. author profiles.
  • Pharmacogenomics Knowledge Base. meta-databases - Pharmacogenomic Annotation 827851551 for PMID:16508919 [PharmGKB] .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16508919.001).
  • [ISSN] 0022-3417
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Grant] United States / NIGMS NIH HHS / GM / GM61218; United States / NIGMS NIH HHS / GM / GM63340; United States / NCI NIH HHS / CA / P30 CA091842
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Enzyme Inhibitors; 0 / Multidrug Resistance-Associated Proteins; 0 / Neoplasm Proteins; 7673326042 / irinotecan; 9035-51-2 / Cytochrome P-450 Enzyme System; XT3Z54Z28A / Camptothecin
  •  go-up   go-down


51. Milczarek R, Klimek J: [Aromatase--key enzyme of estrogen biosynthesis]. Postepy Biochem; 2005;51(4):430-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Estrogens control a large range pivotal life functions as reproductive development and fertility, bone growth and sexual behavior.
  • The property, structure and reaction mechanism of aromatase as well as detailed structure of human aromatase cytochrome P450 gene (CYP19) was discussed in this article.
  • It was pointed that unique human CYP19 gene expression results from presence of many tissue specific promoters and alternative splicing.
  • The molecular mechanism of control aromatase cytochrome P450 gene expression in various species ovaries, testes and human adipose tissue and placenta was discussed in details.
  • Because of a very important role of estrogen in breast cancer a molecular base of aberrant expression CYP19 gene in breast tumor and adipose tissue proximal to breast tumor and potential possibility of pharmacological silencing of this gene expression was discussed in the article.
  • [MeSH-minor] Adipose Tissue / metabolism. Animals. Antineoplastic Agents / pharmacology. Bone Development / physiology. Breast Neoplasms / drug therapy. Breast Neoplasms / genetics. Breast Neoplasms / metabolism. Female. Fertility / physiology. Gene Expression / drug effects. Humans. Male. Placenta / metabolism. Reproduction / physiology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16676578.001).
  • [ISSN] 0032-5422
  • [Journal-full-title] Postepy biochemii
  • [ISO-abbreviation] Postepy Biochem.
  • [Language] pol
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Estrogens; EC 1.14.14.1 / Aromatase
  • [Number-of-references] 66
  •  go-up   go-down


52. Zhang J, Wu X, Huang J: [Clinical study on the expression level of lymphocyte function-related antigen of breast cancer patients]. Zhongguo Zhong Xi Yi Jie He Za Zhi; 2000 Feb;20(2):110-2
Hazardous Substances Data Bank. METHOTREXATE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Clinical study on the expression level of lymphocyte function-related antigen of breast cancer patients].
  • OBJECTIVE: To explore the protein expression level of the lymphocyte function-related antigen CD11a, CD18, CD54 of breast cancer patients' blood, cancer tissue and drainage lymph node, and the effect of chemotherapy as well as Yiqi Yangxue Granule on its expression level.
  • METHODS: The immunohistochemical assay and flow cytometry were used to determine the change of the protein expression level of CD11a, CD18, CD54 on the lymphocyte of blood, cancer tissue and lymph node between before and after chemotherapy and chemotherapy plus Yiqi Yangxue Granule in 72 patients suffering from breast cancer.
  • RESULTS: In breast cancer patients, the level of CD54 was increased more obviously than that of control group, the CD11a, CD18, CD54 of lymphocytes in cancer tissue increased remarkably, while the CD54 expression positive rate reached 100%, the expression level of CD11a, CD18, CD54 which increased significantly in negative lymph node obviously higher than that of positive lymph node.
  • CONCLUSION: The level of adherence cell was markedly abnormal in breast cancer patients, whose immune adherence function disturbed.
  • Although chemotherapy kills the tumor cells, it damages the immune adherence function, Yiqi Yangxue Granule could improve the immune function and enhance the anti-cancer effect of patients.

  • Genetic Alliance. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • Hazardous Substances Data Bank. FLUOROURACIL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11783310.001).
  • [ISSN] 1003-5370
  • [Journal-full-title] Zhongguo Zhong xi yi jie he za zhi Zhongguo Zhongxiyi jiehe zazhi = Chinese journal of integrated traditional and Western medicine
  • [ISO-abbreviation] Zhongguo Zhong Xi Yi Jie He Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Drugs, Chinese Herbal; 0 / Lymphocyte Function-Associated Antigen-1; 126547-89-5 / Intercellular Adhesion Molecule-1; 8N3DW7272P / Cyclophosphamide; U3P01618RT / Fluorouracil; YL5FZ2Y5U1 / Methotrexate
  •  go-up   go-down


53. Abdah-Bortnyak R, Bernstein Z, Ramon N, Zalman D, Shnaider J, Kuten A: [Gynecomastia as a complication of hormonotherapy for prostate cancer: effect of prophylactic breast irradiation]. Harefuah; 2007 Feb;146(2):126-8, 164-5
Hazardous Substances Data Bank. BICALUTAMIDE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Gynecomastia as a complication of hormonotherapy for prostate cancer: effect of prophylactic breast irradiation].
  • Gynecomastia is a benign condition characterized by proliferation of mammary glandular tissue.
  • Hormonotherapy with bicalutamide for prostate cancer is one of the causes of gynecomastia.
  • The well known aim of treatment is to decrease psychological distress and to improve cosmetic appearance.
  • Prophylactic breast irradiation may prevent the appearance of gynecomastia.
  • [MeSH-major] Androgen Antagonists / adverse effects. Anilides / adverse effects. Breast / radiation effects. Gynecomastia / chemically induced. Nitriles / adverse effects. Prostatic Neoplasms / drug therapy. Tosyl Compounds / adverse effects
  • [MeSH-minor] Humans. Male

  • Genetic Alliance. consumer health - Prostate cancer.
  • Genetic Alliance. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17352282.001).
  • [ISSN] 0017-7768
  • [Journal-full-title] Harefuah
  • [ISO-abbreviation] Harefuah
  • [Language] heb
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Israel
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Anilides; 0 / Nitriles; 0 / Tosyl Compounds; A0Z3NAU9DP / bicalutamide
  • [Number-of-references] 23
  •  go-up   go-down


54. Meaney PM, Fanning MW, di Florio-Alexander RM, Kaufman PA, Geimer SD, Zhou T, Paulsen KD: Microwave tomography in the context of complex breast cancer imaging. Conf Proc IEEE Eng Med Biol Soc; 2010;2010:3398-401
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Microwave tomography in the context of complex breast cancer imaging.
  • The notion of applying microwave imaging to breast cancer imaging has been studied at various levels by numerous scientists.
  • The earliest appeal of this concept related to the presumably high property contrast between benign and malignant tissue that was unique to the breast.
  • Subsequent published studies have shown that this assumption was overly simplistic and that the tissue property heterogeneity is considerable within the breast.
  • As we have expanded the clinical use of our microwave tomographic system, we are now using this approach to monitor tumor progressions during neoadjuvant chemotherapy.
  • In these cases, while we can still characterize and track the tumor progression, we have observed a new phenomenon.
  • Very often these cancer patients exhibit skin thickening near the tumor site.
  • Our images have reconstructed elevated dielectric properties along the breast surface associated with the accompanying edema.
  • These observations further add to the complex nature of breast dielectric properties and the challenges for imaging them using microwave interrogation.

  • Genetic Alliance. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] IEEE Trans Med Imaging. 2001 Feb;20(2):104-16 [11321590.001]
  • [Cites] J Microw Power. 1981 Jun;16(2):107-19 [7033539.001]
  • [Cites] Magn Reson Med. 1991 Apr;18(2):371-83 [2046518.001]
  • [Cites] IEEE Trans Biomed Eng. 1995 Oct;42(10):1017-26 [8582719.001]
  • [Cites] Breast Cancer Res. 2013;15(2):R35 [23621959.001]
  • [Cites] Acad Radiol. 2007 Feb;14(2):207-18 [17236994.001]
  • [Cites] Radiology. 2007 May;243(2):350-9 [17400760.001]
  • [Cites] Med Phys. 2007 Jun;34(6):2014-23 [17654905.001]
  • [Cites] Phys Med Biol. 2007 Oct 21;52(20):6093-115 [17921574.001]
  • [Cites] IEEE Trans Med Imaging. 1999 Jun;18(6):496-507 [10463128.001]
  • (PMID = 21097245.001).
  • [ISSN] 1557-170X
  • [Journal-full-title] Conference proceedings : ... Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE Engineering in Medicine and Biology Society. Annual Conference
  • [ISO-abbreviation] Conf Proc IEEE Eng Med Biol Soc
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA080139; United States / NCI NIH HHS / CA / P30 CA023108; United States / NCI NIH HHS / CA / P01-CA080139
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS512905; NLM/ PMC3757128
  •  go-up   go-down


55. Andreev OA, Dupuy AD, Segala M, Sandugu S, Serra DA, Chichester CO, Engelman DM, Reshetnyak YK: Mechanism and uses of a membrane peptide that targets tumors and other acidic tissues in vivo. Proc Natl Acad Sci U S A; 2007 May 8;104(19):7893-8
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mechanism and uses of a membrane peptide that targets tumors and other acidic tissues in vivo.
  • The pH-selective insertion and folding of a membrane peptide, pHLIP [pH (low) insertion peptide], can be used to target acidic tissue in vivo, including acidic foci in tumors, kidneys, and inflammatory sites.
  • In a mouse breast adenocarcinoma model, fluorescently labeled pHLIP finds solid acidic tumors with high accuracy and accumulates in them even at a very early stage of tumor development.
  • The fluorescence signal is stable for >4 days and is approximately five times higher in tumors than in healthy counterpart tissue.
  • In a rat antigen-induced arthritis model, pHLIP preferentially accumulates in inflammatory foci. pHLIP also maps the renal cortical interstitium; however, kidney accumulation can be reduced significantly by providing mice with bicarbonate-containing drinking water.
  • The peptide has three states: soluble in water, bound to the surface of a membrane, and inserted across the membrane as an alpha-helix.
  • At physiological pH, the equilibrium is toward water, which explains its low affinity for cells in healthy tissue; at acidic pH, titration of Asp residues shifts the equilibrium toward membrane insertion and tissue accumulation.
  • The replacement of two key Asp residues located in the transmembrane part of pHLIP by Lys or Asn led to the loss of pH-sensitive insertion into membranes of liposomes, red blood cells, and cancer cells in vivo, as well as to the loss of specific accumulation in tumors. pHLIP nanotechnology introduces a new method of detecting, targeting, and possibly treating acidic diseased tissue by using the selective insertion and folding of membrane peptides.

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Am J Physiol. 1996 Jul;271(1 Pt 2):F132-42 [8760254.001]
  • [Cites] Biophys J. 1981 Oct;36(1):1-19 [7284547.001]
  • [Cites] J Rheumatol. 1998 Sep;25(9):1772-7 [9733459.001]
  • [Cites] J Rheumatol. 1999 Sep;26(9):2018-24 [10493685.001]
  • [Cites] Cardiology. 2005;103(1):10-6 [15528895.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Dec 21;101(51):17867-72 [15601762.001]
  • [Cites] Curr Med Chem. 2005;12(7):795-805 [15853712.001]
  • [Cites] Nature. 2006 Jan 19;439(7074):353-7 [16273092.001]
  • [Cites] Mol Cancer Res. 2006 Feb;4(2):61-70 [16513837.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Apr 25;103(17):6460-5 [16608910.001]
  • [Cites] Science. 2006 May 26;312(5777):1168-71 [16728630.001]
  • [Cites] JAMA. 2006 Jul 26;296(4):445-8 [16868303.001]
  • [Cites] Nature. 2006 Jul 27;442(7101):461-5 [16688182.001]
  • [Cites] Med Chem. 2006 May;2(3):315-27 [16948479.001]
  • [Cites] Cell Oncol. 2006;28(4):127-39 [16988468.001]
  • [Cites] Arthritis Rheum. 2007 Jan;56(1):108-16 [17195213.001]
  • [Cites] Mol Med Today. 2000 Jan;6(1):15-9 [10637570.001]
  • [Cites] Biophys J. 2001 Sep;81(3):1735-58 [11509384.001]
  • [Cites] J Appl Toxicol. 2001 Nov-Dec;21(6):513-9 [11746200.001]
  • [Cites] Atherosclerosis. 2002 Sep;164(1):27-35 [12119190.001]
  • [Cites] Nature. 2002 Dec 19-26;420(6917):860-7 [12490959.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Dec 24;99(26):16766-9 [12471152.001]
  • [Cites] Cancer Treat Rev. 2003 Dec;29(6):541-9 [14585264.001]
  • [Cites] Cell. 2004 Sep 17;118(6):665-6 [15369664.001]
  • [Cites] Cell. 2004 Sep 17;118(6):687-98 [15369669.001]
  • [Cites] Crit Care. 2004 Oct;8(5):331-6 [15469594.001]
  • [Cites] Proc Natl Acad Sci U S A. 1974 Nov;71(11):4457-61 [4530994.001]
  • [Cites] Biochemistry. 1997 Dec 9;36(49):15177-92 [9398245.001]
  • (PMID = 17483464.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / R01 GM070895; United States / NCRR NIH HHS / RR / P20 RR016457; United States / NIGMS NIH HHS / GM / GM073857; United States / NCRR NIH HHS / RR / P20RR016457; United States / NIGMS NIH HHS / GM / GM070895; United States / NIGMS NIH HHS / GM / R01 GM073857
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Lipid Bilayers; 0 / Membrane Proteins
  • [Other-IDs] NLM/ PMC1861852
  •  go-up   go-down


56. Wang HJ, Zhu JS, Zhang Q, Sun Q, Guo H: High level of ezrin expression in colorectal cancer tissues is closely related to tumor malignancy. World J Gastroenterol; 2009 Apr 28;15(16):2016-9
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High level of ezrin expression in colorectal cancer tissues is closely related to tumor malignancy.
  • AIM: To investigate the ezrin expression in normal colorectal mucosa and colorectal cancer tissues, and study the correlation between ezrin expression in colorectal cancer tissues and tumor invasion and metastasis.
  • METHODS: Eighty paraffin-embedded cancer tissue samples were selected from primary colorectal adenocarcinoma.
  • Forty-five patients were of Dukes A to B stage, and 35 were of C to D stage.
  • Another 22 paraffin-embedded tissue blocks of normal colorectal epithelium (> 5 cm away from the edge of the tumor) were selected as the control group.
  • All patients with colorectal cancer were treated surgically and diagnosed histologically, without preoperative chemotherapy or radiotherapy.
  • The immunohistochemistry was used to detect the ezrin expression in paraffin-embedded normal colorectal mucosa tissues and colorectal cancer tissue samples.
  • RESULTS: Ezrin expression in colorectal cancer was significantly higher than in normal colorectal mucosa (75.00% vs 9.09%, P < 0.01), and there was a close relationship between ezrin expression and the degree of tumor differentiation, lymph node metastasis and Dukes stage (88.46% vs 50.00%, P < 0.01; 94.28% vs 51.11%, P < 0.01; 94.28% vs 51.11%, P < 0.01).
  • CONCLUSION: Ezrin expression is obviously higher in colorectal cancer tissues than in normal colorectal mucosa tissues, and the high level of ezrin expression is closely related to the colorectal cancer invasion and metastasis process.
  • [MeSH-major] Colorectal Neoplasms. Cytoskeletal Proteins / metabolism. Neoplasm Invasiveness / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Animals. Female. Humans. Intestinal Mucosa / cytology. Intestinal Mucosa / metabolism. Intestinal Mucosa / pathology. Lymphatic Metastasis / pathology. Male. Middle Aged. Neoplasm Staging

  • Genetic Alliance. consumer health - Colorectal Cancer.
  • MedlinePlus Health Information. consumer health - Colorectal Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cancer Res. 2001 May 1;61(9):3750-9 [11325848.001]
  • [Cites] Maturitas. 2008 May 20;60(1):31-41 [18486367.001]
  • [Cites] Gynecol Oncol. 2003 Aug;90(2):273-81 [12893187.001]
  • [Cites] Nat Rev Cancer. 2003 Nov;3(11):877-83 [14668818.001]
  • [Cites] Microvasc Res. 2004 Jan;67(1):18-28 [14709399.001]
  • [Cites] Gut. 2004 Feb;53(2):235-40 [14724156.001]
  • [Cites] Nat Med. 2004 Feb;10(2):175-81 [14704789.001]
  • [Cites] Nat Med. 2004 Feb;10(2):182-6 [14704791.001]
  • [Cites] Cancer Cell. 2004 Feb;5(2):113-4 [14998486.001]
  • [Cites] Urology. 2004 Mar;63(3):609-12 [15028477.001]
  • [Cites] Trends Mol Med. 2004 May;10(5):201-4 [15121044.001]
  • [Cites] Trends Mol Med. 2004 Jun;10(6):249-50 [15177187.001]
  • [Cites] J Cell Biol. 1994 Jul;126(2):391-401 [7518464.001]
  • [Cites] J Biol Chem. 1996 Mar 22;271(12):7224-9 [8636161.001]
  • [Cites] J Pathol. 1996 May;179(1):74-9 [8691349.001]
  • [Cites] Oncogene. 1996 Sep 19;13(6):1231-7 [8808697.001]
  • [Cites] EMBO J. 1997 Jan 2;16(1):35-43 [9009265.001]
  • [Cites] Trends Biochem Sci. 1996 Dec;21(12):455-8 [9009824.001]
  • [Cites] Curr Biol. 1997 Sep 1;7(9):682-8 [9285722.001]
  • [Cites] J Cell Biol. 1998 Feb 23;140(4):885-95 [9472040.001]
  • [Cites] Biochem Biophys Res Commun. 1999 May 10;258(2):395-400 [10329398.001]
  • [Cites] Breast Cancer Res. 2005;7(3):R365-73 [15987432.001]
  • [Cites] Apoptosis. 2005 Oct;10(5):941-7 [16151629.001]
  • [Cites] Cancer Res. 2006 Apr 1;66(7):3629-38 [16585188.001]
  • [Cites] Infect Immun. 2007 Dec;75(12):5669-77 [17908813.001]
  • [Cites] Cancer Lett. 2008 Mar 8;261(1):55-63 [18155831.001]
  • [Cites] Ai Zheng. 2008 Feb;27(2):165-9 [18279614.001]
  • [Cites] J Cell Sci. 2008 Mar 1;121(Pt 5):644-54 [18270268.001]
  • [Cites] Pediatr Blood Cancer. 2008 Apr;50(4):752-6 [17886294.001]
  • [Cites] Pol J Pathol. 2007;58(4):235-43 [18459457.001]
  • [Cites] Mol Biol Cell. 2003 May;14(5):2181-91 [12802084.001]
  • (PMID = 19399936.001).
  • [ISSN] 2219-2840
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Cytoskeletal Proteins; 0 / ezrin
  • [Other-IDs] NLM/ PMC2675094
  •  go-up   go-down


