[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 22 of about 22
1. Taccioli C, Wan SG, Liu CG, Alder H, Volinia S, Farber JL, Croce CM, Fong LY: Zinc replenishment reverses overexpression of the proinflammatory mediator S100A8 and esophageal preneoplasia in the rat. Gastroenterology; 2009 Mar;136(3):953-66
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In the rat esophagus, it induces cell proliferation, modulates genetic expression, and enhances carcinogenesis.
  • We characterized the role of the top-up-regulated gene S100A8 in esophageal hyperplasia/reversal and in chemically induced esophageal carcinogenesis in zinc-modulated animals by immunohistochemistry and real-time quantitative polymerase chain reaction.
  • The finding that zinc regulates an inflammatory pathway in esophageal carcinogenesis may lead to prevention and therapy for this cancer.

  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • COS Scholar Universe. author profiles.
  • Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .
  • Hazardous Substances Data Bank. ZINC, ELEMENTAL .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • SciCrunch. ArrayExpress: Data: Microarray .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Ann Thorac Surg. 2005 Sep;80(3):1007-16 [16122475.001]
  • [Cites] Cancer Cell. 2005 Mar;7(3):211-7 [15766659.001]
  • [Cites] Exp Cell Res. 2006 Jan 15;312(2):184-97 [16297907.001]
  • [Cites] Nature. 2000 May 18;405(6784):354-60 [10830965.001]
  • [Cites] Cancer Res. 2000 Aug 15;60(16):4589-95 [10969811.001]
  • [Cites] Int J Cancer. 2001 Jan 20;95(1):39-43 [11241309.001]
  • [Cites] J Natl Cancer Inst. 2001 Oct 17;93(20):1525-33 [11604475.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Nov 20;98(24):13507-13 [11717422.001]
  • [Cites] Clin Cancer Res. 2001 Dec;7(12):3971-6 [11751489.001]
  • [Cites] Cancer Lett. 2002 Sep 26;183(2):205-13 [12065096.001]
  • [Cites] Oncogene. 2006 Jan 5;25(1):111-21 [16247483.001]
  • [Cites] J Trace Elem Med Biol. 2006;20(1):3-18 [16632171.001]
  • [Cites] Carcinogenesis. 2006 Jul;27(7):1489-96 [16543248.001]
  • [Cites] Carcinogenesis. 2006 Aug;27(8):1556-66 [16537558.001]
  • [Cites] Carcinogenesis. 2006 Oct;27(10):1980-90 [16606632.001]
  • [Cites] Biochem Pharmacol. 2006 Nov 30;72(11):1622-31 [16846592.001]
  • [Cites] Biogerontology. 2006 Oct-Dec;7(5-6):409-19 [16964525.001]
  • [Cites] Int J Cancer. 2007 Jan 15;120(2):230-42 [17068819.001]
  • [Cites] Scand J Gastroenterol. 2007 Aug;42(8):902-10 [17613918.001]
  • [Cites] Int J Cancer. 2007 Dec 1;121(11):2373-80 [17893866.001]
  • [Cites] Int J Cancer. 2008 Mar 1;122(5):978-89 [17985342.001]
  • [Cites] J Exp Med. 2008 Feb 18;205(2):275-85 [18208974.001]
  • [Cites] J Leukoc Biol. 2008 Jun;83(6):1484-92 [18339893.001]
  • [Cites] J Nutr. 2003 Apr;133(4):1004-10 [12672911.001]
  • [Cites] Methods Mol Biol. 2003;224:149-57 [12710672.001]
  • [Cites] Genome Biol. 2003;4(5):P3 [12734009.001]
  • [Cites] J Invest Dermatol. 2003 Nov;121(5):1168-74 [14708622.001]
  • [Cites] Oncogene. 2004 Feb 12;23(6):1291-9 [14647409.001]
  • [Cites] Cancer Lett. 2004 Apr 8;206(2):193-9 [15013524.001]
  • [Cites] Neoplasia. 2004 Mar-Apr;6(2):128-35 [15140401.001]
  • [Cites] Cancer Res. 2004 Sep 1;64(17):5982-7 [15342377.001]
  • [Cites] Free Radic Biol Med. 2004 Oct 15;37(8):1182-90 [15451058.001]
  • [Cites] Cancer Res. 1980 Aug;40(8 Pt 1):2633-44 [6992989.001]
  • [Cites] J Natl Cancer Inst. 1981 Aug;67(2):243-51 [6943364.001]
  • [Cites] Science. 1996 Feb 23;271(5252):1081-5 [8599083.001]
  • [Cites] Carcinogenesis. 1996 Sep;17(9):1841-8 [8824504.001]
  • [Cites] Adv Cancer Res. 1998;72:141-96 [9338076.001]
  • [Cites] J Natl Cancer Inst. 2005 Jan 5;97(1):40-50 [15632379.001]
  • [Cites] J Natl Cancer Inst. 2005 Feb 16;97(4):301-6 [15713965.001]
  • [Cites] CA Cancer J Clin. 2005 Mar-Apr;55(2):74-108 [15761078.001]
  • [Cites] Cancer Res. 2005 Sep 1;65(17):7790-9 [16140947.001]
  • (PMID = 19111725.001).
  • [ISSN] 1528-0012
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA118560-02; United States / NCI NIH HHS / CA / R01 CA118560; United States / NCI NIH HHS / CA / CA118560; United States / NCI NIH HHS / CA / R01 CA118560-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Advanced Glycosylation End Product-Specific Receptor; 0 / Calgranulin A; 0 / Receptors, Immunologic; 0 / Transcription Factor RelA; EC 1.14.99.1 / Cyclooxygenase 2; J41CSQ7QDS / Zinc
  • [Other-IDs] NLM/ NIHMS85525; NLM/ PMC2650087
  •  go-up   go-down