57. Clarke BL, Khosla S: Modulators of androgen and estrogen receptor activity. Crit Rev Eukaryot Gene Expr; 2010;20(4):275-94
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Modulators of androgen and estrogen receptor activity.
  • This review focuses on significant recent findings regarding modulators of androgen and estrogen receptor activity.
  • Selective androgen receptor modulators (SARMs) interact with androgen receptors (ARs), and selective estrogen receptor modulators (SERMs) interact with estrogen receptors (ERs), with variable tissue selectivity.
  • SERMs, which interact with both ERб and ERв in a tissue-specific manner to produce diverse outcomes in multiple tissues, continue to generate significant interest for clinical application.
  • Development of SARMs for clinical application has been slower to date because of potential adverse effects, but these diverse compounds continue to be investigated for use in disorders in which modulation of the AR is important.
  • These compounds have been evaluated mostly for application in different stages of prostate cancer to date, but they hold promise for multiple other applications.
  • Publication of the large STAR and RUTH clinical trials demonstrated that the SERMs tamoxifen and raloxifene have interesting similarities and differences in tissues that contain ERs.
  • Both SARMs and SERMs hold great promise for therapeutic use in multiple disorders in which tissue-specific effects are mediated by their respective receptors.
  • [MeSH-major] Androgen Receptor Antagonists / pharmacology. Receptors, Androgen / drug effects. Receptors, Estrogen / drug effects. Selective Estrogen Receptor Modulators / pharmacology
  • [MeSH-minor] Breast Neoplasms / drug therapy. Clinical Trials as Topic. Female. Humans. Male. Osteoporosis / drug therapy. Prostatic Neoplasms / drug therapy. Raloxifene Hydrochloride / pharmacology. Tamoxifen / pharmacology

  • Hazardous Substances Data Bank. TAMOXIFEN .
  • Hazardous Substances Data Bank. RALOXIFENE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 21395502.001).
  • [ISSN] 1045-4403
  • [Journal-full-title] Critical reviews in eukaryotic gene expression
  • [ISO-abbreviation] Crit. Rev. Eukaryot. Gene Expr.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgen Receptor Antagonists; 0 / Receptors, Androgen; 0 / Receptors, Estrogen; 0 / Selective Estrogen Receptor Modulators; 094ZI81Y45 / Tamoxifen; 4F86W47BR6 / Raloxifene Hydrochloride
  •  go-up   go-down


58. Takeuchi Y: [Cytokines in bone diseases. Involvement of cytokines in bone metastasis]. Clin Calcium; 2010 Oct;20(10):1504-9
MedlinePlus Health Information. consumer health - Bone Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Cytokines in bone diseases. Involvement of cytokines in bone metastasis].
  • Bone metastases are critically involved in both QOL and ADL in patients with malignant diseases.
  • This issue is seriously important for many patients with cancer expecting rather good prognosis.
  • Recent studies indicate that there are several factors either specific to cancer cells or to bone tissue that participate in establishing bone metastasis.
  • Development of therapeutic tools against bone metastasis is now focusing on blocking actions of cytokines that are involved in establishment of bone metastasis.
  • [MeSH-major] Bone Neoplasms / secondary. Cytokines / physiology
  • [MeSH-minor] Activities of Daily Living. Breast Neoplasms / pathology. Drug Discovery. Female. Humans. Male. Molecular Targeted Therapy. Prostatic Neoplasms / pathology. Quality of Life. Thyroid Neoplasms / pathology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20890032.001).
  • [ISSN] 0917-5857
  • [Journal-full-title] Clinical calcium
  • [ISO-abbreviation] Clin Calcium
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Cytokines
  •  go-up   go-down


59. Rosti G, Ferrante P, Ledermann J, Leyvraz S, Ladenstein R, Koscileniak E, Crown J, Dazzi C, Cariello A, Marangolo M: High-dose chemotherapy for solid tumors: results of the EBMT. Crit Rev Oncol Hematol; 2002 Feb;41(2):129-40
MedlinePlus Health Information. consumer health - Cancer Chemotherapy.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High-dose chemotherapy for solid tumors: results of the EBMT.
  • The European Group for Blood and Marrow Transplantation (EBMT), formerly known as European Group for Bone Marrow Transplantation, was established in 1974 in the Netherlands to share experiences, to promote research and clinical studies and to set up registries in the field of hematopoietic tissue transplantation.
  • At the present time more 400 European and non-European centers are members of the EBMT group.
  • In 1984 a new Working Party was created (Solid Tumors) with the aim to investigate the role of high-dose chemotherapy and stem cell support in the fields of adult and pediatric solid tumors.
  • By January 2000 more than 14000 patients were registered, and at the present time this Registry is the world largest database on this subject.
  • Several phase III randomized clinical trials have recently started on behalf of the Group in different diseases (breast carcinoma, small cell lung cancer, ovarian carcinoma, germ cell tumors and Ewing's family sarcoma).
  • Hundreds of randomized patients will finally produce clearer information on this still experimental therapeutic modality.
  • This paper will describe the EBMT Solid Tumors Working Party Registry updated results as well as the main ongoing studies.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Neoplasms / drug therapy
  • [MeSH-minor] Female. Humans. Male. Randomized Controlled Trials as Topic

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11856589.001).
  • [ISSN] 1040-8428
  • [Journal-full-title] Critical reviews in oncology/hematology
  • [ISO-abbreviation] Crit. Rev. Oncol. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 38
  •  go-up   go-down


60. Huss WJ, Gray DR, Greenberg NM, Mohler JL, Smith GJ: Breast cancer resistance protein-mediated efflux of androgen in putative benign and malignant prostate stem cells. Cancer Res; 2005 Aug 01;65(15):6640-50
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Breast cancer resistance protein-mediated efflux of androgen in putative benign and malignant prostate stem cells.
  • Malignantly transformed stem cells represent a potential common nidus for the primary cancer and the recurrent cancer that arises after treatment failure.
  • Putative prostate stem cells and prostate tumor stem cells in benign and malignant human prostate tissue, in primary human prostate xenografts, and in the transgenic adenocarcinoma of the mouse prostate (TRAMP) mouse model of prostate cancer, are defined by expression of breast cancer resistance protein (BCRP), a marker of pluripotent hematopoietic, muscle, and neural stem cells, and by an absence of androgen receptor (AR) protein.
  • In both benign and malignant human prostate tissue, the rare epithelial cells that express BCRP and lack AR protein are localized in the basal cell compartment, survive androgen deprivation, and maintain proliferative potential in the hypoxic, androgen-deprived prostate.
  • Putative prostate tumor stem cells that express BCRP but not AR protein in TRAMP are the source of a BCRP-negative and AR-negative, Foxa2- and SV40Tag-expressing, transit amplifying compartment that progresses to the poorly differentiated carcinomas that arise rapidly after castration.
  • Therefore, BCRP expression isolates prostate stem/tumor stem cells from the prostate tissue microenvironment through constitutive efflux of androgen, protecting the putative tumor stem cells from androgen deprivation, hypoxia, or adjuvant chemotherapy, and providing the nidus for recurrent prostate cancer.
  • [MeSH-major] ATP-Binding Cassette Transporters / biosynthesis. Androgens / metabolism. Neoplasm Proteins / biosynthesis. Neoplastic Stem Cells / metabolism. Prostatic Neoplasms / metabolism
  • [MeSH-minor] ATP Binding Cassette Transporter, Sub-Family G, Member 2. Animals. Cell Line. Cell Nucleus / metabolism. Humans. Indoles / pharmacology. Male. Mice. Mice, Inbred C57BL. Mice, Transgenic. Novobiocin / pharmacology. Prostate / metabolism. Protein Processing, Post-Translational. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Rats. Receptors, Androgen / biosynthesis. Receptors, Androgen / deficiency. Receptors, Androgen / genetics. Receptors, Androgen / metabolism. Transplantation, Heterologous

  • Genetic Alliance. consumer health - Prostate cancer.
  • Genetic Alliance. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. NOVOBIOCIN .
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16061644.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA84296; United States / NCI NIH HHS / CA / P01 CA077739; United States / NCI NIH HHS / CA / CA77739; United States / NCI NIH HHS / CA / CA64851; United States / NIEHS NIH HHS / ES / ES07017; United States / NCI NIH HHS / CA / CA64865
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ABCG2 protein, human; 0 / ATP Binding Cassette Transporter, Sub-Family G, Member 2; 0 / ATP-Binding Cassette Transporters; 0 / Androgens; 0 / Indoles; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / Receptors, Androgen; 17EC19951N / Novobiocin; CW5S8OP3VO / tryptoquivaline
  •  go-up   go-down


61. Ghetie C, Davies M, Cornfeld D, Suh N, Saif MW: Expectoration of a lung metastasis in a patient with colorectal carcinoma. Clin Colorectal Cancer; 2008 Jul;7(4):283-6
MedlinePlus Health Information. consumer health - Lung Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expectoration of a lung metastasis in a patient with colorectal carcinoma.
  • Metastatic disease is present in up to 20% of patients at the time of diagnosis of colorectal cancer.
  • A rare form of lung metastatic disease is endobronchial metastases, most commonly seen with breast cancer and colon cancer.
  • Their clinical and imaging profile is similar to primary bronchogenic carcinoma.
  • Tumor expectoration is an unusual manifestation of endobronchial metastases (as well as of the primary lung carcinoma).
  • We report the case of a 75-year-old man with known liver and lung metastatic disease from colon cancer who experienced an episode of tissue expectoration.
  • Pathology examination of the expectorated piece of tissue was consistent with colonic adenocarcinoma.
  • Tumor expectoration is a rare event, with < 30 cases reported in the literature.
  • Most of the cases reported include secondary lung malignancies, with renal cell carcinoma being the most common primary site.
  • Endobronchial metastases from colon cancer are rare.
  • Patients with colon cancer can benefit from sputum cytology because this type of metastases is shown to have exfoliative properties.
  • To assess the need for endobronchial management with stent placement or bracytherapy, bronchoscopy should be considered in certain circumstances (the onset of respiratory symptoms, rapid response to chemotherapy, long history of metastatic disease with multiple systemic therapies given, undulating response in tumor, as well as after a reported episode of tissue expectoration).
  • [MeSH-major] Adenocarcinoma / secondary. Colorectal Neoplasms / pathology. Cough / etiology. Hemoptysis / etiology. Lung Neoplasms / secondary. Sputum
  • [MeSH-minor] Aged. Bronchoscopy. Humans. Liver Neoplasms / secondary. Male. Risk Factors

  • MedlinePlus Health Information. consumer health - Colorectal Cancer.
  • MedlinePlus Health Information. consumer health - Cough.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18650198.001).
  • [ISSN] 1533-0028
  • [Journal-full-title] Clinical colorectal cancer
  • [ISO-abbreviation] Clin Colorectal Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 29
  •  go-up   go-down


62. Twelves C: Vision of the future: capecitabine. Oncologist; 2001;6 Suppl 4:35-9
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Capecitabine is a thymidine phosphorylase (TP)-activated oral fluoropyrimidine, rationally designed to generate 5-fluorouracil (5-FU) preferentially within tumors.
  • This tumor selectivity is achieved through exploitation of the significantly higher activity of TP in tumor compared with healthy tissue.
  • The high single-agent activity of capecitabine in breast and colorectal cancer suggests that capecitabine may have a role in the treatment of other tumor types that are sensitive to 5-FU, such as pancreatic cancer.
  • Tumor types known to have a high level of TP activity, such as renal cancer, are especially attractive targets for capecitabine therapy.
  • Capecitabine has potential as monotherapy in these tumor types, or as a combination partner for other cytotoxic agents with different mechanisms of action and little overlap of key toxicities.
  • In particular, some cytotoxic drugs, such as the taxanes and cyclophosphamide, are known to upregulate TP activity in tumor tissue, offering the potential for synergistic action.
  • The combination of capecitabine and docetaxel has demonstrated significant activity in women with anthracycline-pretreated breast cancer, and is the only cytotoxic combination to significantly increase survival compared with standard therapy in this setting.
  • In addition, capecitabine as monotherapy or in combination with other cytotoxic agents has shown encouraging activity in pancreatic, ovarian, and renal cell cancers.
  • This article discusses recent data from clinical trials investigating capecitabine in a range of tumor types, highlighting the potential future role of capecitabine as an alternative to traditional i.v. chemotherapy.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Breast Neoplasms / drug therapy. Deoxycytidine / analogs & derivatives. Deoxycytidine / therapeutic use. Kidney Neoplasms / drug therapy. Ovarian Neoplasms / drug therapy. Pancreatic Neoplasms / drug therapy
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Capecitabine. Female. Fluorouracil / therapeutic use. Humans. Male


63. Blum R, Prince HM, Hicks RJ, Patrikeos A, Seymour J: Discordant response to chemotherapy detected by PET scanning: unveiling of a second primary cancer. Am J Clin Oncol; 2002 Aug;25(4):368-70
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Discordant response to chemotherapy detected by PET scanning: unveiling of a second primary cancer.
  • Positron emission Tomography (PET) is commonly used to stage malignancies and monitor response to treatment.
  • This report describes two patients, one with metastatic breast cancer and the other with aggressive non-Hodgkin's lymphoma (NHL) whose responses to treatment were monitored by serial computed tomography and PET scans.
  • In both cases after completion of systemic chemotherapy, repeat PET scanning revealed residual metabolically active tissue at the base of the neck.
  • Because of differential therapeutic response, the possibility of different pathologic lesions was raised.
  • Both patients were subsequently treated with definitive surgery.
  • In both described cases, a second primary malignancy was found that affected further management and in the second patient altered prognosis.
  • This report concludes that residual metabolically active tissue on PET scans after treatment is not necessarily resistant primary disease.
  • [MeSH-major] Breast Neoplasms / radionuclide imaging. Head and Neck Neoplasms / diagnosis. Lymphoma, Non-Hodgkin / radionuclide imaging. Neoplasm, Residual / diagnosis. Neoplasms, Second Primary / diagnosis. Thyroid Neoplasms / diagnosis. Tomography, Emission-Computed
  • [MeSH-minor] Adult. Biopsy, Needle. Diagnosis, Differential. Female. Humans. Male

  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Head and Neck Cancer.
  • MedlinePlus Health Information. consumer health - Thyroid Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12151967.001).
  • [ISSN] 0277-3732
  • [Journal-full-title] American journal of clinical oncology
  • [ISO-abbreviation] Am. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


64. Benson AB 3rd, Olopade OI, Ratain MJ, Rademaker A, Mobarhan S, Stucky-Marshall L, French S, Dolan ME: Chronic daily low dose of 4-methyl-5-(2-pyrazinyl)-1,2-dithiole-3-thione (Oltipraz) in patients with previously resected colon polyps and first degree female relatives of breast cancer patients. Clin Cancer Res; 2000 Oct;6(10):3870-7
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chronic daily low dose of 4-methyl-5-(2-pyrazinyl)-1,2-dithiole-3-thione (Oltipraz) in patients with previously resected colon polyps and first degree female relatives of breast cancer patients.
  • The chemoprevention agent oltipraz, one of the most active chemopreventive compounds in preclinical studies, has been shown to induce glutathione-S-transferase (GST) activity in animals.
  • Oltipraz was evaluated in a Phase I trial at daily oral doses of 20 mg (L1), 50 mg (L2), and 100 mg (L3) and twice weekly doses of 125 mg (L4) taken for 6 months with 6 patients entered at L1 and L2 and 7 patients entered at L3 and L4 (26 subjects: 19 females and 7 males).
  • The subject population included patients with previously resected colon polyps and first-degree female relatives of breast cancer patients.
  • Of the 26 subjects, the following completed 6 months of therapy: 4 of 6 patients (L1), 4 of 6 patients (L2), 5 of 7 patients (L3), and 4 of 7 patients (L4).
  • There was a significant difference in mean oltipraz concentration across the four doses, with no significant differences in mean oltipraz concentration over time.
  • Rectal tissue and lymphocyte GSH and GST were variable, with no significant difference in mean levels across doses.
  • At the 100-mg/day dose (L3), 1 patient experienced significant increase in rectal tissue GSH and GST activity, whereas 3 additional patients (L1 and L4) had >50% increase in tissue GSH.
  • There were no significant correlations between plasma oltipraz concentration and lymphocyte GST level nor any significant correlation between plasma concentration and percentage of change in tissue GSH or GST.
  • [MeSH-major] Anticarcinogenic Agents / therapeutic use. Breast Neoplasms / prevention & control. Colonic Polyps / complications. Colonic Polyps / surgery. Pyrazines / therapeutic use
  • [MeSH-minor] Biopsy. Dose-Response Relationship, Drug. Female. Glutathione / blood. Glutathione / metabolism. Glutathione Transferase / blood. Glutathione Transferase / metabolism. Hot Temperature. Humans. Lymphocytes / metabolism. Male. Rectum / metabolism. Time Factors

  • Genetic Alliance. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Colonic Polyps.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11051232.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CN / N01-CN25527
  • [Publication-type] Clinical Trial; Clinical Trial, Phase I; Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Pyrazines; 6N510JUL1Y / oltipraz; EC 2.5.1.18 / Glutathione Transferase; GAN16C9B8O / Glutathione
  •  go-up   go-down


65. Ozcanli H, Ozdemir H, Ozenci AM, Söyüncü Y, Aydin AT: [Metastatic tumors of the hand in three cases]. Acta Orthop Traumatol Turc; 2005;39(5):445-8
MedlinePlus Health Information. consumer health - Bone Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Metastatic tumors of the hand in three cases].
  • Metastatic malignancies of the hand are rare and they usually develop from lung, breast, and kidney tumors.
  • Metastases to the bones of the hand can cause pain, swelling, soft tissue ulceration, and osteolytic destruction.
  • We presented three patients with metastatic tumors of the hand, whose ages were 58 (male), 42 (female), and 40 (male) years.
  • Metastases developed in the thumb and the big toe, metacarpal bone, and the nail bed following treatment for primary tumors of the bladder, colon, and chondrosarcoma of the proximal femur, respectively.
  • One patient underwent amputation of the thumb and the big toe followed by systemic chemotherapy, one patient with metacarpal involvement was treated with Ray amputation, and the latter underwent a biopsy.
  • Histopathological diagnoses were consistent with primary tumors.
  • [MeSH-major] Adenocarcinoma / diagnosis. Bone Neoplasms / diagnosis. Hand
  • [MeSH-minor] Adult. Colonic Neoplasms / diagnosis. Colonic Neoplasms / pathology. Combined Modality Therapy. Diagnosis, Differential. Female. Humans. Male. Middle Aged. Neoplasm Metastasis. Urinary Bladder Neoplasms / diagnosis. Urinary Bladder Neoplasms / pathology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16531705.001).
  • [ISSN] 1017-995X
  • [Journal-full-title] Acta orthopaedica et traumatologica turcica
  • [ISO-abbreviation] Acta Orthop Traumatol Turc
  • [Language] tur
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] Turkey
  • [Number-of-references] 25
  •  go-up   go-down