2. Scarano WR, Vilamaior PS, Taboga SR: Tissue evidence of the testosterone role on the abnormal growth and aging effects reversion in the gerbil (Meriones unguiculatus) prostate. Anat Rec A Discov Mol Cell Evol Biol; 2006 Nov;288(11):1190-200
Hazardous Substances Data Bank. TESTOSTERONE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tissue evidence of the testosterone role on the abnormal growth and aging effects reversion in the gerbil (Meriones unguiculatus) prostate.
  • Tissues from experimental animals were studied by histological and histochemistry procedures, androgen receptor immunohistochemistry assay, morphometric-stereological analysis, and transmission electron microscopy (TEM).
  • After the treatment were observed increase of prostate weight and epithelium height in all ages studied.
  • Increase of the thickness of the smooth muscle cell (SMC) layer was observed in pubescent and adult animals and TEM revealed apparent SMC hypertrophy.
  • These data demonstrate that the gerbil prostate is susceptible to androgenic action at the studied ages and it can serve, for example, as experimental model to studies of prostate neoplastic process induction and hormonal therapy in aged animals.
  • [MeSH-major] Aging. Androgens / toxicity. Prostate / drug effects. Prostatic Hyperplasia / chemically induced. Prostatic Intraepithelial Neoplasia / chemically induced. Prostatic Neoplasms / chemically induced. Testosterone / toxicity
  • [MeSH-minor] Age Factors. Animals. Cell Proliferation / drug effects. Disease Models, Animal. Epithelial Cells / drug effects. Epithelial Cells / ultrastructure. Gerbillinae. Immunohistochemistry. Male. Microscopy, Electron, Transmission. Myocytes, Smooth Muscle / drug effects. Myocytes, Smooth Muscle / ultrastructure. Organ Size / drug effects. Receptors, Androgen / drug effects. Receptors, Androgen / metabolism

  • MedlinePlus Health Information. consumer health - Enlarged Prostate (BPH).
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • MedlinePlus Health Information. consumer health - Seniors' Health.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2006 Wiley-Liss, Inc.
  • (PMID = 17031809.001).
  • [ISSN] 1552-4884
  • [Journal-full-title] The anatomical record. Part A, Discoveries in molecular, cellular, and evolutionary biology
  • [ISO-abbreviation] Anat Rec A Discov Mol Cell Evol Biol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Receptors, Androgen; 3XMK78S47O / Testosterone
  •  go-up   go-down


3. Shi W, Bastianutto C, Li A, Perez-Ordonez B, Ng R, Chow KY, Zhang W, Jurisica I, Lo KW, Bayley A, Kim J, O'Sullivan B, Siu L, Chen E, Liu FF: Multiple dysregulated pathways in nasopharyngeal carcinoma revealed by gene expression profiling. Int J Cancer; 2006 Nov 15;119(10):2467-75
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] Multiple dysregulated pathways in nasopharyngeal carcinoma revealed by gene expression profiling.
  • Gene expression profiling was conducted using primary human nasopharyngeal carcinoma (NPC) biopsy samples to improve the understanding of the molecular pathways defining NPC and to identify novel potential therapeutic targets.
  • NPC was diagnosed in 19 patients, 11 had lymphoid hyperplasia (LH), and 6 were "normal" biopsies.
  • All NPC patients (except the M1) were treated with curative intent, which included radiotherapy alone (4 patients), or combined with chemotherapy (14 patients).
  • Our data provide novel insights into the development and progression of NPC, and suggest survivin as a novel therapeutic target for NPC.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Carcinoma / metabolism. Gene Expression Profiling. Microtubule-Associated Proteins / metabolism. NF-kappa B p52 Subunit / metabolism. Nasopharyngeal Neoplasms / metabolism. Neoplasm Proteins / metabolism
  • [MeSH-minor] Apoptosis. Cell Proliferation. Gene Expression Regulation, Neoplastic. Humans. Inhibitor of Apoptosis Proteins. Integrins / metabolism. RNA Interference. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction. Up-Regulation. Wnt Proteins / metabolism. beta Catenin / metabolism

  • Genetic Alliance. consumer health - Nasopharyngeal carcinoma.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16858677.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BIRC5 protein, human; 0 / Biomarkers, Tumor; 0 / Inhibitor of Apoptosis Proteins; 0 / Integrins; 0 / Microtubule-Associated Proteins; 0 / NF-kappa B p52 Subunit; 0 / NFKB2 protein, human; 0 / Neoplasm Proteins; 0 / Wnt Proteins; 0 / beta Catenin
  •  go-up   go-down


Advertisement
4. Wislez M, Spencer ML, Izzo JG, Juroske DM, Balhara K, Cody DD, Price RE, Hittelman WN, Wistuba II, Kurie JM: Inhibition of mammalian target of rapamycin reverses alveolar epithelial neoplasia induced by oncogenic K-ras. Cancer Res; 2005 Apr 15;65(8):3226-35
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Here, we report that mTOR inhibition blocked malignant progression in K-ras(LA1) mice, which undergo somatic activation of the K-ras oncogene and display morphologic changes in alveolar epithelial cells that recapitulate those of precursors of human lung adenocarcinoma.
  • Levels of phospho-S6(Ser236/235), a downstream mediator of mTOR, increased with malignant progression (normal alveolar epithelial cells to adenocarcinoma) in K-ras(LA1) mice and in patients with lung adenocarcinoma.
  • Atypical alveolar hyperplasia, an early neoplastic change, was prominently associated with macrophages and expressed high levels of phospho-S6(Ser236/235).
  • mTOR inhibition in K-ras(LA1) mice by treatment with the rapamycin analogue CCI-779 reduced the size and number of early epithelial neoplastic lesions (atypical alveolar hyperplasia and adenomas) and induced apoptosis of intraepithelial macrophages.
  • LKR-13, a lung adenocarcinoma cell line derived from K-ras(LA1) mice, was resistant to treatment with CCI-779 in vitro.
  • However, LKR-13 cells grown as syngeneic tumors recruited macrophages, and those tumors regressed in response to treatment with CCI-779.
  • [MeSH-minor] Adenoma / drug therapy. Adenoma / enzymology. Adenoma / genetics. Adenoma / pathology. Animals. Cell Line, Tumor. Cell Transformation, Neoplastic / drug effects. Cell Transformation, Neoplastic / metabolism. Disease Progression. Enzyme Activation. Hyperplasia. Macrophages, Alveolar / drug effects. Macrophages, Alveolar / enzymology. Macrophages, Alveolar / pathology. Mice. Mutation. Protein-Serine-Threonine Kinases / metabolism. Proto-Oncogene Proteins / metabolism. Proto-Oncogene Proteins c-akt. Ribosomal Protein S6 Kinases / biosynthesis. TOR Serine-Threonine Kinases

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. SIROLIMUS .
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • 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
  • (PMID = 15833854.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / P50 CA070907; United States / NCI NIH HHS / CA / R01 CA105155
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protein Kinase Inhibitors; 0 / Proto-Oncogene Proteins; 624KN6GM2T / temsirolimus; EC 2.7.- / Protein Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.1.1 / mTOR protein, mouse; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.1 / Ribosomal Protein S6 Kinases; W36ZG6FT64 / Sirolimus
  •  go-up   go-down