66. Shanle EK, Xu W: Selectively targeting estrogen receptors for cancer treatment. Adv Drug Deliv Rev; 2010 Oct 30;62(13):1265-76
MedlinePlus Health Information. consumer health - Cancer Chemotherapy.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Selectively targeting estrogen receptors for cancer treatment.
  • Estrogens regulate growth and development through the action of two distinct estrogen receptors (ERs), ERα and ERβ, which mediate proliferation and differentiation of cells.
  • For decades, ERα mediated estrogen signaling has been therapeutically targeted to treat breast cancer, most notably with the selective estrogen receptor modulator (SERM) tamoxifen.
  • Selectively targeting ERs occurs at two levels: tissue selectivity and receptor subtype selectivity.
  • SERMs have been developed with emphasis on tissue selectivity to target ER signaling for breast cancer treatment.
  • Additionally, new approaches to selectively target the action of ERα going beyond ligand-dependent activity are under current investigation.
  • As evidence of the anti-proliferative role of ERβ accumulates, selectively targeting ERβ is an attractive approach for designing new cancer therapies with the emphasis shifted to designing ligands with subtype selectivity.
  • This review will present the mechanistic and structural features of ERs that determine tissue and subtype selectivity with an emphasis on current approaches to selectively target ERα and ERβ for cancer treatment.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Published by Elsevier B.V.
  • [Cites] Mol Cell. 2005 May 13;18(4):413-24 [15893725.001]
  • [Cites] Mol Endocrinol. 2005 Jun;19(6):1555-68 [15802376.001]
  • [Cites] Oncol Rep. 2005 Jul;14(1):17-21 [15944762.001]
  • [Cites] Oncogene. 2005 Oct 6;24(44):6605-16 [16007178.001]
  • [Cites] J Urol. 2005 Nov;174(5):2051-3 [16217392.001]
  • [Cites] Endocrine. 2005 Aug;27(3):227-38 [16230778.001]
  • [Cites] N Engl J Med. 2006 Jan 19;354(3):270-82 [16421368.001]
  • [Cites] J Clin Invest. 2006 Mar;116(3):561-70 [16511588.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Feb 21;103(8):2959-64 [16477031.001]
  • [Cites] Breast. 2006 Apr;15(2):142-57 [16289904.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Aug 29;103(35):13162-7 [16938840.001]
  • [Cites] Cancer Res. 2006 Dec 1;66(23):11207-13 [17145865.001]
  • [Cites] Cancer Cell. 2006 Dec;10(6):487-99 [17157789.001]
  • [Cites] Cancer Res. 2007 Apr 15;67(8):3955-62 [17440111.001]
  • [Cites] Breast Cancer Res. 2007;9(2):R25 [17428314.001]
  • [Cites] J Endocrinol. 2007 Jun;193(3):421-33 [17535880.001]
  • [Cites] Physiol Rev. 2007 Jul;87(3):905-31 [17615392.001]
  • [Cites] J Cell Biochem. 2007 Aug 1;101(5):1125-47 [17520659.001]
  • [Cites] Mol Cell. 2007 Sep 7;27(5):691-700 [17803935.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Sep 11;104(37):14718-23 [17785410.001]
  • [Cites] Cancer Res. 2007 Oct 1;67(19):9549-60 [17909066.001]
  • [Cites] Rev Endocr Metab Disord. 2007 Sep;8(3):229-39 [17440819.001]
  • [Cites] J Clin Oncol. 2007 Dec 20;25(36):5815-24 [17893378.001]
  • [Cites] J Steroid Biochem Mol Biol. 2008 Jan;108(1-2):23-31 [17962013.001]
  • [Cites] Steroids. 2008 Mar;73(3):233-44 [18093629.001]
  • [Cites] Mol Cell Endocrinol. 2008 Feb 13;283(1-2):49-57 [18177995.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Feb 19;105(7):2433-8 [18268329.001]
  • [Cites] Nucl Recept Signal. 2008;6:e003 [18301783.001]
  • [Cites] J Steroid Biochem Mol Biol. 2008 Mar;109(1-2):1-10 [18243688.001]
  • [Cites] J Clin Oncol. 2008 Apr 1;26(10):1664-70 [18316794.001]
  • [Cites] FASEB J. 2008 May;22(5):1512-20 [18055862.001]
  • [Cites] J Biol Chem. 2008 May 9;283(19):12819-30 [18337247.001]
  • [Cites] Breast Cancer Res Treat. 2008 May;109(2):241-50 [17638070.001]
  • [Cites] ACS Chem Biol. 2008 May 16;3(5):282-6 [18484708.001]
  • [Cites] Mol Endocrinol. 2008 Jul;22(7):1535-51 [18388150.001]
  • [Cites] J Med Chem. 2008 Oct 23;51(20):6512-30 [18785725.001]
  • [Cites] Cancer Res. 2008 Nov 1;68(21):8695-704 [18974111.001]
  • [Cites] Mol Cell Endocrinol. 2008 Nov 25;295(1-2):94-100 [18762230.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Dec 2;105(48):19012-7 [19022902.001]
  • [Cites] Cancer Prev Res (Phila). 2009 Jan;2(1):52-9 [19139018.001]
  • [Cites] Anticancer Agents Med Chem. 2009 Jun;9(5):481-99 [19519291.001]
  • [Cites] Nat Rev Cancer. 2009 Sep;9(9):631-43 [19701242.001]
  • [Cites] J Cell Physiol. 2010 Jan;222(1):156-67 [19780039.001]
  • [Cites] Mol Endocrinol. 2010 Jan;24(1):33-46 [19901195.001]
  • [Cites] Mol Cell Endocrinol. 2010 Feb 5;315(1-2):201-7 [19744542.001]
  • [Cites] Breast Cancer Res Treat. 2010 Apr;120(3):557-65 [19434490.001]
  • [Cites] Med Res Rev. 2011 May;31(3):364-442 [19967775.001]
  • [Cites] Cancer Res. 2001 Sep 15;61(18):6768-76 [11559549.001]
  • [Cites] Physiol Rev. 2001 Oct;81(4):1535-65 [11581496.001]
  • [Cites] J Med Chem. 2001 Nov 22;44(24):4230-51 [11708925.001]
  • [Cites] Mol Endocrinol. 2007 Jan;21(1):1-13 [16556737.001]
  • [Cites] Endocrinology. 2007 Feb;148(2):566-74 [17068134.001]
  • [Cites] Mol Endocrinol. 2007 Apr;21(4):829-42 [17185393.001]
  • [Cites] Endocrinology. 1999 Dec;140(12):5566-78 [10579320.001]
  • [Cites] J Mol Endocrinol. 2000 Feb;24(1):145-55 [10657006.001]
  • [Cites] J Biol Chem. 2000 Feb 25;275(8):5379-87 [10681512.001]
  • [Cites] J Mammary Gland Biol Neoplasia. 1997 Oct;2(4):323-34 [10935020.001]
  • [Cites] Development. 2000 Oct;127(19):4277-91 [10976058.001]
  • [Cites] J Med Chem. 2000 Dec 28;43(26):4934-47 [11150164.001]
  • [Cites] Cancer Res. 2001 Jan 15;61(2):632-40 [11212261.001]
  • [Cites] J Steroid Biochem Mol Biol. 2000 Nov 30;74(5):311-7 [11162939.001]
  • [Cites] J Steroid Biochem Mol Biol. 2001 Jan-Mar;76(1-5):61-70 [11384864.001]
  • [Cites] Nucleic Acids Res. 2001 Jul 15;29(14):2905-19 [11452016.001]
  • [Cites] Clin Ther. 2002;24 Suppl A:A17-30 [11911506.001]
  • [Cites] Science. 2002 Mar 29;295(5564):2380-1 [11923515.001]
  • [Cites] Science. 2002 Mar 29;295(5564):2465-8 [11923541.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Nov 26;99(24):15578-83 [12438700.001]
  • [Cites] Prostate. 2003 Feb 1;54(2):79-87 [12497580.001]
  • [Cites] Mol Endocrinol. 2003 Feb;17(2):247-58 [12554752.001]
  • [Cites] Eur J Cancer. 2003 Jun;39(9):1251-8 [12763213.001]
  • [Cites] Breast Cancer Res Treat. 2003 May;79(2):161-73 [12825851.001]
  • [Cites] Anticancer Res. 2003 May-Jun;23(3B):2419-24 [12894523.001]
  • [Cites] Endocrinology. 2003 Oct;144(10):4241-9 [14500559.001]
  • [Cites] Nat Med. 2004 Jan;10(1):40-7 [14702633.001]
  • [Cites] Cancer Res. 2004 Jan 1;64(1):423-8 [14729654.001]
  • [Cites] J Med Chem. 2004 Jan 29;47(3):600-11 [14736241.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Feb 10;101(6):1566-71 [14745018.001]
  • [Cites] FEBS Lett. 2004 May 21;566(1-3):169-72 [15147889.001]
  • [Cites] Endocrinology. 2004 Jul;145(7):3473-86 [15033914.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Jun 22;101(25):9375-80 [15187231.001]
  • [Cites] Science. 1986 Mar 7;231(4742):1150-4 [3753802.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Dec 1;90(23):11162-6 [8248223.001]
  • [Cites] J Cell Sci. 1993 Dec;106 ( Pt 4):1377-88 [8126115.001]
  • [Cites] J Natl Cancer Inst. 1995 Jul 19;87(14):1067-71 [7616598.001]
  • [Cites] Mol Endocrinol. 1995 Apr;9(4):443-56 [7659088.001]
  • [Cites] Nat Struct Biol. 1996 Jan;3(1):87-94 [8548460.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Jun 11;93(12):5925-30 [8650195.001]
  • [Cites] Endocrinology. 1997 Mar;138(3):863-70 [9048584.001]
  • [Cites] Nature. 1997 Jun 12;387(6634):733-6 [9192902.001]
  • [Cites] Science. 1997 Sep 5;277(5331):1508-10 [9278514.001]
  • [Cites] Nature. 1997 Oct 16;389(6652):753-8 [9338790.001]
  • [Cites] J Clin Endocrinol Metab. 1997 Dec;82(12):4258-65 [9398750.001]
  • [Cites] Mol Endocrinol. 1998 Feb;12(2):302-13 [9482670.001]
  • [Cites] Science. 1998 Jun 12;280(5370):1747-9 [9624051.001]
  • [Cites] Biochem Biophys Res Commun. 1998 Jun 9;247(1):75-8 [9636657.001]
  • [Cites] Curr Opin Cell Biol. 1998 Jun;10(3):384-91 [9640540.001]
  • [Cites] Nucleic Acids Res. 1998 Aug 1;26(15):3505-12 [9671811.001]
  • [Cites] Endocrinology. 1998 Oct;139(10):4252-63 [9751507.001]
  • [Cites] J Natl Cancer Inst. 1998 Oct 21;90(20):1552-8 [9790548.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Dec 22;95(26):15677-82 [9861029.001]
  • [Cites] Cell. 1998 Dec 23;95(7):927-37 [9875847.001]
  • [Cites] Endocr Rev. 1999 Jun;20(3):358-417 [10368776.001]
  • [Cites] J Steroid Biochem Mol Biol. 1999 Apr-Jun;69(1-6):165-75 [10418990.001]
  • [Cites] EMBO J. 1999 Sep 1;18(17):4608-18 [10469641.001]
  • [Cites] Mol Endocrinol. 1999 Oct;13(10):1672-85 [10517669.001]
  • [Cites] J Am Chem Soc. 2004 Nov 24;126(46):15106-19 [15548008.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Feb 1;102(5):1484-9 [15665095.001]
  • [Cites] Eur J Cancer. 2005 Feb;41(3):346-56 [15691633.001]
  • [Cites] Annu Rev Physiol. 2005;67:285-308 [15709960.001]
  • [Cites] J Mol Endocrinol. 2005 Apr;34(2):553-66 [15821116.001]
  • [Cites] Lancet. 2005 May 14-20;365(9472):1687-717 [15894097.001]
  • (PMID = 20708050.001).
  • [ISSN] 1872-8294
  • [Journal-full-title] Advanced drug delivery reviews
  • [ISO-abbreviation] Adv. Drug Deliv. Rev.
  • [Language] ENG
  • [Grant] United States / NIMH NIH HHS / MH / R03MH089442; United States / NIMH NIH HHS / MH / R03 MH089442; United States / NCI NIH HHS / CA / R01CA125387; United States / NCI NIH HHS / CA / R01 CA125387; United States / NIEHS NIH HHS / ES / T32 ES007015
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Estrogen Receptor alpha; 0 / Estrogen Receptor beta; 0 / Ligands; 0 / Selective Estrogen Receptor Modulators
  • [Other-IDs] NLM/ NIHMS229613; NLM/ PMC2991615
  •  go-up   go-down


67. Mercatante DR, Mohler JL, Kole R: Cellular response to an antisense-mediated shift of Bcl-x pre-mRNA splicing and antineoplastic agents. J Biol Chem; 2002 Dec 20;277(51):49374-82
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Overexpression of Bcl-xL, an anti-apoptotic member of the Bcl-2 family, negatively correlates with the sensitivity of various cancers to chemotherapeutic agents.
  • It also suggests a specificity of the oligonucleotide effects since non-cancerous cells with low levels of Bcl-xL should resist the treatment.
  • 5'Bcl-x AS sensitized cells to several antineoplastic agents and radiation and was effective in promoting apoptosis of MCF-7/ADR cells, a breast cancer cell line resistant to doxorubicin via overexpression of the mdr1 gene.
  • Efficacy of 5'Bcl-x AS combined with chemotherapeutic agents in the PC3 prostate cancer cell line may be translated to clinical prostate cancer since recurrent prostate cancer tissue samples expressed higher levels of Bcl-xL than benign prostate tissue.
  • Treatment with 5'Bcl-x AS may enhance the efficacy of standard anti-cancer regimens and should be explored, especially in recurrent prostate cancer.
  • [MeSH-minor] Alternative Splicing. Apoptosis. Blotting, Western. Breast Neoplasms / drug therapy. Cisplatin / pharmacology. Dose-Response Relationship, Drug. Dose-Response Relationship, Radiation. Doxorubicin / pharmacology. Female. Humans. Male. Models, Genetic. Oligonucleotides / pharmacology. Prostate / drug effects. Prostate / metabolism. Prostatic Neoplasms / metabolism. Protein Binding. RNA / metabolism. RNA Splicing. Radiation-Sensitizing Agents / pharmacology. Recurrence. Reverse Transcriptase Polymerase Chain Reaction. Ribonucleases / metabolism. Time Factors. Transfection. Tumor Cells, Cultured. bcl-X Protein

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. CIS-DIAMINEDICHLOROPLATINUM .
  • Hazardous Substances Data Bank. DOXORUBICIN .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12381725.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01 CA 77739; United States / NIGMS NIH HHS / GM / P01 GM 59299-01
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / BCL2L1 protein, human; 0 / Oligonucleotides; 0 / Oligonucleotides, Antisense; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Messenger; 0 / Radiation-Sensitizing Agents; 0 / bcl-X Protein; 63231-63-0 / RNA; 80168379AG / Doxorubicin; EC 3.1.- / Ribonucleases; Q20Q21Q62J / Cisplatin
  •  go-up   go-down


68. Safe S, McDougal A: Mechanism of action and development of selective aryl hydrocarbon receptor modulators for treatment of hormone-dependent cancers (Review). Int J Oncol; 2002 Jun;20(6):1123-8
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mechanism of action and development of selective aryl hydrocarbon receptor modulators for treatment of hormone-dependent cancers (Review).
  • Ligand-activated receptors are extensively used as targets for developing tissue-selective drugs for treatment of multiple diseases including cancers.
  • The high affinity ligand TCDD induces several AhR-mediated changes in gene expression, tissue/species-specific toxicities, and both tumorigenic and anticarcinogenic responses including inhibition of estrogen-dependent mammary and uterine tumor formation and growth.
  • Research in this laboratory has demonstrated that TCDD inhibits E2-induced responses in the rodent uterus and mammary tumors (growth inhibition) and in breast and endometrial cancer cell lines through complex inhibitory AhR-estrogen receptor (ER) crosstalk.
  • These compounds are relatively non-toxic and inhibit ER-positive and ER-negative mammary tumor growth, and synergize with tamoxifen to inhibit breast cancer growth and block tamoxifen-induced estrogenic activity in the uterus.
  • Preliminary studies also indicate that SAhRMs inhibit prostate cancer cell growth, and there is evidence for inhibitory AhR-androgen receptor crosstalk.
  • SAhRMs represent a novel class of drugs for treatment of hormone-dependent cancers, and combined therapies of SAhRMs with tamoxifen and other selective ER modulators (SERMs) provides a new approach for treating women with breast cancer.
  • [MeSH-major] Neoplasms, Hormone-Dependent / drug therapy. Receptors, Aryl Hydrocarbon / drug effects
  • [MeSH-minor] Animals. Breast Neoplasms / drug therapy. Female. Humans. Male. Receptors, Estrogen / analysis. Receptors, Estrogen / antagonists & inhibitors. Receptors, Estrogen / drug effects. Selective Estrogen Receptor Modulators / therapeutic use. Tetrachlorodibenzodioxin / pharmacology

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12011988.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA64081; United States / NIEHS NIH HHS / ES / ES04176; United States / NIEHS NIH HHS / ES / ES09106
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Receptors, Aryl Hydrocarbon; 0 / Receptors, Estrogen; 0 / Selective Estrogen Receptor Modulators; DO80M48B6O / Tetrachlorodibenzodioxin
  •  go-up   go-down


69. Ivanov O, Chen F, Wiley EL, Keswani A, Diaz LK, Memmel HC, Rademaker A, Gradishar WJ, Morrow M, Khan SA, Cryns VL: alphaB-crystallin is a novel predictor of resistance to neoadjuvant chemotherapy in breast cancer. Breast Cancer Res Treat; 2008 Oct;111(3):411-7
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] alphaB-crystallin is a novel predictor of resistance to neoadjuvant chemotherapy in breast cancer.
  • AIMS: alphaB-crystallin is an anti-apoptotic protein commonly expressed in poor prognosis basal-like breast tumors, which are largely triple (estrogen receptor (ER), progesterone receptor (PR), and HER2) negative.
  • We examined whether alphaB-crystallin expression in breast cancer was associated with a poor response to neoadjuvant (preoperative) chemotherapy.
  • METHODS: One hundred and twelve breast cancer patients who received neoadjuvant chemotherapy and who had post-chemotherapy tumor specimens available for analysis were included in the study.
  • Forty-nine percent of patients were treated with doxorubicin and cyclophosphamide (AC), 37% received AC in combination with a taxane, and 14% received other regimens.
  • Paired pre- and post-chemotherapy tumor specimens were available for 33 patients. alphaB-crystallin expression was determined by immunohistochemistry in tissue microarrays.
  • RESULTS: Seventeen percent of tumors were alphaB-crystallin positive. alphaB-crystallin expression was identical in 32 of 33 cases for which both pre- and post-chemotherapy tumor tissue was available. alphaB-crystallin expression was associated with ER-negative (P = 0.0024) and triple negative status (P = 0.005).
  • Overall response rates (ORR) defined as > or =50% reduction in tumor size after treatment were 53% (clinical ORR) and 61% (pathological ORR).
  • Although tumor grade, size, ER, PR, HER2 or triple negative status was not associated with response, alphaB-crystallin-positive tumors had poorer overall response rates than alphaB-crystallin-negative tumors (clinical ORR, 21% vs. 59%, respectively, P = 0.0045; pathological ORR, 16% vs. 70%, respectively, P < 0.0001).
  • CONCLUSION: alphaB-crystallin is a novel biomarker expressed predominantly in triple negative breast tumors that identifies a subset of chemotherapy-resistant tumors, which may contribute to their poor prognosis.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biomarkers, Tumor / analysis. Breast Neoplasms / chemistry. Breast Neoplasms / drug therapy. Drug Resistance, Neoplasm. alpha-Crystallin B Chain / analysis
  • [MeSH-minor] Adult. Aged. Chemotherapy, Adjuvant. Female. Humans. Male. Middle Aged. Neoadjuvant Therapy. Receptor, ErbB-2 / analysis. Receptors, Estrogen / analysis. Receptors, Progesterone / analysis. Treatment Failure

  • Genetic Alliance. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17968656.001).
  • [ISSN] 0167-6806
  • [Journal-full-title] Breast cancer research and treatment
  • [ISO-abbreviation] Breast Cancer Res. Treat.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01CA097198; United States / NCI NIH HHS / CA / R21CA125181
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Receptors, Estrogen; 0 / Receptors, Progesterone; 0 / alpha-Crystallin B Chain; EC 2.7.10.1 / ERBB2 protein, human; EC 2.7.10.1 / Receptor, ErbB-2
  •  go-up   go-down


70. Morré DJ, Hostetler B, Weston N, Kim C, Morré DM: Cancer type-specific tNOX isoforms: A putative family of redox protein splice variants with cancer diagnostic and prognostic potential. Biofactors; 2008;34(3):201-7
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cancer type-specific tNOX isoforms: A putative family of redox protein splice variants with cancer diagnostic and prognostic potential.
  • A proteomics approach with detection on western blots using an S-peptide tagged pan-tNOX (ENOX2) recombinant (scFv) antibody followed by alkaline phosphatase-linked anti S has revealed a family of more than 20 ENOX2 isoforms of varying molecular weights (34 to 94 kDa) and mostly of low isoelectric points (4.6 +/- 0.7) based on serum analysis.
  • Different isoforms characterize cancers of different tissue origins indicative of both cancer presence and tissue site of origin.
  • ENOX2 proteins are cancer-associated and differ from constitutive (CNOX or ENOX1) proteins primarily by the absence of a drug binding site to which the cancer-specific scFv is directed.
  • The tNOX isoform technology is under development as a clinical aid to identify unknown or uncertain primary cancers, evaluation of metastatic spread in post surgery patients, monitoring remission following cessation of therapy and for early diagnosis in at-risk populations.
  • [MeSH-major] NADH, NADPH Oxidoreductases / analysis. NADH, NADPH Oxidoreductases / metabolism. Neoplasms / metabolism. Protein Isoforms / analysis. Protein Isoforms / metabolism
  • [MeSH-minor] Blotting, Western. Breast Neoplasms / metabolism. Colonic Neoplasms / metabolism. Electrophoresis, Gel, Two-Dimensional. Female. Humans. Lung Neoplasms / metabolism. Lymphoma, Non-Hodgkin / metabolism. Male. Melanoma / metabolism. Ovarian Neoplasms / metabolism. Pancreatic Neoplasms / mortality. Prostatic Neoplasms / metabolism. Uterine Cervical Neoplasms

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19734121.001).
  • [ISSN] 1872-8081
  • [Journal-full-title] BioFactors (Oxford, England)
  • [ISO-abbreviation] Biofactors
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Protein Isoforms; EC 1.6.- / NADH, NADPH Oxidoreductases; EC 1.6.- / tumor-associated NADH oxidase
  •  go-up   go-down


71. Di Somma S, Di Benedetto MP, Salvatore G, Agozzino L, Ferranti F, Esposito S, La Dogana P, Scarano MI, Caputo G, Cotrufo M, Santo LD, de Divitiis O: Desmin-free cardiomyocytes and myocardial dysfunction in end stage heart failure. Eur J Heart Fail; 2004 Jun;6(4):389-98
MedlinePlus Health Information. consumer health - Heart Failure.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Our aim was to evaluate the desmin content in the myocardial tissue of patients with end-stage heart failure of ischaemic origin and to assess its role on cardiac function.
  • Control myocardial tissue was obtained from the cardiac biopsies of six women with breast cancer taken prior to commencing chemotherapy with anthracyclines, four male donors for heart transplantation and two autoptic hearts from patients who died due to non-cardiac events.
  • Myocardial tissue, obtained from the left ventricle (remote zone from infarcted area), was analyzed by light and confocal immunochemistry (desmin) microscopy.
  • The desmin content of myocardial tissue was obtained by real-time PCR.
  • At real-time PCR evaluation, there was a reduction (P<0.01) in desmin content in the ICM patients compared to controls.
  • In conclusion, the myocardial tissue of patients with end-stage heart failure of ischaemic origin, shows a decreased number in desmin-positive myocytes at immunochemistry evaluation compared to normal individuals.
  • This deficiency in cytoskeletal intermediate filament content is associated with reduced cardiac function.
  • [MeSH-minor] Cardiomyopathy, Dilated / complications. Cardiomyopathy, Dilated / physiopathology. Coronary Angiography. Echocardiography, Doppler. Female. Heart Transplantation. Heart Ventricles / pathology. Heart Ventricles / radiography. Heart Ventricles / ultrasonography. Humans. Immunohistochemistry. Male. Microscopy, Polarization. Myocardial Infarction / complications. Myocardial Infarction / physiopathology. Severity of Illness Index. Staining and Labeling. Stroke Volume / physiology. Treatment Outcome

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15182762.001).
  • [ISSN] 1388-9842
  • [Journal-full-title] European journal of heart failure
  • [ISO-abbreviation] Eur. J. Heart Fail.
  • [Language] eng
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Desmin
  •  go-up   go-down


72. Nio Y, Toga T, Maruyama R, Fukushima M: Expression of orotate phosphoribosyl transferase in human pancreatic cancer: implication for the efficacy of uracil and tegafur-based adjuvant chemotherapy. Oncol Rep; 2007 Jul;18(1):59-64
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of orotate phosphoribosyl transferase in human pancreatic cancer: implication for the efficacy of uracil and tegafur-based adjuvant chemotherapy.
  • The enzyme orotate phosphoribosyl transferase (OPRT) is involved in the metabolism of the anticancer drug 5-fluorouracil (5-FU), and is a key enzyme for conversion of 5-FU to its active form in tumor tissue.
  • Little is known regarding the significance of OPRT in human pancreatic cancer.
  • The present study was designed to assess the association between the activity of OPRT in the tumor, and the clinicopathological status and prognosis of human resectable pancreatic cancer, especially regarding its relevance to the efficacy of adjuvant chemotherapy with uracil and tegafur (UFT), cyclophosphamide (CPA) and/or gemcitabine (GEM).
  • The present study included 99 resectable pancreatic cancers, which were all invasive ductal tubular carcinomas.
  • OPRT was immunostained with a rabbit anti-human OPRT polyclonal antibody.
  • OPRT was positively stained in 54 (54.5%) of 99 pancreatic cancers.
  • The post-surgical survival rate of the OPRT (+) pancreatic cancers was significantly higher than that of the OPRT (-) ones.
  • In the OPRT (+) group, the survival rate of the patients, who received adjuvant chemotherapy (ACT) with UFT, CPA or GEM, was significantly higher than that of the patients without ACT; however, in the OPRT (-) group, there was no difference in the survival between the ACT (+) and (-) groups.
  • Multivariate analyses demonstrated that for all patients, primary tumor, status of nodal involvement (pN), residual tumor, level of dissection and CPA were significant variables for the prognosis: in OPRT (+) groups, primary tumor, nodal involvement, GEM and CPA were significant variables.
  • The present study is the first report on the significance of OPRT in human pancreatic cancer, and the results indicate that the expression of OPRT may be useful to predict the response to adjuvant chemotherapy in human pancreatic cancer.
  • [MeSH-major] Adenocarcinoma, Mucinous / enzymology. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Pancreatic Ductal / enzymology. Carcinoma, Papillary / enzymology. Orotate Phosphoribosyltransferase / metabolism. Pancreatic Neoplasms / enzymology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Chemotherapy, Adjuvant. Cyclophosphamide / administration & dosage. Deoxycytidine / administration & dosage. Deoxycytidine / analogs & derivatives. Female. Fluorouracil / administration & dosage. Humans. Male. Middle Aged. Neoplasm Staging. Prognosis. Survival Rate. Tegafur / administration & dosage

  • Genetic Alliance. consumer health - Pancreatic cancer.
  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • Hazardous Substances Data Bank. FLUOROURACIL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17549346.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0W860991D6 / Deoxycytidine; 1548R74NSZ / Tegafur; 8N3DW7272P / Cyclophosphamide; B76N6SBZ8R / gemcitabine; EC 2.4.2.10 / Orotate Phosphoribosyltransferase; U3P01618RT / Fluorouracil
  •  go-up   go-down


73. Dai J, Lu Y, Yu C, Keller JM, Mizokami A, Zhang J, Keller ET: Reversal of chemotherapy-induced leukopenia using granulocyte macrophage colony-stimulating factor promotes bone metastasis that can be blocked with osteoclast inhibitors. Cancer Res; 2010 Jun 15;70(12):5014-23
Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Reversal of chemotherapy-induced leukopenia using granulocyte macrophage colony-stimulating factor promotes bone metastasis that can be blocked with osteoclast inhibitors.
  • Hematopoietic growth factors are used to reverse chemotherapy-induced leukopenia.
  • However, some factors such as granulocyte macrophage colony-stimulating factor (GM-CSF) induce osteoclast-mediated bone resorption that can promote cancer growth in the bone.
  • Accordingly, we evaluated the ability of GM-CSF to promote bone metastases of breast cancer or prostate cancer in a mouse model of chemotherapy-induced leukopenia.
  • In this model, GM-CSF reversed cyclophosphamide-induced leukopenia but also promoted breast cancer and prostate cancer growth in the bone but not in soft tissue sites.
  • Bone growth was associated with the induction of osteoclastogenesis, yet in the absence of tumor GM-CSF, it did not affect osteoclastogenesis.
  • Two osteoclast inhibitors, the bisphosphonate zoledronic acid and the RANKL inhibitor osteoprotegerin, each blocked GM-CSF-induced tumor growth in the bone but did not reverse the ability of GM-CSF to reverse chemotherapy-induced leukopenia.
  • Our findings indicate that it is possible to dissociate the bone-resorptive effects of GM-CSF, to reduce metastatic risk, from the benefits of this growth factor in reversing leukopenia caused by treatment with chemotherapy.

  • MedlinePlus Health Information. consumer health - Bone Cancer.
  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Br J Cancer. 2000 Apr;82(8):1459-68 [10780527.001]
  • [Cites] Endocrinology. 2005 Apr;146(4):1727-36 [15637291.001]
  • [Cites] J Bone Miner Res. 2000 Aug;15(8):1459-66 [10934644.001]
  • [Cites] Br J Cancer. 2001 Apr 20;84(8):1126-34 [11308265.001]
  • [Cites] J Clin Invest. 2001 May;107(10):1235-44 [11375413.001]
  • [Cites] Curr Pharm Des. 2001 May;7(8):613-35 [11375772.001]
  • [Cites] Drugs Today (Barc). 2002 Feb;38(2):91-102 [12532187.001]
  • [Cites] Clin Cancer Res. 2003 Jan;9(1):295-306 [12538482.001]
  • [Cites] J Bone Miner Res. 2004 Feb;19(2):190-9 [14969388.001]
  • [Cites] Exp Cell Res. 2004 Mar 10;294(1):149-58 [14980510.001]
  • [Cites] BJU Int. 2004 Jul;94(1):164-70 [15217454.001]
  • [Cites] Crit Care. 2004 Oct;8(5):R291-8 [15469571.001]
  • [Cites] J Natl Cancer Inst. 1974 Sep;53(3):661-74 [4412247.001]
  • [Cites] Infect Immun. 1989 Jun;57(6):1792-9 [2656523.001]
  • [Cites] Haematologica. 1990 Jan-Feb;75 Suppl 1:95-8 [2190885.001]
  • [Cites] Toxicol Appl Pharmacol. 1998 May;150(1):91-7 [9630457.001]
  • [Cites] Blood. 1998 Nov 1;92(9):3465-73 [9787189.001]
  • [Cites] Am J Pathol. 1999 Feb;154(2):553-66 [10027413.001]
  • [Cites] Genes Dev. 1999 Sep 15;13(18):2412-24 [10500098.001]
  • [Cites] J Bone Miner Res. 2005 Feb;20(2):318-29 [15647826.001]
  • [Cites] Oncology (Williston Park). 2005 Apr;19(4 Suppl 2):5-9 [15934493.001]
  • [Cites] J Mammary Gland Biol Neoplasia. 2005 Apr;10(2):169-80 [16025223.001]
  • [Cites] J Clin Oncol. 2005 Aug 1;23(22):4821-2 [15983398.001]
  • [Cites] Prostate Cancer Prostatic Dis. 2005;8(3):253-9 [15999121.001]
  • [Cites] Cancer Res. 2005 Sep 1;65(17):7554-60 [16140917.001]
  • [Cites] Anticancer Drugs. 2005 Oct;16(9):969-76 [16162973.001]
  • [Cites] Clin Exp Immunol. 2006 Oct;146(1):146-58 [16968409.001]
  • [Cites] Nat Med. 2007 Jan;13(1):62-9 [17159986.001]
  • [Cites] Nat Med. 2007 Jan;13(1):25-6 [17206127.001]
  • [Cites] Blood. 2007 Apr 15;109(8):3424-31 [17192391.001]
  • [Cites] Acta Oncol. 2007;46(5):669-77 [17562444.001]
  • [Cites] J Clin Oncol. 2007 Jul 20;25(21):3158-67 [17634496.001]
  • [Cites] J Cell Biochem. 2007 Dec 15;102(6):1333-42 [17907152.001]
  • [Cites] Biochem Biophys Res Commun. 2008 Mar 21;367(4):881-7 [18201554.001]
  • [Cites] J Natl Compr Canc Netw. 2008 Feb;6(2):109-18 [18319047.001]
  • [Cites] Cancer Treat Rev. 2008 Aug;34(5):453-75 [18423992.001]
  • [Cites] Clin Exp Metastasis. 2008;25(5):559-67 [18421566.001]
  • [Cites] Nature. 2008 Jul 24;454(7203):436-44 [18650914.001]
  • [Cites] PLoS One. 2009;4(9):e6896 [19727403.001]
  • [Cites] Cancer Res. 2000 Jun 1;60(11):2949-54 [10850442.001]
  • (PMID = 20501834.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA093900-06A1; United States / NCI NIH HHS / CA / CA093900-06A18688; United States / NCI NIH HHS / CA / P01CA093900; United States / NCI NIH HHS / CA / CA093900-06A1; United States / NCI NIH HHS / CA / P01 CA093900-06A18688; United States / NCI NIH HHS / CA / P01 CA093900
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Bone Density Conservation Agents; 0 / Diphosphonates; 0 / Imidazoles; 0 / Osteoprotegerin; 0 / RANK Ligand; 6XC1PAD3KF / zoledronic acid; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor; 8N3DW7272P / Cyclophosphamide
  • [Other-IDs] NLM/ NIHMS199063; NLM/ PMC2888854
  •  go-up   go-down


74. Tsavaris N, Lazaris A, Kosmas C, Gouveris P, Kavantzas N, Kopterides P, Papathomas T, Agrogiannis G, Zorzos H, Kyriakou V, Patsouris E: Topoisomerase I and IIalpha protein expression in primary colorectal cancer and recurrences following 5-fluorouracil-based adjuvant chemotherapy. Cancer Chemother Pharmacol; 2009 Jul;64(2):391-8
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Topoisomerase I and IIalpha protein expression in primary colorectal cancer and recurrences following 5-fluorouracil-based adjuvant chemotherapy.
  • In the present study, we correlate topo-I and -II expression and outcome after chemotherapy in primary and relapsed colorectal cancer.
  • PATIENTS AND METHODS: Patients with colorectal cancer that had recurred, following surgery and adjuvant chemotherapy and underwent a second operation were included in the present study.
  • All had undergone surgical resection of the primary tumor and received post-operatively 5-FU-based (5FU + Leucovorin, Mayo Clinic regimen) adjuvant chemotherapy.
  • Tumor tissue was collected at the initial operation from the primary tumor and at the time of recurrence (during the second operation following chemotherapy).
  • All tissue samples were analyzed for levels of expression of both topo-I and topo-IIa using standard three-step immunohistochemistry on paraffin sections.
  • Levels of expression of topo-I and topo-II were higher in malignant cells from tumor recurrences compared to primary tumors (P = 0.0001 for both).
  • CONCLUSIONS: The study results reported here underscore the role of topoisomerase expression in colorectal cancer and suggest a potential role in tumor recurrence.
  • [MeSH-major] Antigens, Neoplasm / metabolism. Antimetabolites, Antineoplastic / therapeutic use. Biomarkers, Tumor / metabolism. Colorectal Neoplasms / drug therapy. DNA Topoisomerases, Type I / metabolism. DNA Topoisomerases, Type II / metabolism. DNA-Binding Proteins / metabolism. Fluorouracil / therapeutic use. Neoplasm Recurrence, Local / drug therapy
  • [MeSH-minor] Adult. Aged. Chemotherapy, Adjuvant. Combined Modality Therapy. DNA / genetics. Female. Humans. Immunoenzyme Techniques. Male. Middle Aged. Neoplasm Staging. Ploidies. Prognosis. Survival Rate. Treatment Outcome