5. Sekine Y, Demosky SJ, Stonik JA, Furuya Y, Koike H, Suzuki K, Remaley AT: High-density lipoprotein induces proliferation and migration of human prostate androgen-independent cancer cells by an ABCA1-dependent mechanism. Mol Cancer Res; 2010 Sep;8(9):1284-94
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Androgen deprivation therapy for prostate cancer leads to a significant increase of high-density lipoprotein (HDL), which is generally viewed as beneficial, particularly for cardiovascular disease, but the effect of HDL on prostate cancer is unknown.
  • In this study, we investigated the effect of HDL on prostate cancer cell proliferation, migration, intracellular cholesterol levels, and the role of cholesterol transporters, namely ABCA1, ABCG1, and SR-BI in these processes.
  • HDL induced cell proliferation and migration of the androgen-independent PC-3 and DU145 cells by a mechanism involving extracellular signal-regulated kinase (ERK) 1/2 and Akt, but had no effect on the androgen-dependent LNCaP cell, which did not express ABCA1 unlike the other cell lines.
  • Treatment with HDL did not significantly alter the cholesterol content of the cell lines.
  • Knockdown of ABCA1 but not ABCG1 or SR-BI by small interfering RNA (siRNA) inhibited HDL-induced cell proliferation, migration, and ERK1/2 and Akt signal transduction in PC-3 cells.
  • Moreover, after treatment of LNCaP cells with charcoal-stripped fetal bovine serum, ABCA1 was induced ∼10-fold, enabling HDL to induce ERK1/2 activation, whereas small interfering RNA knockdown of ABCA1 inhibited HDL-induced ERK1/2 activation.
  • Simvastatin, which inhibited ABCA1 expression in PC-3 and DU145 cells, attenuated HDL-induced PC-3 and DU145 cell proliferation, migration, and ERK1/2 and Akt phosphorylation.
  • In human prostate biopsy samples, ABCA1 mRNA expression was ∼2-fold higher in the androgen deprivation therapy group than in subjects with benign prostatic hyperplasia or pretreatment prostate cancer groups.
  • [MeSH-major] ATP-Binding Cassette Transporters / metabolism. Cell Movement / drug effects. Lipoproteins, HDL / pharmacology. Prostatic Neoplasms / metabolism. Prostatic Neoplasms / pathology
  • [MeSH-minor] ATP Binding Cassette Transporter 1. Androgens / metabolism. Cell Line, Tumor. Cell Proliferation / drug effects. Cholesterol / metabolism. Enzyme Activation / drug effects. Extracellular Signal-Regulated MAP Kinases / metabolism. Gene Expression Regulation, Neoplastic / drug effects. Humans. Intracellular Space / drug effects. Intracellular Space / metabolism. Male. Proto-Oncogene Proteins c-akt / metabolism. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Small Interfering / metabolism. Simvastatin / pharmacology

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • Hazardous Substances Data Bank. CHOLESTEROL .
  • Hazardous Substances Data Bank. SIMVASTATIN .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • 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 .
  • 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] © 2010 AACR.
  • [Cites] Curr Opin Lipidol. 2004 Dec;15(6):659-65 [15529025.001]
  • [Cites] Cancer Res. 2004 Nov 1;64(21):7682-5 [15520169.001]
  • [Cites] J Clin Invest. 2005 Apr;115(4):959-68 [15776112.001]
  • [Cites] Carcinogenesis. 2005 May;26(5):883-91 [15705602.001]
  • [Cites] Am J Epidemiol. 2005 Aug 15;162(4):318-25 [16014776.001]
  • [Cites] Trends Cardiovasc Med. 2005 Oct;15(7):265-71 [16226682.001]
  • [Cites] Biochem Biophys Res Commun. 2006 May 26;344(1):226-32 [16600185.001]
  • [Cites] Mol Cancer Ther. 2006 Sep;5(9):2310-6 [16985065.001]
  • [Cites] J Natl Cancer Inst. 2006 Dec 20;98(24):1819-25 [17179483.001]
  • [Cites] Prostate. 2007 Apr 1;67(5):463-71 [17252538.001]
  • [Cites] Prostate. 2007 Jul 1;67(10):1061-9 [17469127.001]
  • [Cites] Clin Chim Acta. 2007 Aug;383(1-2):78-84 [17512923.001]
  • [Cites] Atherosclerosis. 2008 Jan;196(1):180-9 [17466310.001]
  • [Cites] J Am Coll Cardiol. 2008 Apr 22;51(16):1604-12 [18420105.001]
  • [Cites] Expert Rev Cardiovasc Ther. 2008 Oct;6(9):1203-15 [18939908.001]
  • [Cites] J Urol. 2009 May;181(5):1998-2006; discussion 2007-8 [19286225.001]
  • [Cites] Endocr J. 2009;56(3):317-34 [18753704.001]
  • [Cites] Prostate. 2009 Oct 1;69(14):1493-506 [19536794.001]
  • [Cites] Int J Cancer. 2000 Jan 1;85(1):60-7 [10585584.001]
  • [Cites] J Urol. 2000 Mar;163(3):1027-32 [10688043.001]
  • [Cites] Carcinogenesis. 2001 May;22(5):701-7 [11323387.001]
  • [Cites] J Lipid Res. 2001 Jun;42(6):967-75 [11369805.001]
  • [Cites] J Biol Chem. 2001 Aug 24;276(34):31780-5 [11427538.001]
  • [Cites] Circulation. 2001 Oct 16;104(16):1978-83 [11602504.001]
  • [Cites] Methods. 2001 Dec;25(4):402-8 [11846609.001]
  • [Cites] Int J Cancer. 2002 Jun 20;99(6):846-52 [12115487.001]
  • [Cites] Mol Cell Biol. 2002 Aug;22(16):5962-74 [12138205.001]
  • [Cites] Biochem Biophys Res Commun. 2002 Sep 6;296(5):1051-7 [12207878.001]
  • [Cites] J Biol Chem. 2003 Mar 14;278(11):9142-9 [12511559.001]
  • [Cites] Lancet. 2003 Mar 8;361(9360):859-64 [12642065.001]
  • [Cites] Arterioscler Thromb Vasc Biol. 2003 May 1;23(5):712-9 [12615688.001]
  • [Cites] Arterioscler Thromb Vasc Biol. 2003 May 1;23(5):802-8 [12637339.001]
  • [Cites] J Cell Biochem. 2004 Jan 1;91(1):54-69 [14689582.001]
  • [Cites] Cancer Res. 2004 Feb 15;64(4):1515-21 [14973113.001]
  • [Cites] Biochem Biophys Res Commun. 2004 Apr 9;316(3):790-4 [15033469.001]
  • [Cites] Cancer. 1973 Jul;32(1):196-205 [4123791.001]
  • [Cites] Anal Biochem. 1975 May 12;65(1-2):42-9 [165752.001]
  • [Cites] Methods Enzymol. 1986;129:628-44 [3523160.001]
  • [Cites] Cancer. 1989 Aug 1;64(3):598-604 [2743254.001]
  • [Cites] J Natl Cancer Inst. 1993 Oct 6;85(19):1571-9 [8105097.001]
  • [Cites] Science. 1996 Jan 26;271(5248):518-20 [8560269.001]
  • [Cites] J Urol. 2005 Feb;173(2):342-59 [15643172.001]
  • (PMID = 20671065.001).
  • [ISSN] 1557-3125
  • [Journal-full-title] Molecular cancer research : MCR
  • [ISO-abbreviation] Mol. Cancer Res.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / NIH0013975756; United States / PHS HHS / / NIH0013975756; United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ABCA1 protein, human; 0 / ATP Binding Cassette Transporter 1; 0 / ATP-Binding Cassette Transporters; 0 / Androgens; 0 / Lipoproteins, HDL; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 97C5T2UQ7J / Cholesterol; AGG2FN16EV / Simvastatin; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases
  • [Other-IDs] NLM/ NIHMS222887; NLM/ PMC2941551
  •  go-up   go-down