  • Genetic Alliance. consumer health - Colorectal Cancer.
  • MedlinePlus Health Information. consumer health - Colorectal Cancer.
  • Hazardous Substances Data Bank. FLUOROURACIL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Jpn J Cancer Res. 1994 Feb;85(2):187-93 [8144400.001]
  • [Cites] Nature. 1993 Sep 16;365(6443):227-32 [8396729.001]
  • [Cites] J Med Chem. 1995 Feb 3;38(3):395-401 [7853331.001]
  • [Cites] Anticancer Drugs. 1994 Dec;5(6):645-9 [7888702.001]
  • [Cites] Tumori. 1995 Jan-Feb;81(1):36-8 [7754538.001]
  • [Cites] Biochim Biophys Acta. 1995 May 17;1262(1):1-14 [7772596.001]
  • [Cites] Am J Clin Oncol. 1995 Aug;18(4):300-2 [7625370.001]
  • [Cites] Eur J Cancer. 1995 Jun;31A(6):894-8 [7646917.001]
  • [Cites] J Clin Oncol. 1996 Mar;14(3):709-15 [8622015.001]
  • [Cites] Br J Cancer. 1996 May;73(10):1265-7 [8630290.001]
  • [Cites] Oncol Res. 1996;8(1):17-25 [8704283.001]
  • [Cites] Anticancer Res. 1996 Nov-Dec;16(6B):3467-74 [9042208.001]
  • [Cites] Mod Pathol. 1997 May;10(5):409-13 [9160303.001]
  • [Cites] J Clin Oncol. 1997 Oct;15(10):3223-9 [9336359.001]
  • [Cites] Anticancer Drugs. 1998 Jan;9(1):18-28 [9491788.001]
  • [Cites] Science. 1998 Mar 6;279(5356):1534-41 [9488652.001]
  • [Cites] Mol Pathol. 1997 Oct;50(5):247-53 [9497914.001]
  • [Cites] Biochim Biophys Acta. 1998 Oct 1;1400(1-3):83-105 [9748515.001]
  • [Cites] Biochim Biophys Acta. 1998 Oct 1;1400(1-3):139-54 [9748545.001]
  • [Cites] Cancer Res. 1994 Jul 15;54(14):3723-5 [8033091.001]
  • [Cites] Biochim Biophys Acta. 1998 Oct 1;1400(1-3):173-84 [9748560.001]
  • [Cites] Bull Cancer. 1998 Dec;Spec No:26-32 [9932081.001]
  • [Cites] Bull Cancer. 1998 Dec;Spec No:33-7 [9932082.001]
  • [Cites] Bull Cancer. 1998 Dec;Spec No:38-42 [9932083.001]
  • [Cites] Hum Pathol. 1999 Apr;30(4):384-91 [10208458.001]
  • [Cites] Mod Pathol. 1999 Apr;12(4):356-61 [10229499.001]
  • [Cites] Nature. 1957 Mar 30;179(4561):663-6 [13418758.001]
  • [Cites] J Chemother. 2006 Oct;18(5):538-44 [17127232.001]
  • [Cites] Biochemistry. 2007 Jul 17;46(28):8217-25 [17580961.001]
  • [Cites] Chemotherapy. 2007;53(4):282-91 [17496414.001]
  • [Cites] J Cancer Res Clin Oncol. 2007 Dec;133(12):1011-5 [17605046.001]
  • [Cites] Hum Pathol. 2000 Feb;31(2):214-9 [10685636.001]
  • [Cites] Hum Pathol. 2000 Jun;31(6):728-33 [10872667.001]
  • [Cites] J Clin Pathol. 2001 Apr;54(4):309-13 [11304849.001]
  • [Cites] Anticancer Res. 2001 Mar-Apr;21(2A):1167-72 [11396158.001]
  • [Cites] Breast J. 2001 May-Jun;7(3):176-80 [11469931.001]
  • [Cites] J Cancer Res Clin Oncol. 2002 Feb;128(2):114-8 [11862483.001]
  • [Cites] Chemotherapy. 2002 May;48(2):94-9 [12011542.001]
  • [Cites] Hum Pathol. 2002 Jun;33(6):599-607 [12152158.001]
  • [Cites] Med Sci Monit. 2002 Sep;8(9):PI65-9 [12218954.001]
  • [Cites] J Chemother. 2002 Aug;14(4):406-11 [12420860.001]
  • [Cites] Hum Pathol. 2002 Nov;33(11):1114-9 [12454816.001]
  • [Cites] Am J Clin Pathol. 2003 Feb;119(2):265-71 [12579998.001]
  • [Cites] Pathology. 2003 Aug;35(4):315-8 [12959767.001]
  • [Cites] Cancer Chemother Pharmacol. 2003 Dec;52(6):514-9 [14504920.001]
  • [Cites] Oncol Rep. 2004 Apr;11(4):899-903 [15010892.001]
  • [Cites] Hum Pathol. 2004 Jun;35(6):745-51 [15188142.001]
  • [Cites] Int J Cancer. 2004 Aug 20;111(2):252-8 [15197779.001]
  • [Cites] Proc Natl Acad Sci U S A. 1988 Feb;85(4):1086-90 [2829215.001]
  • [Cites] Am J Clin Oncol. 1989 Dec;12(6):491-3 [2589229.001]
  • [Cites] Am J Clin Oncol. 1990 Oct;13(5):455-8 [2220666.001]
  • [Cites] Ann Oncol. 1991 Oct;2(9):687-8 [1742225.001]
  • [ErratumIn] Cancer Chemother Pharmacol. 2009 Jul;64(2):399. Arapogiannis, George [corrected to Agrogiannis, George]; Patsouris, Efstathios [corrected to Patsouris, Efstratios]
  • (PMID = 19083133.001).
  • [ISSN] 1432-0843
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Antimetabolites, Antineoplastic; 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 9007-49-2 / DNA; EC 5.99.1.2 / DNA Topoisomerases, Type I; EC 5.99.1.3 / DNA Topoisomerases, Type II; EC 5.99.1.3 / DNA topoisomerase II alpha; U3P01618RT / Fluorouracil
  • [Other-IDs] NLM/ PMC2688619
  •  go-up   go-down


75. Meirow D: Reproduction post-chemotherapy in young cancer patients. Mol Cell Endocrinol; 2000 Nov 27;169(1-2):123-31

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Reproduction post-chemotherapy in young cancer patients.
  • High-dose chemotherapy and radiotherapy has increased long-term survival of young patients with cancer.
  • With conventional chemotherapy, there is significant differences in ovarian failure rate according to patients age, disease for which patients are treated for, and the drugs used.
  • Bone marrow transplantation in cancer patients almost invariably induced ovarian failure, irrespective of patient age, treatment protocol or administration of hormonal treatment.
  • Moreover, normal reproductive parameters post-chemotherapy does not necessarily imply that the ovaries escaped damage; ovarian injury is not an all or none phenomenon--partial loss of primordial follicle reserve can result in premature menopause as a delayed reaction to treatment.
  • This should be taken into account while consulting former cancer patients about future planed pregnancies.
  • The direct mechanisms of chemotherapy induced ovarian failure are poorly understood.
  • An in vitro study has demonstrated that in the human ovary chemotherapy acts primarily on primordial follicles through induction of apoptotic changes in pregranulosa cells which lead to follicle loss.
  • Protecting fertility potential in females exposed to chemotherapy with IVF and embryo cryopreservation or cryopreservation of ovarian tissue is practiced.
  • Ovarian tissue cryopreservation: A recent study has demonstrated that laparoscopic ovarian biopsy performed with the round biopter is a safe and efficient method for collecting ovarian tissue for cryopreservation in cancer patients.
  • In order to avoid possible hazards of transferring malignant cells, genetic and immunohistochemical markers for detection of minimal residual cancer cells in ovarian tissue are currently used.
  • IVF: IVF and embryocryopreservation is currently used in infertile patients, however, several obstacles prevent it's wide implementation in cancer patients such as the need for male partner and the time needed for ovarian stimulation.
  • A highly important issue is the possible risk of performing IVF and embryo cryopreservation to preserve fertility in females already exposed to chemotherapy.
  • An animal study has raised serious concerns regarding the consequences of chemotherapy on future pregnancies.
  • High abortion and malformation rates related to the different stages of oocyte maturation at the time of exposure to chemotherapy were demonstrated.
  • These results should be taken into account when considering the use of IVF and embryo cryopreservation following chemotherapy treatment in cancer patients.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Neoplasms / complications. Reproductive Techniques
  • [MeSH-minor] Adolescent. Adult. Age Factors. Bone Marrow Transplantation / adverse effects. Breast Neoplasms / complications. Breast Neoplasms / physiopathology. Breast Neoplasms / therapy. Cohort Studies. Cryopreservation / methods. Female. Fertilization in Vitro / methods. Humans. Leukemia, Myeloid, Acute / complications. Leukemia, Myeloid, Acute / physiopathology. Leukemia, Myeloid, Acute / therapy. Lymphoma / complications. Lymphoma / physiopathology. Lymphoma / therapy. Ovary / cytology. Primary Ovarian Insufficiency / chemically induced. Primary Ovarian Insufficiency / etiology. Primary Ovarian Insufficiency / pathology. Retrospective Studies. Risk Factors. Statistics, Nonparametric

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11155944.001).
  • [ISSN] 0303-7207
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  •  go-up   go-down


76. Marquard L, Petersen KD, Persson M, Hoff KD, Jensen PB, Sehested M: Monitoring the effect of belinostat in solid tumors by H4 acetylation. APMIS; 2008 May;116(5):382-92
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Monitoring the effect of belinostat in solid tumors by H4 acetylation.
  • One of them is the hydroxamic acid belinostat (PXD101) that has demonstrated therapeutic efficacy for several clinical indications.
  • Acetylation of histones is a key event after treatment with HDAC inhibitors, and could thus be used as a marker for monitoring cellular response to HDAC inhibitor treatment.
  • Here we describe the utility of a newly described monoclonal antibody against acetylated H4 for immunohistochemistry on paraffin-embedded fine needle biopsies from nude mice carrying A2780 human ovarian cancer xenografts.
  • Acetylated H4 was monitored in vivo by immunohistochemistry during treatment with belinostat, and compared with pharmacokinetics in plasma and tumor tissue.
  • We found an increased level of acetylated H4 15 min after a single treatment (200 mg/kg i.v.) with maximum level reached after 1 h.
  • H4 acetylation intensity reflected the belinostat concentration in plasma and tumor tissue.
  • The threshold level for belinostat activity, indicated by acetylated H4, correlated with belinostat plasma concentrations above 1,000 ng/ml.
  • In conclusion, examination of H4 acetylation in fine needle biopsies using the T25 antibody may prove useful in monitoring HDAC inhibitor efficacy in clinical trials involving humans with solid tumors.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Histones / metabolism. Hydroxamic Acids / therapeutic use. Neoplasms, Experimental / drug therapy. Neoplasms, Experimental / metabolism
  • [MeSH-minor] Acetylation / drug effects. Animals. Antibodies, Monoclonal. Breast Neoplasms / drug therapy. Breast Neoplasms / enzymology. Cell Line, Tumor. Female. HCT116 Cells. Histone Deacetylase Inhibitors. Histone Deacetylases / immunology. Humans. Leukemia P388 / drug therapy. Leukemia P388 / enzymology. Liver Neoplasms, Experimental / drug therapy. Liver Neoplasms, Experimental / enzymology. Male. Mice. Mice, Nude. Ovarian Neoplasms / drug therapy. Ovarian Neoplasms / enzymology. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / enzymology. Sulfonamides. Transplantation, Heterologous

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Natl Cancer Inst. 2000 Aug 2;92(15):1210-6 [10922406.001]
  • [Cites] Nat Med. 2001 Apr;7(4):437-43 [11283670.001]
  • [Cites] Oncogene. 2001 May 28;20(24):2988-90 [11420713.001]
  • [Cites] Clin Cancer Res. 2002 Mar;8(3):718-28 [11895901.001]
  • [Cites] Nat Rev Cancer. 2001 Dec;1(3):194-202 [11902574.001]
  • [Cites] Nat Rev Drug Discov. 2002 Apr;1(4):287-99 [12120280.001]
  • [Cites] Mol Cancer Ther. 2003 Aug;2(8):721-8 [12939461.001]
  • [Cites] Clin Cancer Res. 2003 Sep 1;9(10 Pt 1):3578-88 [14506144.001]
  • [Cites] Cancer Cell. 2004 May;5(5):455-63 [15144953.001]
  • [Cites] Am J Respir Cell Mol Biol. 1998 Nov;19(5):777-85 [9806742.001]
  • [Cites] Blood. 2005 Feb 1;105(3):959-67 [15466934.001]
  • [Cites] APMIS. 2005 Apr;113(4):264-8 [15865607.001]
  • [Cites] J Clin Oncol. 2005 Jun 10;23(17):3912-22 [15851766.001]
  • [Cites] Cytometry A. 2005 Jul;66(1):52-61 [15915507.001]
  • [Cites] Cancer. 2005 Dec 15;104(12):2717-25 [16294345.001]
  • [Cites] J Clin Oncol. 2006 Jan 1;24(1):166-73 [16330674.001]
  • [Cites] Clin Cancer Res. 2006 Mar 1;12(5):1547-55 [16533780.001]
  • [Cites] J Clin Oncol. 2006 Aug 1;24(22):3678-85 [16877737.001]
  • [Cites] Brief Funct Genomic Proteomic. 2006 Sep;5(3):209-21 [16877467.001]
  • [Cites] Brief Funct Genomic Proteomic. 2006 Sep;5(3):190-208 [16980317.001]
  • [Cites] Cell Mol Immunol. 2006 Aug;3(4):285-90 [16978537.001]
  • [Cites] Blood. 2006 Nov 15;108(10):3271-9 [16882711.001]
  • [Cites] Cell. 2007 Feb 23;128(4):707-19 [17320508.001]
  • [Cites] Blood. 2007 Apr 1;109(7):2781-90 [17179232.001]
  • [Cites] J Clin Oncol. 2007 May 20;25(15):1979-85 [17513804.001]
  • (PMID = 18452428.001).
  • [ISSN] 0903-4641
  • [Journal-full-title] APMIS : acta pathologica, microbiologica, et immunologica Scandinavica
  • [ISO-abbreviation] APMIS
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antineoplastic Agents; 0 / Histone Deacetylase Inhibitors; 0 / Histones; 0 / Hydroxamic Acids; 0 / Sulfonamides; EC 3.5.1.98 / Histone Deacetylases; F4H96P17NZ / belinostat
  • [Other-IDs] NLM/ PMC2774150
  •  go-up   go-down


77. Abrahamsen JF, Kristoffersen EK, Hervig T, Ekanger R, Nesthus I, Ulvestad E: [High dose chemotherapy with autologous stem cell support in cancer patients]. Tidsskr Nor Laegeforen; 2000 May 20;120(13):1523-8

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [High dose chemotherapy with autologous stem cell support in cancer patients].
  • INTRODUCTION: In 1996 it was decided that high-dose chemotherapy with peripheral stem cell support should be offered by all five university hospitals in Norway.
  • RESULTS: All patients had a total of > 2-10(6) CD34 positive cells/kg collected before high-dose chemotherapy.
  • To achieve this critical stem cell dose, five patients had to have three or more stem cell collections; four of them had to be mobilised several times.
  • Poor stem cell mobilisation was mostly marked in patients with soft tissue sarcoma and testicular cancer, but was also observed in a few heavily pre-treated patients with non-Hodgkins lymphoma.
  • With the exception of one lymphoma patient who developed a rapid bone marrow relapse, all patients had satisfactory sign of bone marrow regeneration after reinfusion of the stem cells.
  • No treatment-related deaths have occurred.
  • Four to 38 months after high-dose therapy, 33% of patients with multiple myeloma and 52% of patients with malignant lymphoma were alive and in complete remission.
  • Three of the four patients with soft tissue sarcoma relapsed 3-7 months after high-dose chemotherapy.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Hematopoietic Stem Cell Transplantation. Neoplasms / therapy
  • [MeSH-minor] Adolescent. Adult. Antigens, CD34. Breast Neoplasms / drug therapy. Breast Neoplasms / immunology. Breast Neoplasms / therapy. Combined Modality Therapy. Dose-Response Relationship, Drug. Female. Hematopoietic Stem Cell Mobilization. Humans. Lymphoma / drug therapy. Lymphoma / immunology. Lymphoma / therapy. Male. Middle Aged. Multiple Myeloma / drug therapy. Multiple Myeloma / immunology. Multiple Myeloma / therapy. Prognosis. Sarcoma / drug therapy. Sarcoma / immunology. Sarcoma / therapy. Testicular Neoplasms / drug therapy. Testicular Neoplasms / immunology. Testicular Neoplasms / therapy. Transplantation, Autologous

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 10916472.001).
  • [ISSN] 0029-2001
  • [Journal-full-title] Tidsskrift for den Norske lægeforening : tidsskrift for praktisk medicin, ny række
  • [ISO-abbreviation] Tidsskr. Nor. Laegeforen.
  • [Language] nor
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] NORWAY
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Antineoplastic Agents
  •  go-up   go-down


78. Dummer R, Bergh J, Karlsson Y, Horowitz JA, Mulder NH, Huinink DTB, Burg G, Hofbauer G, Osanto S: Biological activity and safety of adenoviral vector-expressed wild-type p53 after intratumoral injection in melanoma and breast cancer patients with p53-overexpressing tumors. Cancer Gene Ther; 2000 Jul;7(7):1069-76
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Biological activity and safety of adenoviral vector-expressed wild-type p53 after intratumoral injection in melanoma and breast cancer patients with p53-overexpressing tumors.
  • p53 mutations are common genetic alterations in human cancer.
  • Gene transfer of a wild-type (wt) p53 gene reverses the loss of normal p53 function in vitro and in vivo.
  • A phase I dose escalation study of single intratumoral (i.t.) injection of a replication-defective adenoviral expression vector containing wt p53 was carried out in patients with metastatic melanoma or breast cancer with increased p53 protein immunoreactivity in pretreatment tumor biopsies.
  • The biological activity of the injected wt p53 was assayed by reverse transcriptase-polymerase chain reaction in tumor tissue.
  • A total of six (five melanoma and one breast adenocarcinoma) patients were treated at dose levels dependent upon tumor size/dose escalation sequence.
  • Five of six patients became positive for the transfer of wt p53 into tumor tissue 2 days after injection of the vector.
  • Of the four patients assayed, all developed anti-adenoviral antibodies.
  • Adverse reactions associated with i.t. injection were mild, with no obvious correlation between the incidence, severity, or relationship of the events and drug dose. p53 gene therapy by i.t. injection of a replication-defective adenoviral expression vector is safe, feasible, and biologically effective (with respect to transduction frequency) in patients with either metastatic melanoma or breast cancer.
  • [MeSH-major] Adenocarcinoma / therapy. Adenoviridae / genetics. Breast Neoplasms / therapy. Genes, p53 / genetics. Genetic Therapy. Melanoma / therapy. Skin Neoplasms / therapy
  • [MeSH-minor] Adult. Aged. Antibodies, Viral / analysis. Defective Viruses. Female. Genetic Vectors. Humans. Male. Middle Aged. Neoplasm Staging. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction. Safety. Transfection. Virus Shedding