6. De J, Brown RE: Tissue-microarray based immunohistochemical analysis of survival pathways in nodular sclerosing classical Hodgkin lymphoma as compared with Non-Hodgkin's lymphoma. Int J Clin Exp Med; 2010 Jan 30;3(1):55-68
antibodies-online. View related products from antibodies-online.com (subscription/membership/fee required).

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tissue-microarray based immunohistochemical analysis of survival pathways in nodular sclerosing classical Hodgkin lymphoma as compared with Non-Hodgkin's lymphoma.
  • Neoplastic cells rely on key oncogenic pathways for their gain of proliferative and/or loss of apoptotic potential.
  • Therapy targeted at specific points in these pathways has the potential to eliminate cancer cells by inducing differentiation or apoptosis.
  • Concurrent immunophenotypic evaluation of survival pathways in nodular sclerosing classical Hodgkin lymphoma (cHL-NS) tissues has not previously been undertaken.
  • We took the tissue microarray (TMA)-based approach to retrospectively evaluate the activation state of key oncogenic pathways by immunohisto-chemistry (IHC) in a series of 6 cases of cHL-NS (with predominantly syncitial areas).
  • For comparison, 2 cases of diffuse large B-cell lymphoma (DLBCL), and 1 case of follicular hyperplasia (FH) were included in the study.
  • Differential upregulation of the mitogen-activated protein kinase (MAPK)-extracellular signal related kinase (ERK), signal transducers and activators of transcription (STAT)3, and protein kinase c - alpha (PKC-alpha) pathways was seen among the cHL cases, whereas nuclear factor - kappa B (NF-kB) and phosphoinositide 3 kinase (PI3 K)-AKT-mammalian target of rapamycin (mTOR) pathways were equally activated in the neoplastic Reed-Sternberg cells of the 6 cHL-NS cases.
  • In this pilot study, concurrent evaluation of oncogenic pathways in cHL-NS and DLBCL offers powerful insights in the putative therapeutic targets for an individualized approach to diagnosis and therapy.


7. Oliver L, Olivier C, Marhuenda FB, Campone M, Vallette FM: Hypoxia and the malignant glioma microenvironment: regulation and implications for therapy. Curr Mol Pharmacol; 2009 Nov;2(3):263-84
MedlinePlus Health Information. consumer health - Brain Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hypoxia and the malignant glioma microenvironment: regulation and implications for therapy.
  • Glioblastoma Multiforme (GBM) tumors are the most common type of brain tumors.
  • The pathological characteristics of these tumors are exemplified by an active invasiveness, necrosis and a specialized form of angiogenesis, known as microvascular hyperplasia.
  • These pathological features are thought to be due to tissue hypoxia.
  • Cells that are under hypoxic stress can either develop an adaptive response that includes increasing the rate of glycolysis and angiogenesis or undergo cell death by promoting apoptosis and/or necrosis.
  • The ability of tumor cells to maintain a balance between an adaptation to hypoxia and cell death is regulated by a family of transcription factors called hypoxia-inducing factors (HIF), which are essential for the regulation of the expression of a large number of hypoxia-responsive genes.
  • The hypothesis that tumor hypoxia would facilitate the likelihood of metastases, tumor recurrence, resistance to chemotherapy and radiotherapy and the invasive potential; all of which culminate in a decrease in patient survival.
  • In this review we will summarize the role of hypoxia in GBM with regard to drug therapy and toxicity and attempt to describe the possible interactions between hypoxia and apoptosis.
  • [MeSH-major] Apoptosis. Brain Neoplasms / metabolism. Brain Neoplasms / pathology. Cell Hypoxia. Glioblastoma / metabolism. Glioblastoma / pathology. Hypoxia-Inducible Factor 1 / genetics
  • [MeSH-minor] Animals. Drug Resistance, Neoplasm. Drug Therapy. Gene Expression Regulation, Neoplastic. Glycolysis. Humans. Necrosis. Neoplasm Invasiveness. Neoplasm Recurrence, Local. Neovascularization, Pathologic. Radiotherapy. Signal Transduction

  • Genetic Alliance. consumer health - Glioma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20021464.001).
  • [ISSN] 1874-4702
  • [Journal-full-title] Current molecular pharmacology
  • [ISO-abbreviation] Curr Mol Pharmacol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United Arab Emirates
  • [Chemical-registry-number] 0 / Hypoxia-Inducible Factor 1
  • [Number-of-references] 217
  •  go-up   go-down