79. Zanca C, Garofalo M, Quintavalle C, Romano G, Acunzo M, Ragno P, Montuori N, Incoronato M, Tornillo L, Baumhoer D, Briguori C, Terracciano L, Condorelli G: PED is overexpressed and mediates TRAIL resistance in human non-small cell lung cancer. J Cell Mol Med; 2008 Dec;12(6A):2416-26
MedlinePlus Health Information. consumer health - Lung Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] PED is overexpressed and mediates TRAIL resistance in human non-small cell lung cancer.
  • PED (phosphoprotein enriched in diabetes) is a death-effector domain (DED) family member with a broad anti-apoptotic action.
  • Recently, we reported that the expression of PED is increased in breast cancer cells and determines the refractoriness of these cells to anticancer therapy.
  • In the present study, we focused on the role of PED in non-small cell lung cancer (NSCLC), a tumour frequently characterized by evasion of apoptosis and drug resistance.
  • Immunohistochemical analysis of a tissue microarray, containing 160 lung cancer samples, indicated that PED was strongly expressed in different lung tumour types.
  • Western blotting performed with specimens from NSCLC-affected patients showed that PED was strongly up-regulated (>6 fold) in the areas of tumour compared to adjacent normal tissue.
  • Furthermore, PED expression levels in NSCLC cell lines correlated with their resistance to tumour necrosis factor related apoptosis-inducing ligand (TRAIL)-induced cell death.
  • In conclusion, PED is specifically overexpressed in lung tumour tissue and contributes to TRAIL resistance.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / drug therapy. Carcinoma, Non-Small-Cell Lung / metabolism. Intracellular Signaling Peptides and Proteins / metabolism. Lung Neoplasms / drug therapy. Lung Neoplasms / metabolism. Phosphoproteins / metabolism. TNF-Related Apoptosis-Inducing Ligand / pharmacology
  • [MeSH-minor] Aged. Aged, 80 and over. Apoptosis / drug effects. Apoptosis / physiology. Cell Line, Tumor. Drug Resistance, Neoplasm. Female. Humans. Male. Middle Aged. Protein Array Analysis. RNA, Small Interfering / genetics. Receptors, TNF-Related Apoptosis-Inducing Ligand / metabolism. Recombinant Proteins / pharmacology. Transfection. Up-Regulation

  • Genetic Alliance. consumer health - Lung Cancer.
  • Genetic Alliance. consumer health - Non-small cell lung cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18284607.001).
  • [ISSN] 1582-1838
  • [Journal-full-title] Journal of cellular and molecular medicine
  • [ISO-abbreviation] J. Cell. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Romania
  • [Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; 0 / PEA15 protein, human; 0 / Phosphoproteins; 0 / RNA, Small Interfering; 0 / Receptors, TNF-Related Apoptosis-Inducing Ligand; 0 / Recombinant Proteins; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFSF10 protein, human
  • [Other-IDs] NLM/ PMC4514119
  •  go-up   go-down


80. Mailliez A, Baldini C, Van JT, Servent V, Mallet Y, Bonneterre J: Nasal septum perforation: a side effect of bevacizumab chemotherapy in breast cancer patients. Br J Cancer; 2010 Sep 7;103(6):772-5
MedlinePlus Health Information. consumer health - Breast Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Nasal septum perforation: a side effect of bevacizumab chemotherapy in breast cancer patients.
  • BACKGROUND: Bevacizumab is an anti-vascular endothelial growth factor approved in association with paclitaxel or docetaxel as first line in patients (pts) with metastatic breast cancer.
  • We report our experience of nasal perforation in breast cancer pts receiving bevacizumab and chemotherapy either in the adjuvant or in the metastatic settings.
  • METHODS: Between 1 January and 31 December 2009, 70 pts received bevacizumab together with chemotherapy.
  • Bevacizumab was associated with docetaxel (100 mg m(-2) every 3 weeks) in two pts and with weekly paclitaxel in one.
  • In these two cases, nasal septum perforation occurred at the time of docetaxel treatment.
  • CONCLUSION: A high incidence of nasal septum perforation has been shown in pts with breast cancer receiving bevacizumab together with chemotherapy.
  • Several mechanisms could be involved (mucositis, delayed tissue repair, antiangiogenic action of taxanes).
  • [MeSH-major] Antibodies, Monoclonal / adverse effects. Antineoplastic Agents / adverse effects. Breast Neoplasms / drug therapy. Nasal Septum / drug effects
  • [MeSH-minor] Adult. Aged. Antibodies, Monoclonal, Humanized. Bevacizumab. Female. Humans. Male. Middle Aged. Treatment Outcome

  • Genetic Alliance. consumer health - Breast Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Nat Med. 1999 Dec;5(12):1359-64 [10581076.001]
  • [Cites] J Clin Oncol. 2011 Nov 10;29(32):4286-93 [21990397.001]
  • [Cites] Rev Med Interne. 2002 Nov;23(11):919-26 [12481392.001]
  • [Cites] Int J Cancer. 2003 Mar 10;104(1):121-9 [12532428.001]
  • [Cites] J Otolaryngol. 1985 Apr;14(2):125-31 [4068101.001]
  • [Cites] Nature. 1992 Oct 29;359(6398):845-8 [1279432.001]
  • [Cites] Clin Cancer Res. 1996 Nov;2(11):1843-9 [9816139.001]
  • [Cites] Oncologist. 2006 Jan;11(1):85-6 [16401718.001]
  • [Cites] Intern Med J. 2006 Jul;36(7):471-2 [16780459.001]
  • [Cites] Oncologist. 2006 Nov-Dec;11(10):1070-1 [17110625.001]
  • [Cites] J Clin Oncol. 2007 Aug 1;25(22):3376-7 [17664487.001]
  • [Cites] N Engl J Med. 2007 Dec 27;357(26):2666-76 [18160686.001]
  • [Cites] Laryngoscope. 2008 Sep;118(9):1539-41 [18622319.001]
  • [Cites] Ann Oncol. 2009 Nov;20(11):1901-2 [19752003.001]
  • [Cites] Med Oncol. 2010 Dec;27(4):1057-9 [19847680.001]
  • [Cites] Med Oncol. 2011 Mar;28(1):89-93 [20213219.001]
  • [Cites] Mol Cancer Ther. 2002 Nov;1(13):1191-200 [12479700.001]
  • (PMID = 20736943.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 2S9ZZM9Q9V / Bevacizumab
  • [Other-IDs] NLM/ PMC2966623
  •  go-up   go-down


81. Devi GR, Beer TM, Corless CL, Arora V, Weller DL, Iversen PL: In vivo bioavailability and pharmacokinetics of a c-MYC antisense phosphorodiamidate morpholino oligomer, AVI-4126, in solid tumors. Clin Cancer Res; 2005 May 15;11(10):3930-8
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] In vivo bioavailability and pharmacokinetics of a c-MYC antisense phosphorodiamidate morpholino oligomer, AVI-4126, in solid tumors.
  • AVI-4126, a PMO targeted against c-MYC, has been extensively characterized in multiple cancer and other disease models and is currently in human clinical trials.
  • A phase I clinical study was conducted to address the issue of PMO bioavailability in malignant tumors surgically excised from patients with adenocarcinoma of prostate and breast 1 day after i.v. administration of a single dose of 90 mg AVI-4126 PMO.
  • The study objectives were to evaluate safety, to determine AVI-4126 concentration in tissue samples of the tumors, and to examine the distribution of AVI-4126 (margin versus tumor core).
  • Significant concentrations of intact PMO similar to the animal models were detected in both human prostate and breast tumor tissues with increased distribution in the tumor core for the vascular breast tumors.
  • No serious adverse events (graded according to National Cancer Institute Common Toxicity Criteria) were reported.
  • Another phase I study was conducted in normal human volunteers to assess AVI-4126 plasma pharmacokinetics following single i.v. administration of 90 mg AVI-4126.
  • Data from both human studies indicated similar plasma concentration-time profile.
  • These studies show PMO bioavailability in tumor tissue and establish the feasibility of using PMO targeting specific genes in human cancer clinical trials.
  • [MeSH-major] Breast Neoplasms / drug therapy. Morpholines / adverse effects. Morpholines / pharmacokinetics. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Animals. Biological Availability. Female. Genes, myc. Humans. Infusions, Intravenous. Male. Mice. Mice, Nude. Morpholinos

  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15897595.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase I; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Morpholines; 0 / Morpholinos
  •  go-up   go-down


82. Martinez-Balibrea E, Martínez-Cardús A, Musulén E, Ginés A, Manzano JL, Aranda E, Plasencia C, Neamati N, Abad A: Increased levels of copper efflux transporter ATP7B are associated with poor outcome in colorectal cancer patients receiving oxaliplatin-based chemotherapy. Int J Cancer; 2009 Jun 15;124(12):2905-10
Hazardous Substances Data Bank. FLUOROURACIL .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Increased levels of copper efflux transporter ATP7B are associated with poor outcome in colorectal cancer patients receiving oxaliplatin-based chemotherapy.
  • Recently, the copper efflux transporters ATP7B and ATP7A have been implicated in the transport of and resistance to platinum drugs in breast and ovarian cancers.
  • Because of the extensive use of oxaliplatin in colorectal cancer (CRC), we examined the expression of both transporters in tumors from CRC patients treated with oxaliplatin/5FU and sought to determine whether their expression can predict clinical outcome in these patients.
  • ATP7B and ATP7A levels were determined by quantitative real-time PCR in 50 primary tumors of previously untreated patients with advanced colorectal adenocarcinoma who were subsequently treated with oxaliplatin/5FU.
  • Additionally, ATP7B protein expression was assessed by immunohistochemical staining using a tissue microarray.
  • Patients with the lowest mRNA expression levels of ATP7B had a significantly longer time to progression (TTP) (p = 0.0009) than patients with the highest levels (12.14 months vs. 6.43 months) who also had an increased risk of progression (HR = 3.56; 95% CI, 1.6-7.9; p = 0.002).
  • In conclusion, ATP7B mRNA and protein expression in colorectal tumors is associated with clinical outcome to oxaliplatin/5FU.
  • Prospective studies are required to evaluate the role of this marker in tailoring chemotherapy.
  • [MeSH-major] Adenosine Triphosphatases / metabolism. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cation Transport Proteins / metabolism. Colorectal Neoplasms / drug therapy. Colorectal Neoplasms / metabolism
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / metabolism. Adenocarcinoma / secondary. Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. Chemotherapy, Adjuvant. Female. Fluorouracil / administration & dosage. Follow-Up Studies. Humans. Immunoenzyme Techniques. Liver Neoplasms / drug therapy. Liver Neoplasms / metabolism. Liver Neoplasms / secondary. Lung Neoplasms / drug therapy. Lung Neoplasms / metabolism. Lung Neoplasms / secondary. Male. Middle Aged. Neoplasm Invasiveness. Organoplatinum Compounds / administration & dosage. Prognosis. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Survival Rate. Tissue Array Analysis. Treatment Outcome

  • Genetic Alliance. consumer health - Colorectal Cancer.
  • MedlinePlus Health Information. consumer health - Colorectal Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2008 UICC.
  • (PMID = 19296535.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cation Transport Proteins; 0 / Organoplatinum Compounds; 0 / RNA, Messenger; 04ZR38536J / oxaliplatin; EC 3.6.1.- / Adenosine Triphosphatases; EC 3.6.3.4 / ATP7A protein, human; EC 3.6.3.4 / Wilson disease protein; U3P01618RT / Fluorouracil
  •  go-up   go-down


83. Bacci G, Ferrari C, Longhi A, Ferrari S, Forni C, Bacchini P, Palmerini E, Briccoli A, Pignotti E, Balladelli A, Picci P: Second malignant neoplasm in patients with osteosarcoma of the extremities treated with adjuvant and neoadjuvant chemotherapy. J Pediatr Hematol Oncol; 2006 Dec;28(12):774-80
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Second malignant neoplasm in patients with osteosarcoma of the extremities treated with adjuvant and neoadjuvant chemotherapy.
  • We evaluated the rate of second malignancies in 1205 patients with osteosarcoma of the extremity treated at our Institution with different protocols of adjuvant and neoadjuvant chemotherapy.
  • Twenty-six patients (2.15%) developed a second malignant neoplasm at a median of 7.6 years (1 to 25 y) after primary osteosarcoma treatment.
  • Of these, 2 developed a third cancer which were not considered in the series.
  • Second neoplasms were leukemia (10), breast (7), lung (2), kidney (2), central nervous system cancer (2), soft tissue (1), parotid (1), and colon (1).
  • The rate of second neoplasms was significantly higher in female patients, and the latent period shorter in hematologic tumors compared with solid tumors.
  • Ten of these 26 patients are disease free at a median of 7.7 years (range 1 to 15 y) after the last treatment.
  • The rate of second malignancies observed in the osteosarcoma group was significantly higher than that observed in the control group of 1160 patients with benign tumors treated in the same period at our Institute (2.2% vs. 0.8%, P<0.009).
  • Our study showed that the risk of second neoplasm within 15 years increased and then leveled off and that although secondary solid tumors could be explained as unrelated cases, leukemias seem to be over represented.
  • [MeSH-major] Neoplasms, Second Primary / epidemiology. Osteosarcoma
  • [MeSH-minor] Adolescent. Adult. Chemotherapy, Adjuvant / methods. Child. Child, Preschool. Disease-Free Survival. Female. Humans. Incidence. Infant. Male. Neoplasms / drug therapy. Neoplasms / epidemiology. Retrospective Studies. Risk Factors. Sex Factors. Time Factors

  • Genetic Alliance. consumer health - Osteosarcoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17164644.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  •  go-up   go-down


84. Folkerd EJ, Dowsett M: Influence of sex hormones on cancer progression. J Clin Oncol; 2010 Sep 10;28(26):4038-44

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Influence of sex hormones on cancer progression.
  • To review the influence of sex hormones on the progression of breast, prostate, gynecologic, and colorectal cancer.
  • The literature was reviewed in an informal manner utilizing the authors' prior knowledge to collate the current evidence for the involvement of sex hormones, particularly estrogens and androgens in the progression of a range of hormonally responsive cancers.
  • In particular, the effect of treatment involving hormone withdrawal treatment was considered strong evidence for involvement.
  • Data from clinical trials indicate the efficacy of therapeutic interventions that result in ablation or antagonism of host steroids for a range of cancers.
  • Demonstration of the correlation of the completeness of withdrawal with clinical outcome together with direct evidence of progression from studies looking at the influence of tissue and circulating levels of sex hormones more recently in conjunction with gene expression profiles all provide compelling evidence for the involvement of steroids in the progression of disease.
  • The involvement of steroids in the progression of cancer in hormone-sensitive tissues is well established and an important target for therapy.
  • [MeSH-major] Gonadal Steroid Hormones / physiology. Neoplasms / etiology
  • [MeSH-minor] Breast Neoplasms / drug therapy. Breast Neoplasms / etiology. Colorectal Neoplasms / drug therapy. Colorectal Neoplasms / etiology. Disease Progression. Drug Resistance, Neoplasm. Female. Humans. Male. Prognosis. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / etiology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] J Clin Oncol. 2011 Feb 1;29(4):e94-5; author reply e96 [21172886.001]
  • (PMID = 20644089.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Gonadal Steroid Hormones
  • [Number-of-references] 82
  •  go-up   go-down


85. Czajka-Oraniec I, Simpson ER: Aromatase research and its clinical significance. Endokrynol Pol; 2010 Jan-Feb;61(1):126-34
Genetics Home Reference. consumer health - CYP19A1 gene.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The enzyme is active in various tissues in both females and males, thus oestrogens are produced not only in gonads but also in extra-gonadal localizations such as brain, adipose tissue, breast, skin, and bone.
  • Aromatase gene CYP19A1 located on chromosome 15 comprises nine coding exons and a number of alternative non-coding first exons that regulate tissue-specific expression.
  • Studies on local regulation of aromatase expression and activity are important for understanding processes such as growth of oestrogen-dependent breast cancer.
  • Research on aromatase was important for its practical outcome as it contributed to the development of aromatase inhibitors (AIs), an effective and safe group of drugs for the first-line endocrine therapy of breast cancer.
  • Further studies are needed to establish AIs application in other oestrogen-dependent conditions, to overcome the resistance in breast cancer patients, and to develop tissue-specific selective inhibitors. (Pol J Endocrinol 2010; 61 (1): 126-134).
  • [MeSH-minor] Animals. Aromatase Inhibitors / therapeutic use. Bone and Bones / metabolism. Breast Neoplasms / drug therapy. Breast Neoplasms / enzymology. Estrogens / biosynthesis. Female. Humans. Male. Mice. Polymorphism, Genetic

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20205115.001).
  • [ISSN] 0423-104X
  • [Journal-full-title] Endokrynologia Polska
  • [ISO-abbreviation] Endokrynol Pol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Aromatase Inhibitors; 0 / Estrogens; EC 1.14.14.1 / Aromatase
  • [Number-of-references] 129
  •  go-up   go-down


86. Yeh IT, Ludueña RF: The betaII isotype of tubulin is present in the cell nuclei of a variety of cancers. Cell Motil Cytoskeleton; 2004 Feb;57(2):96-106
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The betaII isotype of tubulin is present in the cell nuclei of a variety of cancers.
  • More recently, we examined a variety of cancerous and non-cancerous cell lines and found betaII in the nuclei of all of the former and only a few of the latter (Walss-Bass et al., 2002: Cell Tissue Res. 308:215-223].
  • In order to determine if betaII-tubulin occurs in the nuclei of actual cancers as well as in cancer cell lines, we used the immunoperoxidase method to look for nuclear betaII in a variety of tumors excised from 201 patients.
  • We found that 75% of these tumors contain betaII in their nuclei.
  • Distribution of nuclear betaII was highly dependent on the type of cancer, with 100% of the colon and prostate cancers, but only 19% of the skin tumors, having nuclear betaII.
  • Nuclear betaII was particularly marked in tumors of epithelial origin, of which 83% showed nuclear betaII, in contrast to 54% in tumors of non-epithelial origin.
  • In many cases, particularly metastases, otherwise normal cells adjacent to the tumor also showed nuclear betaII, suggesting that cancer cells may influence nearby cells to synthesize betaII and localize it to their nuclei.
  • Our results have implications for the diagnosis, biology, and chemotherapy of cancer.
  • [MeSH-major] Cell Nucleus / metabolism. Neoplasms / metabolism. Tubulin / metabolism
  • [MeSH-minor] Bone Neoplasms / metabolism. Brain Neoplasms / metabolism. Breast Neoplasms / metabolism. Colonic Neoplasms / metabolism. Female. Humans. Liver Neoplasms / metabolism. Lung Neoplasms / metabolism. Lymph Nodes / metabolism. Lymph Nodes / pathology. Male. Ovarian Neoplasms / metabolism. Pancreatic Neoplasms / metabolism. Prostatic Neoplasms / metabolism. Skin Neoplasms / metabolism. Stomach Neoplasms / metabolism