8. Midorikawa Y, Ishikawa T, Kubota K, Mori M, Takayama T, Makuuchi M: Development of well-differentiated hepatocellular carcinoma in large adenomatous hyperplasia after long-term follow-up: a case report. Hepatogastroenterology; 2002 Jul-Aug;49(46):1098-101
MedlinePlus Health Information. consumer health - Liver Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Development of well-differentiated hepatocellular carcinoma in large adenomatous hyperplasia after long-term follow-up: a case report.
  • This report describes a 63-year-old man with a large adenomatous hyperplasia that had been followed over 10 years without any apparent change of size or profile, but grew rapidly after completion of interferon therapy.
  • This patient was a sustained responder, in whom serum alanine aminotransferase levels remained within the normal range and the serum hepatitis C virus-RNA level was undetectable after completion of interferon therapy.
  • However, the tumors, located in segments 5 and 8 of the liver, which had both been followed as adenomatous hyperplasia, grew rapidly two months after completion of interferon therapy; imaging modalities revealed that the former was a typical hepatocellular carcinoma and the latter a large adenomatous hyperplasia.
  • Histological examination showed that the tumor in segment 8 had mosaic proliferation of hepatocytes without fibrosis, indicating adenomatous hyperplasia, in which a small focus of well-differentiated hepatocellular carcinoma was present.
  • This case suggests that even in sustained responders to interferon, administration of this drug cannot suppress malignant transformation of adenomatous hyperplasia to hepatocellular carcinoma.
  • [MeSH-major] Adenoma, Liver Cell / surgery. Carcinoma, Hepatocellular / chemically induced. Cell Transformation, Neoplastic / chemically induced. Hepatitis C, Chronic / drug therapy. Interferon-beta / adverse effects. Liver Neoplasms / chemically induced. Precancerous Conditions / surgery
  • [MeSH-minor] Follow-Up Studies. Hepatectomy. Humans. Hyperplasia. Liver / pathology. Male. Middle Aged. Tomography, X-Ray Computed. Ultrasonography

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12143212.001).
  • [ISSN] 0172-6390
  • [Journal-full-title] Hepato-gastroenterology
  • [ISO-abbreviation] Hepatogastroenterology
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 77238-31-4 / Interferon-beta
  •  go-up   go-down


9. Wüstenberg EG, Theissig F, Offergeld C, Hüttenbrink KB: [Necrotizing lymphadenitis (Kikuchi-Fujimoto disease) as a rare cause of cervical lymphadenopathies. Diagnosis and differential diagnosis]. Laryngorhinootologie; 2000 Feb;79(2):93-5
Genetic Alliance. consumer health - Kikuchi disease.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Common causes include inflammations, neoplastic, or autoimmune diseases.
  • We report on three cases of Kikuchi-Fujimoto disease as a benign self-limiting lymphadenopathy of unknown etiology, which is usually found in young women between 20 and 30 years of age.
  • In two of the three cases, histologic lymph node examination revealed T-cell lymphoma and Hodgkin's disease and in one case led to initial chemotherapeutic treatment.
  • Chemotherapy was discontinued.
  • CONCLUSIONS: Kikuchi-Fujimoto disease is a benign, self-limiting lymphadenopathy which is usually diagnosed in young women.
  • In order to minimize the risk of misdiagnosis and incorrect treatment, the ENT specialist should inform the pathologist about the differential diagnosis of Kikuchi-Fujimoto disease in such cases.
  • [MeSH-minor] Adolescent. Adult. Cell Division / physiology. Diagnosis, Differential. Female. Humans. Hyperplasia. T-Lymphocytes / pathology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 10738716.001).
  • [ISSN] 0935-8943
  • [Journal-full-title] Laryngo- rhino- otologie
  • [ISO-abbreviation] Laryngorhinootologie
  • [Language] ger
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] GERMANY
  •  go-up   go-down


10. Wang B, Rouzier R, Albarracin CT, Sahin A, Wagner P, Yang Y, Smith TL, Meric-Bernstam F, Marcelo Aldaz C, Hortobagyi GN, Pusztai L: Expression of sigma 1 receptor in human breast cancer. Breast Cancer Res Treat; 2004 Oct;87(3):205-14
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.
  • The sigma 1 receptor (S1R) represents a unique drug-binding site that is distinct from any other receptors.
  • We examined S1R expression in human breast cancer and assessed the activity of S1R ligands in breast cancer cell lines.
  • One-hundred nine breast specimens from normal breast, benign breast disease and cancer were examined with immunohistochemistry or RT-PCR and six different cell lines were also evaluated.
  • S1R mRNA overexpression was detected in 64% of breast cancers compared to normal breast tissue.
  • Immunohistochemistry showed positive epithelial cell staining in 60% of invasive and 41% of in situ cancers, 75% of ductal hyperplasia and in 33% of normal breast.
  • The pattern of expression was more diffuse in invasive breast carcinoma compared to other conditions (p = 0.02).
  • S1R expression was neither a prognostic nor a predictive factor for efficacy of adjuvant chemotherapy but the study only included 58 cancer patients and therefore the statistical power is limited.
  • The S1R-specific ligand, SKF 10047 demonstrated the least growth inhibitory activity and showed no interaction with chemotherapy.
  • These results demonstrate that some normal and most neoplastic breast epithelial cells and cell lines commonly express S1R.
  • High concentrations of haloperidol inhibit the growth of these cells and potentiate the effect of chemotherapy in vitro.
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / pharmacology. Blotting, Western. Cell Line, Tumor / drug effects. Cell Line, Tumor / metabolism. DNA Primers. Female. Humans. Immunohistochemistry. RNA, Messenger / analysis. RNA, Neoplasm / analysis. Reverse Transcriptase Polymerase Chain Reaction

  • Genetic Alliance. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [ErratumIn] Breast Cancer Res Treat. 2005 Jan;89(1):95. Marcelo, AC [corrected to Marcelo Aldaz, C]
  • (PMID = 15528963.001).
  • [ISSN] 0167-6806
  • [Journal-full-title] Breast cancer research and treatment
  • [ISO-abbreviation] Breast Cancer Res. Treat.
  • [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] Netherlands
  • [Chemical-registry-number] 0 / DNA Primers; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Receptors, sigma
  •  go-up   go-down


11. Gironet N, De Muret A, Machet L, Diot P, Rivollier C, Dumont P, Lorette G, Vaillant L: [Paraneoplastic pemphigus revealing dendritic cell sarcoma originating from Castleman's disease of the neck]. Ann Dermatol Venereol; 2005 Jan;132(1):41-4
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] [Paraneoplastic pemphigus revealing dendritic cell sarcoma originating from Castleman's disease of the neck].
  • [Transliterated title] Pemphigus paranéoplasique révélateur du développement d'un sarcome à cellules dendritiques à partir d'une tumeur de Castleman pulmonaire.
  • We report a case of paraneoplastic pemphigus at the stage of the sarcomatous transformation of Castleman's disease, present for many years but without concomitant paraneoplastic pemphigus.
  • Following surgical treatment, the respiratory failure worsened.
  • The patient improved with systemic corticosteroids at the dose of 2 mg/kg/d and chemotherapy was initiated.
  • [MeSH-major] Giant Lymph Node Hyperplasia / complications. Paraneoplastic Syndromes / etiology. Pemphigus / etiology. Sarcoma / complications. Sarcoma / etiology
  • [MeSH-minor] Adrenal Cortex Hormones / therapeutic use. Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cell Transformation, Neoplastic. Dendritic Cells. Diagnosis, Differential. Fatal Outcome. Humans. Male. Oral Ulcer / etiology. Oral Ulcer / pathology. Respiratory Insufficiency