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2004 Wiley-Liss, Inc.
  • (PMID = 14691949.001).
  • [ISSN] 0886-1544
  • [Journal-full-title] Cell motility and the cytoskeleton
  • [ISO-abbreviation] Cell Motil. Cytoskeleton
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 26376; United States / NCI NIH HHS / CA / P30 CA54174
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Tubulin
  •  go-up   go-down


87. Miyake H, Hara I, Fujisawa M, Gleave ME: The potential of clusterin inhibiting antisense oligodeoxynucleotide therapy for prostate cancer. Expert Opin Investig Drugs; 2006 May;15(5):507-17
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The potential of clusterin inhibiting antisense oligodeoxynucleotide therapy for prostate cancer.
  • This review summarise the authors' recent experience in the development of antisense (AS) oligodeoxynucleotide (ODN) therapy that targets a cytoprotective gene, clusterin, for the treatment of prostate cancer.
  • The acquisition of resistance to a wide variety of proapototic stimuli was initially demonstrated by introducing the clusterin gene into prostate cancer cells.
  • Furthermore, silencing clusterin expression using AS ODN synergistically enhanced the effects of several conventional therapeutic modalities through the effective induction of apoptosis in prostate cancer xenograft models.
  • Based on these outcomes, Phase I clinical trials were conducted using AS clusterin ODN incorporating 2'-O-(2-methoxy)ethyl-gapmer backbone (OGX-011), and the optimal dose of OGX-011 capable of inducing </= 90% suppression of clusterin in human prostate cancer tissue was determined.
  • Collectively, these findings suggest the utility of inactivating clusterin function using AS ODN technology as a novel therapeutic strategy for prostate cancer treatment.
  • There have been four kinds of Phase II studies that have begun to further evaluate the efficacy of OGX-011 in patients with prostate, breast and lung cancers.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Clusterin / antagonists & inhibitors. Oligonucleotides, Antisense / therapeutic use. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Animals. Humans. Male

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16634689.001).
  • [ISSN] 1744-7658
  • [Journal-full-title] Expert opinion on investigational drugs
  • [ISO-abbreviation] Expert Opin Investig Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Clusterin; 0 / Oligonucleotides, Antisense
  • [Number-of-references] 113
  •  go-up   go-down


88. Huang DZ, He XH, Yang S, Shi YK: [Clinical and pathological analysis of 15 cases with primary breast lymphoma]. Ai Zheng; 2004 Aug;23(8):939-42
Hazardous Substances Data Bank. VINCRISTINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Clinical and pathological analysis of 15 cases with primary breast lymphoma].
  • BACKGROUND & OBJECTIVE: Primary breast lymphoma (PBL), a rare disease, is likely to be misdiagnosed, and its treatment still remains controversial.
  • This study was to investigate the clinical and pathological features of PBL, summarize the treatment experience, and obtain a better profile of the disease.
  • METHODS: The clinical and pathological records of 15 PBL patients admitted in the Cancer Hospital, Chinese Academy of Medical Science from January 1986 to December 2003 were analyzed.
  • Of all cases, 93.3%(14/15) were B-cell origin, 6.7% (1/15) were T-cell origin, 40% (6/15) were diffuse large B-cell lymphoma, and 26.6% (4/15) were mucosa associated lymphoid tissue lymphoma.
  • No local relapse occurred in the 8 patients who were given local mastectomy combined with chemoradiotherapy, with a median follow-up of 34.5 months (ranging from 4 to 214 months).
  • Two of the 6 patients with low grade PBL, who did not receive chemotherapy, relapsed after a short remission; 2 of the remaining 4 patients who received chemotherapy gained a constant remission, while after salvage chemoradiotherapy the other 2 gained a second remission up to now.
  • CONCLUSION: The majority of PBL was B-cell origin, diffuse large B-cell lymphoma and mucosa associated lymphoid tissue lymphoma were the most frequent entities.
  • PBL must be regarded as a kind of systemic disease in spite of its pathologic type.
  • Chemotherapy should be included in the multi-modality treatment of PBL.
  • [MeSH-major] Breast Neoplasms / therapy. Lymphoma, B-Cell / therapy. Mastectomy / methods
  • [MeSH-minor] Adult. Aged. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Combined Modality Therapy. Cyclophosphamide / administration & dosage. Doxorubicin / administration & dosage. Female. Follow-Up Studies. Humans. Male. Middle Aged. Neoplasm Recurrence, Local. Neoplasm Staging. Postoperative Period. Prednisone / administration & dosage. Prognosis. Retrospective Studies. Survival Rate. Vincristine / administration & dosage

  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Mastectomy.
  • Hazardous Substances Data Bank. DOXORUBICIN .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • Hazardous Substances Data Bank. PREDNISONE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15301719.001).
  • [Journal-full-title] Ai zheng = Aizheng = Chinese journal of cancer
  • [ISO-abbreviation] Ai Zheng
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; CHOP protocol
  •  go-up   go-down


89. Choi YW, Munden RF, Erasmus JJ, Park KJ, Chung WK, Jeon SC, Park CK: Effects of radiation therapy on the lung: radiologic appearances and differential diagnosis. Radiographics; 2004 Jul-Aug;24(4):985-97; discussion 998
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effects of radiation therapy on the lung: radiologic appearances and differential diagnosis.
  • Radiation-induced lung disease (RILD) due to radiation therapy is common.
  • Radiologic manifestations are usually confined to the lung tissue within the radiation port and are dependent on the interval after completion of treatment.
  • However, the use of oblique beam angles and the development of newer irradiation techniques such as three-dimensional conformal radiation therapy can result in an unusual distribution of these findings.
  • Awareness of the atypical manifestations of RILD can be useful in preventing confusion with infection, recurrent malignancy, lymphangitic carcinomatosis, and radiation-induced tumors.
  • In addition, knowledge of radiologic findings that are outside the expected pattern for RILD can be useful in diagnosis of infection or recurrent malignancy.
  • Such findings include the late appearance or enlargement of a pleural effusion; development of consolidation, a mass, or cavitation; and occlusion of bronchi within an area of radiation-induced fibrosis.
  • A comprehensive understanding of the full spectrum of these manifestations is important to facilitate diagnosis and management in cancer patients treated with radiation therapy.
  • [MeSH-minor] Adenocarcinoma / radiography. Adenocarcinoma / radiotherapy. Adult. Aged. Antineoplastic Agents / adverse effects. Antineoplastic Agents / pharmacology. Breast Neoplasms / radiotherapy. Bronchiectasis / etiology. Bronchiectasis / radiography. Carcinoma, Non-Small-Cell Lung / radiography. Carcinoma, Non-Small-Cell Lung / radiotherapy. Diagnosis, Differential. Disease Progression. Dose Fractionation. Esophageal Neoplasms / radiotherapy. Female. Hodgkin Disease / radiotherapy. Humans. Lung Neoplasms / diagnosis. Lung Neoplasms / radiotherapy. Male. Middle Aged. Neoplasm Recurrence, Local / radiography. Neoplasms, Radiation-Induced / diagnosis. Radiation Tolerance / drug effects. Radiotherapy Dosage. Radiotherapy, Conformal / adverse effects

  • MedlinePlus Health Information. consumer health - Radiation Therapy.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright RSNA, 2004
  • (PMID = 15256622.001).
  • [ISSN] 1527-1323
  • [Journal-full-title] Radiographics : a review publication of the Radiological Society of North America, Inc
  • [ISO-abbreviation] Radiographics
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 59
  •  go-up   go-down


90. Kursova LV, Konoplyannikov AG, Pasov VV, Ivanova IN, Poluektova MV, Konoplyannikova OA: Possibilities for the use of autologous mesenchymal stem cells in the therapy of radiation-induced lung injuries. Bull Exp Biol Med; 2009 Apr;147(4):542-6

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Possibilities for the use of autologous mesenchymal stem cells in the therapy of radiation-induced lung injuries.
  • Possible therapeutic effect of systemic (intravenous) transplantation of autologous mesenchymal stem cells was studied in experiments (C57Bl/6 mice) and pilot clinical trial.
  • Clinical trial was performed on 11 patients with radiation-induced lung injuries developed after combined chemotherapy and radiation therapy for lymphogranulomatosis or breast cancer.
  • The patients were subjected to single transplantation of mesenchymal stem cells and course of standard pharmacotherapy.
  • Clinical trial showed that cell therapy with autologous mesenchymal stem cells does not induce progression of the underlying oncological disease.
  • Parameters of spirography, immune status, lung scintigraphy, and markers for inflammation and tissue hypoxia in the patients remained practically unchanged 1 year after the treatment.
  • [MeSH-minor] Adult. Animals. Disease Progression. Humans. Male. Mice. Mice, Inbred C57BL. Pilot Projects. Radiation Pneumonitis / blood. Radiation Pneumonitis / pathology. Radiation Pneumonitis / surgery. Radiotherapy / adverse effects. Transplantation, Autologous. Treatment Outcome

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19704968.001).
  • [ISSN] 1573-8221
  • [Journal-full-title] Bulletin of experimental biology and medicine
  • [ISO-abbreviation] Bull. Exp. Biol. Med.
  • [Language] eng; rus
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


91. Yamada N, Ohira M, Hirakawa K: [COX and study of cancer therapy]. Gan To Kagaku Ryoho; 2004 Aug;31(8):1147-51

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [COX and study of cancer therapy].
  • The increased expression of COX-2 in carcinoma tissue is found in gastric cancer, lung cancer and breast cancer as well as colon cancer.
  • Food and Drug Administration (FDA) approved administration of a COX-2 inhibitor to FAP patients.
  • COX-2 plays an important role in proliferation, invasion and metastasis of cancer.
  • COX-2 expression was reportedly enhanced in lung cancer by an anticancer agent and radiotherapy, and clinical application of a COX-2 inhibitor is attempted.
  • In addition, the experimental examination showed the inhibitory effect of a COX-2 inhibitor on hematogenous metastasis of colon cancer.
  • Clinical application of the COX-2 inhibitor to an effective anti-tumor agent is expected after more studies have been conducted on its molecular biologic function.
  • [MeSH-major] Cyclooxygenase Inhibitors / therapeutic use. Isoenzymes / biosynthesis. Neoplasms / enzymology. Prostaglandin-Endoperoxide Synthases / biosynthesis
  • [MeSH-minor] Adenomatous Polyposis Coli / drug therapy. Animals. Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Breast Neoplasms / enzymology. Colonic Neoplasms / enzymology. Cyclooxygenase 2. Cyclooxygenase 2 Inhibitors. Female. Humans. Lung Neoplasms / enzymology. Male. Membrane Proteins. Mice. Mice, Knockout. Neoplastic Cells, Circulating / drug effects. Stomach Neoplasms / enzymology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15332534.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Cyclooxygenase 2 Inhibitors; 0 / Cyclooxygenase Inhibitors; 0 / Isoenzymes; 0 / Membrane Proteins; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases
  • [Number-of-references] 27
  •  go-up   go-down


92. Chen HL, Chang WH, Shih SC, Pang KK, Bair MJ: Trismus and trigeminal neuralgia in one patient with colon cancer. J Natl Med Assoc; 2008 Jun;100(6):740-2
MedlinePlus Health Information. consumer health - Trigeminal Neuralgia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Trismus and trigeminal neuralgia in one patient with colon cancer.
  • A 64-year-old man got trismus and trigeminal neuralgia under the diagnosis of colon cancer with mandibular metastasis after emergency appendectomy and elective hemicolectomy.
  • The patient chose to forgo further surgery and was given only palliative chemotherapy and radiotherapy.
  • He died six months after diagnosis.
  • Metastatic tumors to the oral cavity are relatively uncommon.
  • They are found most commonly in the mandible, and 70% of cases are adenocarcinoma-most commonly from breast and lung, followed by adrenals, kidneys, prostate, thyroid and colon.
  • Mandibular mass is usually the first sign, then soft-tissue swelling, pain and paresthesias.
  • Tissue proof is needed to confirm the diagnosis.
  • The treatment depends on the nature of the primary, the degree of dissemination and the precise location.
  • However, the prognosis is grim, with the mean survival after diagnosis being only about 6-7 months.
  • [MeSH-major] Adenocarcinoma / secondary. Colonic Neoplasms / pathology. Mandibular Neoplasms / secondary. Trigeminal Neuralgia / etiology. Trismus / etiology
  • [MeSH-minor] Appendectomy. Colectomy. Fatal Outcome. Humans. Male. Middle Aged. Palliative Care. Tomography, X-Ray Computed

  • Genetic Alliance. consumer health - Trigeminal neuralgia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18595580.001).
  • [ISSN] 1943-4693
  • [Journal-full-title] Journal of the National Medical Association
  • [ISO-abbreviation] J Natl Med Assoc
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


93. Gaja A: [Diurnal rhythm of serum leptin in patients with solid tumors]. Vnitr Lek; 2004 Apr;50(4):300-4
MedlinePlus Health Information. consumer health - Colorectal Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Diurnal rhythm of serum leptin in patients with solid tumors].
  • [Transliterated title] Diurnální rytmus sérového leptinu u pacientů se solidními nádory.
  • Leptin is a protein produced by fat tissue.
  • It has many regulatory effects in the area of energetic metabolism, immunity and haematopoiesis.
  • Its role in tumour diseases especially in states with cachexia is studied.
  • There is lack of information about diurnal rhythm of leptin in tumour diseases except some endocrine tumours.
  • In this study 10 patients with breast and colorectal cancer without marks of kachexia and mostly without pre-existing chemotherapy were examined.
  • The diurnal rhythm of leptin was preserved in cancer patients (morning minimum 10.5 +/- 4.2 ng/ml and nocturnal maximum 17.9 +/- 10.1 ng/ml).
  • The difference between males and females (p < 0.01) and correlation of concentrations of leptin with BMI (r = 0.61, p < 0.001) were preserved too.
  • Maybe preservation of diurnal rhythm of leptin can be important in planning of cytostatic and immunomodulatory therapy in future.
  • [MeSH-major] Breast Neoplasms / blood. Circadian Rhythm. Colorectal Neoplasms / blood. Leptin / blood
  • [MeSH-minor] Female. Humans. Male. Middle Aged

  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15214301.001).
  • [ISSN] 0042-773X
  • [Journal-full-title] Vnitr̆ní lékar̆ství
  • [ISO-abbreviation] Vnitr Lek
  • [Language] cze
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Czech Republic
  • [Chemical-registry-number] 0 / Leptin
  •  go-up   go-down


94. Kuttesch JF Jr, Krailo MD, Madden T, Johansen M, Bleyer A, Children's Oncology Group: Phase II evaluation of intravenous vinorelbine (Navelbine) in recurrent or refractory pediatric malignancies: a Children's Oncology Group study. Pediatr Blood Cancer; 2009 Oct;53(4):590-3
Hazardous Substances Data Bank. VINBLASTINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase II evaluation of intravenous vinorelbine (Navelbine) in recurrent or refractory pediatric malignancies: a Children's Oncology Group study.
  • BACKGROUND: A Phase II trial was developed to determine the efficacy and toxicity of intravenous vinorelbine, a semi-synthetic vinca alkaloid, in children, adolescent, and young adults with recurrent or refractory solid malignancies.
  • PROCEDURES: Fifty patients were enrolled among three strata: soft tissue sarcomas [rhabdomyosarcoma (RMS), non-rhabdomyosarcoma, primitive neuroepithelial tumor] (20 patients); brain tumors [astrocytoma (4 patients), medulloblastoma (2 patients), other (16 patients)] (22 patients); neuroblastoma (8 patients).
  • Four responses (one complete, three partial) occurred within the soft tissue sarcoma strata (all with RMS) and two occurred in the brain tumor group (medulloblastoma and astrocytoma).
  • The most common toxicities were hematological and neurological.
  • CONCLUSION: Vinorelbine at dose of 30 mg/m(2) can be safely administered to children with recurrent or refractory solid malignancies.
  • The study design identified vinorelbine to be active in the sarcoma category, with a response rate of 36% (4/11) among RMS patients.