  • Genetic Alliance. consumer health - Castleman's Disease.
  • Genetic Alliance. consumer health - Pemphigus.
  • MedlinePlus Health Information. consumer health - Pemphigus.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15746607.001).
  • [ISSN] 0151-9638
  • [Journal-full-title] Annales de dermatologie et de vénéréologie
  • [ISO-abbreviation] Ann Dermatol Venereol
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones
  •  go-up   go-down


12. Elsässer-Beile U, Ruhnau T, Freudenberg N, Wetterauer U, Mengs U: Antitumoral effect of recombinant mistletoe lectin on chemically induced urinary bladder carcinogenesis in a rat model. Cancer; 2001 Mar 1;91(5):998-1004
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.
  • The control group (n = 39 + 17 rats) received no other treatment.
  • The four therapy groups also received rML twice weekly according to one of the following instillation regimens:.
  • To study the immunomodulatory effects of intravesically applied rML, 17 animals from the control group and 15 animals from Group b were asphyxiated at Week 13, and urinary bladder tissue was analyzed by semiquantitative reverse transcriptase-polymerase chain reaction analysis for mRNA expression of interferon-gamma, interleukin-10, and Fas ligand.
  • RESULTS: By Week 21, atypical hyperplasia and neoplastic transformation were found in 82% of the animals in the control group.
  • In contrast, in all four cohorts that were treated with rML, significantly lower rates of atypical hyperplasia and neoplastic transformation were found (Group a, 50%; Group b, 52%; Group c, 45%; and Group d, 42%).
  • By Week 13, in the bladder tissue of 15 rML-treated animals from Group b, lower expression of interleukin-10 mRNA was measured, whereas the expression levels of interferon-gamma mRNA and Fas ligand mRNA were comparable to those of 17 animals from the control group.
  • [MeSH-major] Adjuvants, Immunologic / pharmacology. Plant Preparations. Plant Proteins. Recombinant Proteins / pharmacology. Toxins, Biological / pharmacology. Urinary Bladder Neoplasms / drug therapy
  • [MeSH-minor] Administration, Intravesical. Alkylating Agents / administration & dosage. Animals. Cell Transformation, Neoplastic. Female. Methylnitrosourea / administration & dosage. Neoplasms, Experimental. Rats. Ribosome Inactivating Proteins, Type 2. Urothelium / drug effects. Urothelium / pathology

  • MedlinePlus Health Information. consumer health - Bladder Cancer.
  • Hazardous Substances Data Bank. N-NITROSO-N-METHYLUREA .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2001 American Cancer Society.
  • (PMID = 11251952.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / Alkylating Agents; 0 / Plant Preparations; 0 / Plant Proteins; 0 / Recombinant Proteins; 0 / Ribosome Inactivating Proteins, Type 2; 0 / Toxins, Biological; 0 / ribosome inactivating protein, Viscum; 684-93-5 / Methylnitrosourea
  •  go-up   go-down


13. Zhu B, Liu GT, Wu RS, Strada SJ: Chemoprevention of bicyclol against hepatic preneoplastic lesions. Cancer Biol Ther; 2006 Dec;5(12):1665-73
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.
  • Bicyclol reduced densities of number and area of gamma-glutamyltransferase positive foci, indexes for neoplastic hyperplasia; and also suppressed protein expressions for glutathione S transferase P isoform (GST-P) and alpha-fetal protein and mRNA for N-ras, c-myc and PKCalpha genes.
  • Bicyclol also suppressed TPA-stimulated Balb/c 3T3 cell proliferation in both cell number and 3H-thymidine incorporation.
  • These data demonstrate that Bicyclol prevents carcinogens-induced animal neoplasm and cell malignant transformation via mechanisms at stages of initiation and promotion.
  • It substantiates those evidences that Bicyclol would be used as potential a chemopreventive agent for hepatocarcinogenesis along with its major therapy against chronic anti-hepatitis.
  • [MeSH-major] Biphenyl Compounds / therapeutic use. Gene Expression Regulation / drug effects. Liver Neoplasms / prevention & control. Precancerous Conditions / prevention & control
  • [MeSH-minor] Animals. Antineoplastic Agents / therapeutic use. Cell Transformation, Neoplastic. Chemoprevention. Diethylnitrosamine. Disease Models, Animal. Genes, myc. Genes, ras. Male. RNA, Messenger / genetics. Rats. Rats, Wistar

  • MedlinePlus Health Information. consumer health - Liver Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. N-NITROSODIETHYLAMINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Cancer Biol Ther. 2006 Dec;5(12):1674-6 [17421070.001]
  • (PMID = 17106253.001).
  • [ISSN] 1538-4047
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biphenyl Compounds; 0 / RNA, Messenger; 0 / bicyclol; 3IQ78TTX1A / Diethylnitrosamine
  •  go-up   go-down


14. Imai T, Onose J, Hasumura M, Ueda M, Takizawa T, Hirose M: Sequential analysis of development of invasive thyroid follicular cell carcinomas in inflamed capsular regions of rats treated with sulfadimethoxine after N-bis(2-hydroxypropyl)nitrosamine-initiation. Toxicol Pathol; 2004 Mar-Apr;32(2):229-36
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] Sequential analysis of development of invasive thyroid follicular cell carcinomas in inflamed capsular regions of rats treated with sulfadimethoxine after N-bis(2-hydroxypropyl)nitrosamine-initiation.
  • A 2-stage thyroid follicular carcinogenesis model in rats initiated with N-bis(2-hydroxypropyl)nitrosamine (DHPN) is widely used to detect modifying effects of chemicals on thyroid carcinogenesis.
  • A number of goitrogens are known to strongly promote carcinogenesis, and the carcinomas often originate adjacent to the thyroid capsule and show invasive growth into the capsule or adjacent tissues.
  • In DHPN-SDM-treated rats, multiple focal hyperplasias and adenomas developed in thyroid follicular parenchyma at weeks 4 to 6.
  • Apart from the proliferative lesions, capsular thickening with inflammatory cell infiltration, mainly consisting of macrophages, and migration of follicular epithelium into the capsule were also observed.
  • Focal hyperplasias/adenomas adjacent to the capsule progressively developed to invasive carcinomas at weeks 6 to 10.
  • In thyroid parenchyma, malignant lesions were seldom observed.
  • With SDM-treatment alone, although no neoplastic lesions were observed, capsular thickening with inflammation and epithelial migration resulted in intracapsular residual follicles.
  • Intracapsular residual follicular cells as well as invasive and intrathyroidal carcinoma cells generally showed increased cell proliferative activity, coincidental with cytoplasmic/nuclear positivity for beta-catenin.
  • [MeSH-major] Adenocarcinoma, Follicular / chemically induced. Carcinogens / toxicity. Nitrosamines / toxicity. Sulfadimethoxine / toxicity. Thyroid Gland / drug effects. Thyroid Neoplasms / chemically induced
  • [MeSH-minor] Adenoma / chemically induced. Adenoma / pathology. Administration, Oral. Animals. Biomarkers, Tumor. Cytoskeletal Proteins / metabolism. Drug Therapy, Combination. Hyperplasia. Injections, Subcutaneous. Male. Neoplasm Invasiveness. Rats. Rats, Inbred F344. Trans-Activators / metabolism. Water Supply. beta Catenin

  • MedlinePlus Health Information. consumer health - Thyroid Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15200161.001).
  • [ISSN] 0192-6233
  • [Journal-full-title] Toxicologic pathology
  • [ISO-abbreviation] Toxicol Pathol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Carcinogens; 0 / Ctnnb1 protein, rat; 0 / Cytoskeletal Proteins; 0 / Nitrosamines; 0 / Trans-Activators; 0 / beta Catenin; 30CPC5LDEX / Sulfadimethoxine; 4J072HB2ND / diisopropanolnitrosamine
  •  go-up   go-down


15. Hernando E, Charytonowicz E, Dudas ME, Menendez S, Matushansky I, Mills J, Socci ND, Behrendt N, Ma L, Maki RG, Pandolfi PP, Cordon-Cardo C: The AKT-mTOR pathway plays a critical role in the development of leiomyosarcomas. Nat Med; 2007 Jun;13(6):748-53
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • To determine the role of aberrant PI3K-AKT signaling in leiomyosarcoma pathogenesis, we genetically inactivated Pten in the smooth muscle cell lineage by cross-breeding Pten(loxP/loxP) mice with Tagln-cre mice.
  • Mice carrying homozygous deletion of Pten alleles developed widespread smooth muscle cell hyperplasia and abdominal leiomyosarcomas, with a very rapid onset and elevated incidence (approximately 80%) compared to other animal models.
  • Our data show a new and critical role for the AKT-mTOR pathway in smooth muscle transformation and leiomyosarcoma genesis, and support treatment of selected sarcomas by the targeting of this pathway with new compounds or combinations of these with conventional chemotherapy agents.
  • [MeSH-minor] Animals. Cell Transformation, Neoplastic / genetics. Cell Transformation, Neoplastic / metabolism. Cell Transformation, Neoplastic / pathology. Female. Humans. Hyperplasia. Male. Mice. Mice, Knockout. Mice, Transgenic. Muscle, Smooth / enzymology. Muscle, Smooth / pathology. PTEN Phosphohydrolase / deficiency. PTEN Phosphohydrolase / genetics. Phosphatidylinositol 3-Kinases / physiology. Sarcoma / enzymology. Sarcoma / etiology. Sarcoma / pathology. TOR Serine-Threonine Kinases


16. Zhong C, Yang S, Huang J, Cohen MB, Roy-Burman P: Aberration in the expression of the retinoid receptor, RXRalpha, in prostate cancer. Cancer Biol Ther; 2003 Mar-Apr;2(2):179-84
Hazardous Substances Data Bank. ALITRETINOIN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • To determine the relation of this finding to human prostate cancer, we examined the expression of RXRalpha protein in human prostate cancer cell lines by western blotting and prostate cancer specimens by immunohistochemistry.
  • Relative to the "normal" prostate epithelial cells, there was approximately two- to nine-fold decrease in the full-length 54 kD RXRalpha protein in each of the seven different prostate cancer cell lines tested.
  • Similarly, while RXRalpha immunostaining was uniformly strong in the nuclei of most of the benign prostatic epithelial cells of the thirteen adenocarcinoma specimens tested, a highly heterogeneous pattern of expression was detected in the malignant epithelium, with some areas with low or no staining, others with mostly cytoplasmic staining, and some with both nuclear and cytoplasmic immunoreactivity.
  • To evaluate the effect of RXRalpha modulation on the biologic properties of prostate cancer cell lines, we used a lentivirus expression system to overexpress RXRalpha in CWR22R prostate cancer cells that basally expressed a marginal level of the receptor.
  • A correlation of reduction of cell growth or increased susceptibility to apoptosis with increases in the level of RXRalpha nuclear receptor was demonstrated.
  • These effects were further enhanced when the cell culture medium was supplemented with a retinoid receptor panagonist, 9-cis retinoic acid.
  • [MeSH-major] Prostatic Hyperplasia / metabolism. Prostatic Neoplasms / metabolism. Receptors, Retinoic Acid / metabolism. Transcription Factors / metabolism
  • [MeSH-minor] Animals. Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Blotting, Western. Cell Division / drug effects. Epithelial Cells / metabolism. Epithelial Cells / pathology. Gene Expression Regulation, Neoplastic. Humans. Immunoenzyme Techniques. Lentivirus / genetics. Male. Mice. Prostate / pathology. Retinoid X Receptors. Transfection. Tretinoin / pharmacology. Tumor Cells, Cultured / metabolism. Tumor Cells, Cultured / pathology

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Enlarged Prostate (BPH).
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. ALL-TRANS-RETINOIC ACID .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Cancer Biol Ther. 2003 Mar-Apr;2(2):185-6 [12750560.001]
  • (PMID = 12750559.001).
  • [ISSN] 1538-4047
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01CA59705
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Receptors, Retinoic Acid; 0 / Retinoid X Receptors; 0 / Transcription Factors; 5300-03-8 / alitretinoin; 5688UTC01R / Tretinoin
  •  go-up   go-down