95. Halin S, Rudolfsson SH, Van Rooijen N, Bergh A: Extratumoral macrophages promote tumor and vascular growth in an orthotopic rat prostate tumor model. Neoplasia; 2009 Feb;11(2):177-86
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Extratumoral macrophages promote tumor and vascular growth in an orthotopic rat prostate tumor model.
  • Tumor-associated macrophages are involved in angiogenesis and tumor progression, but their role and specific site of action in prostate cancer remain unknown.
  • To explore this, Dunning R-3327 AT-1 rat prostate tumor cells were injected into the prostate of syngenic and immunocompetent Copenhagen rats and analyzed at different time points for vascular proliferation and macrophage density.
  • Endothelial proliferation increased with tumor size both in the tumor and importantly also in the extratumoral normal prostate tissue.
  • Macrophages accumulated in the tumor and in the extratumoral normal prostate tissue and were most abundant in the invasive zone.
  • Moreover, only extratumoral macrophages showed strong positive associations with tumor size and extratumoral vascular proliferation.
  • Treatment with clodronate-encapsulated liposomes reduced the monocyte/macrophage infiltration and resulted in a significant inhibition of tumor growth.
  • This was accompanied by a suppressed proliferation in microvessels and in the extratumoral prostate tissue also in arterioles and venules.
  • The AT-1 tumors produced, as examined by RT(2) Profiler PCR arrays, numerous factors promoting monocyte recruitment, angiogenesis, and tissue remodeling.
  • Several, namely, chemokine (C-C) ligand 2, fibroblast growth factor 2, matrix metalloproteinase 9, interleukin 1beta, interferon gamma, and transforming growth factor beta, were highly upregulated by the tumor in vivo compared with tumor cells in vitro, suggesting macrophages as a plausible source.
  • In conclusion, we here show the importance of extratumoral monocytes/macrophages for prostate tumor growth, angiogenesis, and extratumoral arteriogenesis.
  • Our findings identify tumor-associated macrophages and several chemotactic and angiogenic factors as potential targets for prostate cancer therapy.
  • [MeSH-major] Disease Models, Animal. Macrophages / metabolism. Neovascularization, Pathologic. Prostatic Neoplasms / blood supply. Prostatic Neoplasms / pathology
  • [MeSH-minor] Angiogenic Proteins / genetics. Animals. Cell Proliferation / drug effects. Chemokines / genetics. Clodronic Acid / pharmacology. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Liposomes / pharmacology. Male. Neoplasm Transplantation. Rats. Reverse Transcriptase Polymerase Chain Reaction. Tumor Cells, Cultured

  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Breast Cancer Res. 2003;5(2):83-8 [12631386.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Mar 4;100(5):2645-50 [12598651.001]
  • [Cites] Nat Rev Cancer. 2004 Jan;4(1):71-8 [14708027.001]
  • [Cites] J Immunol. 2004 Apr 1;172(7):4410-7 [15034056.001]
  • [Cites] Blood. 2004 Oct 15;104(8):2224-34 [15231578.001]
  • [Cites] Prostate. 1986;9(3):261-81 [3774632.001]
  • [Cites] J Immunol Methods. 1994 Sep 14;174(1-2):83-93 [8083541.001]
  • [Cites] Hepatology. 1996 May;23(5):1239-43 [8621159.001]
  • [Cites] Endocrinology. 1998 Feb;139(2):451-6 [9449610.001]
  • [Cites] J Natl Cancer Inst. 1998 Nov 4;90(21):1648-53 [9811314.001]
  • [Cites] Science. 1999 Jun 18;284(5422):1994-8 [10373119.001]
  • [Cites] Endocrinology. 2005 Aug;146(8):3463-70 [15845622.001]
  • [Cites] Cell. 2006 Jan 27;124(2):263-6 [16439202.001]
  • [Cites] Cell. 2006 Feb 10;124(3):615-29 [16469706.001]
  • [Cites] J Leukoc Biol. 2006 Jul;80(1):59-65 [16684892.001]
  • [Cites] Br J Cancer. 2006 Aug 7;95(3):272-81 [16832418.001]
  • [Cites] Clin Cancer Res. 2006 Dec 15;12(24):7431-6 [17189416.001]
  • [Cites] Prostate. 2007 Mar 1;67(4):370-7 [17192959.001]
  • [Cites] J Invest Dermatol. 2007 Aug;127(8):2031-41 [17460736.001]
  • [Cites] Neoplasia. 2007 Jul;9(7):556-62 [17710158.001]
  • [Cites] Cancer Res. 2007 Sep 15;67(18):8874-81 [17875729.001]
  • [Cites] J Cell Biochem. 2008 Feb 15;103(3):691-708 [17668426.001]
  • [Cites] J Immunol. 2008 Feb 15;180(4):2011-7 [18250403.001]
  • [Cites] Mol Cancer Ther. 2008 Apr;7(4):788-99 [18375821.001]
  • [Cites] Cell Transplant. 2008;17(1-2):211-22 [18468252.001]
  • [Cites] Int J Oncol. 2000 Sep;17(3):445-51 [10938382.001]
  • [Cites] Cancer Res. 2000 Oct 15;60(20):5857-61 [11059783.001]
  • [Cites] Cell. 2000 Oct 27;103(3):481-90 [11081634.001]
  • [Cites] Lancet. 2001 Feb 17;357(9255):539-45 [11229684.001]
  • [Cites] Scand J Urol Nephrol. 2001 Dec;35(6):437-52 [11848422.001]
  • [Cites] J Pathol. 2002 Mar;196(3):254-65 [11857487.001]
  • [Cites] Nat Rev Cancer. 2002 Mar;2(3):161-74 [11990853.001]
  • [Cites] Nature. 2002 Dec 19-26;420(6917):860-7 [12490959.001]
  • [Cites] Prostate. 2004 Jan 1;58(1):57-65 [14673953.001]
  • (PMID = 19177202.001).
  • [ISSN] 1476-5586
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Canada
  • [Chemical-registry-number] 0 / Angiogenic Proteins; 0 / Chemokines; 0 / Liposomes; 0813BZ6866 / Clodronic Acid
  • [Other-IDs] NLM/ PMC2631142
  •  go-up   go-down


96. Swerdlow AJ, Barber JA, Hudson GV, Cunningham D, Gupta RK, Hancock BW, Horwich A, Lister TA, Linch DC: Risk of second malignancy after Hodgkin's disease in a collaborative British cohort: the relation to age at treatment. J Clin Oncol; 2000 Feb;18(3):498-509
MedlinePlus Health Information. consumer health - Hodgkin Disease.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Risk of second malignancy after Hodgkin's disease in a collaborative British cohort: the relation to age at treatment.
  • PURPOSE: To assess long-term site-specific risks of second malignancy after Hodgkin's disease in relation to age at treatment and other factors.
  • PATIENTS AND METHODS: A cohort of 5,519 British patients with Hodgkin's disease treated during 1963 through 1993 was assembled and followed-up for second malignancy and mortality.
  • RESULTS: Three hundred twenty-two second malignancies occurred.
  • Relative risks of gastrointestinal, lung, breast, and bone and soft tissue cancers, and of leukemia, increased significantly with younger age at first treatment.
  • Absolute excess risks and cumulative risks of solid cancers and leukemia, however, were greater at older ages than at younger ages.
  • Gastrointestinal cancer risk was greatest after mixed-modality treatment (relative risk [RR] = 3.3; 95% confidence interval [CI], 2.1 to 4.8); lung cancer risks were significantly increased after chemotherapy (RR = 3.
  • 3; 95% CI, 2.4 to 4.7), mixed-modality treatment (RR = 4.3; 95% CI, 2.9 to 6.2), and radiotherapy (RR = 2.9; 95% CI, 1.9 to 4.1); breast cancer risk was increased only after radiotherapy without chemotherapy (RR = 2.5; 95% CI, 1.4 to 4.0); and leukemia risk was significantly increased after chemotherapy (RR = 31.6; 95% CI, 19.7 to 47.6) and mixed-modality treatment (RR = 38.1; 95% CI, 24.6 to 55. 9).
  • These risks were generally greater after treatment at younger ages: for patients treated at ages younger than 25 years, there were RRs of 18.7 (95% CI, 5.8 to 43.5) for gastrointestinal cancer after mixed-modality treatment, 14.4 (95% CI, 5.7 to 29.3) for breast cancer after radiotherapy, and 85.2 (95% CI, 45.3 to 145.7) for leukemia after chemotherapy (with or without radiotherapy).
  • CONCLUSION: Age at treatment has a major effect on risk of second malignancy after Hodgkin's disease.
  • Although absolute excess risks are greater for older patients, RRs of several important malignancies are much greater for patients who are treated when young.
  • The increased risk of gastrointestinal cancers may relate particularly to mixed-modality treatment, and that of lung cancer to chemotherapy as well as radiotherapy; there are also well-known increased risks of breast cancer from radiotherapy and leukemia from chemotherapy.
  • The roles of specific chemotherapeutic agents in the etiology of solid cancers after Hodgkin's disease require detailed investigation.
  • [MeSH-major] Hodgkin Disease / drug therapy. Hodgkin Disease / radiotherapy. Neoplasms, Second Primary / epidemiology
  • [MeSH-minor] Adolescent. Adult. Age Factors. Cohort Studies. Combined Modality Therapy. Female. Humans. Male. Middle Aged. Risk Factors. Time Factors. United Kingdom / epidemiology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 10653865.001).
  • [ISSN] 0732-183X
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  •  go-up   go-down


97. Ensinger C, Sterlacci W: Implications of EGFR PharmDx kit for cetuximab eligibility. Expert Rev Mol Diagn; 2008 Mar;8(2):141-8
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • EGF receptor (EGFR) represents an attractive target for anticancer therapies in a variety of malignant neoplasms, including colorectal, non-small-cell lung, head and neck carcinomas and gliomas.
  • Particularly for application of drugs against extracellular EGFR parts, knowledge about EGFR levels within the cell membrane is of high import, because only EGFR-depending tumors respond to these therapeutic approaches.
  • Immunohistochemical investigation of tissue slides of the primary tumor are performed to screen for EGFR occurrence in tumor cells.
  • It represents the second approved combination of diagnostic tools and dependent application of monoclonal antibody therapies after the successful HercepTest/Herceptin for breast carcinomas.
  • This proceeding represents an important step toward a personalized cancer therapy with major advantages for patients, mainly reduction of toxic side effects and dramatically increased efficiency.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Colonic Neoplasms / drug therapy. Colonic Neoplasms / metabolism. Neoplasm Proteins / biosynthesis. Reagent Kits, Diagnostic. Receptors, Fibroblast Growth Factor / biosynthesis
  • [MeSH-minor] Antibodies, Monoclonal, Humanized. Breast Neoplasms / drug therapy. Breast Neoplasms / metabolism. Cetuximab. Female. Gene Expression Regulation, Neoplastic. Humans. Male. Protein Structure, Tertiary. Trastuzumab. United States. United States Food and Drug Administration

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • Hazardous Substances Data Bank. Trastuzumab .
  • Hazardous Substances Data Bank. CETUXIMAB .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18366301.001).
  • [ISSN] 1744-8352
  • [Journal-full-title] Expert review of molecular diagnostics
  • [ISO-abbreviation] Expert Rev. Mol. Diagn.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / Neoplasm Proteins; 0 / Reagent Kits, Diagnostic; 0 / Receptors, Fibroblast Growth Factor; P188ANX8CK / Trastuzumab; PQX0D8J21J / Cetuximab
  • [Number-of-references] 111
  •  go-up   go-down


98. Buzdar AU: Breast cancer in men. Oncology (Williston Park); 2003 Oct;17(10):1361-4; discussion 1364, 1369-72
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Breast cancer in men.
  • Most men with breast cancer present with a mass in the breast, the evaluation of which should include a tissue diagnosis.
  • If the presence of invasive cancer is established, adequate local therapy includes total removal of the breast.
  • Most tumors are hormone-receptor positive.
  • In high-risk patients, the use of endocrine adjuvant therapy and/or combined endocrine and chemotherapy should be considered.
  • Patients with estrogen-receptor (ER)-negative disease should be offered chemotherapy.
  • In patients with metastatic disease and ER-positive tumors, initial treatment should be endocrine therapy; systemic chemotherapy should be used in patients who are either hormone-receptor negative or resistant to available endocrine therapies.
  • [MeSH-major] Antineoplastic Agents, Hormonal / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Breast Neoplasms, Male / drug therapy. Breast Neoplasms, Male / surgery
  • [MeSH-minor] Chemotherapy, Adjuvant. Drug Resistance, Neoplasm. Humans. Male. Neoplasm Metastasis. Receptors, Estrogen. Risk Factors

  • Genetic Alliance. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Male Breast Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 14606362.001).
  • [ISSN] 0890-9091
  • [Journal-full-title] Oncology (Williston Park, N.Y.)
  • [ISO-abbreviation] Oncology (Williston Park, N.Y.)
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Receptors, Estrogen
  • [Number-of-references] 18
  •  go-up   go-down


99. Robson ME, Chappuis PO, Satagopan J, Wong N, Boyd J, Goffin JR, Hudis C, Roberge D, Norton L, Bégin LR, Offit K, Foulkes WD: A combined analysis of outcome following breast cancer: differences in survival based on BRCA1/BRCA2 mutation status and administration of adjuvant treatment. Breast Cancer Res; 2004;6(1):R8-R17
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A combined analysis of outcome following breast cancer: differences in survival based on BRCA1/BRCA2 mutation status and administration of adjuvant treatment.
  • BACKGROUND: The prognostic significance of germline mutations in BRCA1 and BRCA2 in women with breast cancer remains unclear.
  • METHODS: Two retrospective cohorts of Ashkenazi Jewish women undergoing breast-conserving treatment for invasive cancer between 1980 and 1995 (n = 584) were established.
  • Archived tissue blocks were used as the source of DNA for Ashkenazi Jewish BRCA1/BRCA2 founder mutation analysis.
  • Paraffin-embedded tissue and follow-up information was available for 505 women.
  • After a median follow-up period of 116 months, breast cancer specific survival was worse in women with BRCA1 mutations than in those without (62% at 10 years versus 86%; P < 0.0001), but not in women with the BRCA2 mutation (84% versus 86% at 10 years; P = 0.76).
  • Germline BRCA1 mutations were an independent predictor of breast cancer mortality in multivariate analysis (hazard ratio 2.4, 95% confidence interval 1.2-4.8; P = 0.01).
  • BRCA1 status predicted breast cancer mortality only among women who did not receive chemotherapy (hazard ratio 4.8, 95% confidence interval 2.0-11.7; P = 0.001).
  • The risk for metachronous ipsilateral cancer was not greater in women with germline BRCA1/BRCA2 founder mutations than in those without mutations (P = 0.68).
  • CONCLUSION: BRCA1 mutations, but not BRCA2 mutations, are associated with reduced survival in Ashkenazi women undergoing breast-conserving treatment for invasive breast cancer, but the poor prognosis associated with germline BRCA1 mutations is mitigated by adjuvant chemotherapy.
  • The risk for metachronous ipsilateral disease does not appear to be increased for either BRCA1 or BRCA2 mutation carriers, at least up to 10 years of follow up.
  • [MeSH-major] BRCA1 Protein / genetics. BRCA2 Protein / genetics. Breast Neoplasms / pathology. Germ-Line Mutation
  • [MeSH-minor] Adult. Chemotherapy, Adjuvant. Follow-Up Studies. Humans. Jews / genetics. Male. Middle Aged. Multivariate Analysis. Risk Factors. Survival Analysis. Time Factors. Treatment Outcome

  • Genetic Alliance. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Clin Oncol. 2001 Feb 15;19(4):924-30 [11181654.001]
  • [Cites] Curr Probl Surg. 2001 Jun;38(6):387-480 [11375625.001]
  • [Cites] JAMA. 2001 Nov 14;286(18):2251-6 [11710890.001]
  • [Cites] J Clin Oncol. 2002 Mar 1;20(5):1260-8 [11870168.001]
  • [Cites] J Clin Oncol. 2002 Mar 15;20(6):1480-90 [11896095.001]
  • [Cites] Lancet. 2002 Apr 27;359(9316):1471-7 [11988246.001]
  • [Cites] J Mammary Gland Biol Neoplasia. 2001 Oct;6(4):453-65 [12013534.001]
  • [Cites] J Med Genet. 2002 Aug;39(8):611-4 [12161607.001]
  • [Cites] Int J Cancer. 2002 Oct 20;101(6):555-9 [12237897.001]
  • [Cites] Cancer. 2003 Jan 1;97(1):1-11 [12491499.001]
  • [Cites] J Clin Oncol. 2003 Jan 1;21(1):41-5 [12506168.001]
  • [Cites] Cancer. 2003 Feb 1;97(3):527-36 [12548593.001]
  • [Cites] Cancer. 2003 Apr 1;97(7):1601-8 [12655515.001]
  • [Cites] Br J Cancer. 2003 Apr 22;88(8):1285-91 [12698198.001]
  • [Cites] Am J Hum Genet. 1995 Jan;56(1):265-71 [7825587.001]
  • [Cites] Lancet. 1998 Jan 31;351(9099):316-21 [9652611.001]
  • [Cites] J Natl Cancer Inst. 1998 Aug 5;90(15):1138-45 [9701363.001]
  • [Cites] Clin Cancer Res. 1997 Dec;3(12 Pt 1):2465-9 [9815648.001]
  • [Cites] J Clin Oncol. 1999 Oct;17(10):3017-24 [10506595.001]
  • [Cites] Cancer Res. 2001 Jun 15;61(12):4842-50 [11406561.001]
  • [Cites] Nat Genet. 1996 Oct;14(2):188-90 [8841192.001]
  • [Cites] J Clin Oncol. 1999 Nov;17(11):3396-402 [10550133.001]
  • [Cites] J Natl Cancer Inst. 1999 Dec 15;91(24):2112-7 [10601383.001]
  • [Cites] Breast Cancer Res Treat. 2000 Jan;59(2):185-92 [10817354.001]
  • [Cites] Eur J Cancer. 2000 Jul;36(11):1365-73 [10899649.001]
  • [Cites] J Biol Chem. 2000 Aug 4;275(31):23899-903 [10843985.001]
  • [Cites] J Clin Oncol. 2000 Oct 1;18(19):3360-9 [11013276.001]
  • [Cites] J Clin Oncol. 2000 Dec 15;18(24):4045-52 [11118465.001]
  • [Cites] J Clin Oncol. 2000 Dec 15;18(24):4053-9 [11118466.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2000 Dec 1;48(5):1281-9 [11121624.001]
  • [Cites] Lancet. 2000 Dec 2;356(9245):1876-81 [11130383.001]
  • [Cites] Nat Genet. 1995 Oct;11(2):198-200 [7550349.001]
  • [Cites] Nat Genet. 1996 Oct;14(2):185-7 [8841191.001]
  • [CommentIn] Breast Cancer Res. 2004;6(1):E7 [14680492.001]
  • (PMID = 14680495.001).
  • [ISSN] 1465-542X
  • [Journal-full-title] Breast cancer research : BCR
  • [ISO-abbreviation] Breast Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BRCA1 Protein; 0 / BRCA2 Protein
  • [Other-IDs] NLM/ PMC314444
  •  go-up   go-down


100. Haskell SG: Selective estrogen receptor modulators. South Med J; 2003 May;96(5):469-76
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Because of recent concerns about the long-term risks of estrogen replacement therapy in postmenopausal women, there is growing interest in a group of compounds known as selective estrogen receptor modulators (SERMs).
  • The SERMs bind to estrogen receptors and have tissue-specific effects that allow them to function as estrogen agonists in some tissues and estrogen antagonists in other tissues.
  • Clomid is used primarily in the treatment of infertility.
  • Tamoxifen is indicated for the treatment and prevention of breast cancer.
  • It has an estrogen antagonist effect on breast tissue, but an estrogen-like effect on lipids, bone, and the endometrium.
  • It is thought to be an estrogen antagonist on the uterus and breast tissues and an estrogen agonist with respect to bone and serum lipids.
  • [MeSH-major] Bone and Bones / drug effects. Breast / drug effects. Breast Neoplasms / drug therapy. Cardiovascular System / drug effects. Central Nervous System / drug effects. Endometrium / drug effects. Infertility / drug therapy. Osteoporosis / drug therapy. Receptors, Estrogen / drug effects. Selective Estrogen Receptor Modulators / pharmacology. Selective Estrogen Receptor Modulators / therapeutic use
  • [MeSH-minor] Female. Humans. Male

  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Infertility.
  • MedlinePlus Health Information. consumer health - Osteoporosis.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12911186.001).
  • [ISSN] 0038-4348
  • [Journal-full-title] Southern medical journal
  • [ISO-abbreviation] South. Med. J.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Estrogen; 0 / Selective Estrogen Receptor Modulators
  • [Number-of-references] 84
  •  go-up   go-down






Advertisement