17. Yan J, Katz A: PectaSol-C modified citrus pectin induces apoptosis and inhibition of proliferation in human and mouse androgen-dependent and- independent prostate cancer cells. Integr Cancer Ther; 2010 Jun;9(2):197-203
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Apoptosis and inhibition of cell growth were investigated by Western blotting.
  • RESULTS: Androgen-dependent and -independent human prostate cancer cell lines (LNCaP and PC3, respectively), androgen-dependent and -independent murine prostate cancer cell lines (CASP2.1 and CASP1.1, respectively), as well as noncancerous human benign prostate hyperplasia BPH-1 cell line, were used in the study.
  • MTT assay revealed that 1.0% PectaSol exerted cytotoxicity on LNCaP, PC3, CASP2.1, CASP1.1, and BPH-1 cells for 4-day treatment by 48.0% +/- 2.1%, 54.4% +/- 0.3%, 15.4% +/- 0.8%, 46.1% +/- 1.7%, and 27.4% +/- 1.6%, respectively; whereas 1.0% PectaSol-C showed cytotoxity by 52.2% +/- 1.8%, 48.2% +/- 2.9%, 23.0% +/- 2.6%, 49.0% +/- 1.3%, and 26.8% +/- 2.6%, respectively.
  • CONCLUSION: PectaSol MCP and PectaSol-C MCP can inhibit cell proliferation and apoptosis in prostate cancer cell lines.
  • [MeSH-major] Apoptosis / drug effects. Citrus / chemistry. Pectins / pharmacology. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Androgens / metabolism. Animals. Blotting, Western. Cell Line, Tumor. Cell Proliferation / drug effects. Gene Expression Regulation, Neoplastic / drug effects. Humans. Male. Mice. Prostatic Hyperplasia / drug therapy. Prostatic Hyperplasia / pathology

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • Hazardous Substances Data Bank. PECTIN .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20462856.001).
  • [ISSN] 1552-695X
  • [Journal-full-title] Integrative cancer therapies
  • [ISO-abbreviation] Integr Cancer Ther
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Pectins; 9000-69-5 / pectin
  •  go-up   go-down


18. Ramberg H, Eide T, Krobert KA, Levy FO, Dizeyi N, Bjartell AS, Abrahamsson PA, Taskén KA: Hormonal regulation of beta2-adrenergic receptor level in prostate cancer. Prostate; 2008 Jul 1;68(10):1133-42
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.
  • BACKGROUND: Androgen deprivation is the only effective systemic therapy available for patients with prostatic carcinoma, but is associated with a gradual transition to a hormone-refractory prostate cancer (HRCAP) in which ligand-independent activation of the androgen receptor has been implicated.
  • METHODS: Prostatic cell lines were analyzed using cDNA micro-array, real time RT-PCR, radioligand binding assay, cAMP measurements, transfection and thymidine incorporation assay.
  • The number of beta-adrenergic receptors was modestly up-regulated in androgen independent cell lines (LNCaP-C4, LNCaP-C4-2 and DU145) compared to LNCaP.
  • Immunohistochemical staining of human prostate specimens showed high expression of beta(2)-AR in glandular, epithelial cells and increased expression in malignant cells compared to benign hyperplasia and normal tissue.
  • Interestingly, beta(2)-AR mRNA was strongly down-regulated by androgen ablation therapy of prostate cancer patients.
  • CONCLUSION: The level of beta(2)-AR was increased by T3 in prostatic adenocarcinoma cells and reduced in prostate cancer patients who had received androgen ablation therapy for 3 months.
  • [MeSH-minor] Androgen Antagonists / pharmacology. Androgen Antagonists / therapeutic use. Androgens / metabolism. Anilides / pharmacology. Antineoplastic Agents / pharmacology. Biopsy. Cell Line, Tumor. Down-Regulation. Gene Expression Regulation, Neoplastic / drug effects. Gene Expression Regulation, Neoplastic / physiology. Humans. Immunohistochemistry. Male. Nitriles / pharmacology. Oligonucleotide Array Sequence Analysis. Prostate / metabolism. Prostate / pathology. Receptors, Androgen / metabolism. Signal Transduction / drug effects. Signal Transduction / physiology. Tosyl Compounds / pharmacology. Triiodothyronine / pharmacology. Up-Regulation

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • Hazardous Substances Data Bank. LIOTHYRONINE .
  • Hazardous Substances Data Bank. BICALUTAMIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • (PMID = 18454446.001).
  • [ISSN] 0270-4137
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Androgens; 0 / Anilides; 0 / Antineoplastic Agents; 0 / Nitriles; 0 / Receptors, Adrenergic, beta-2; 0 / Receptors, Androgen; 0 / Tosyl Compounds; 06LU7C9H1V / Triiodothyronine; A0Z3NAU9DP / bicalutamide
  •  go-up   go-down


19. Tan-Chiu E, Wang J, Costantino JP, Paik S, Butch C, Wickerham DL, Fisher B, Wolmark N: Effects of tamoxifen on benign breast disease in women at high risk for breast cancer. J Natl Cancer Inst; 2003 Feb 19;95(4):302-7
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] Effects of tamoxifen on benign breast disease in women at high risk for breast cancer.
  • BACKGROUND: In 1998 the National Surgical Adjuvant Breast and Bowel Project (NSABP) demonstrated that tamoxifen treatment reduced the incidence of both invasive and noninvasive breast cancer in women at high risk for the disease.
  • We examined the effect of tamoxifen treatment on the incidence of benign breast disease and the number of breast biopsies in the same group of women.
  • Included in this analysis were women who had undergone a breast biopsy and who had histologic diagnoses of adenosis, cyst, duct ectasia, fibrocystic disease, fibroadenoma, fibrosis, hyperplasia, or metaplasia.
  • RESULTS: Overall, tamoxifen treatment reduced the risk of benign breast disease by 28% (RR = 0.72, 95% confidence interval [CI] = 0.65 to 0.79).
  • Tamoxifen therapy resulted in statistically significant reductions in the risk of adenosis (RR = 0.59, 95% CI = 0.47 to 0.73), cyst (RR = 0.66, 95% CI = 0.58 to 0.75), duct ectasia (RR = 0.72, 95% CI = 0.53 to 0.97), fibrocystic disease (RR = 0.67, 95% CI = 0.58 to 0.77), hyperplasia (RR = 0.60, 95% CI = 0.50 to 0.71), and metaplasia (RR = 0.51, 95% CI = 0.41 to 0.62).
  • Tamoxifen therapy also reduced the risk for fibroadenoma (RR = 0.77, 95% CI = 0.56 to 1.04) and fibrosis (RR = 0.86, 95% CI = 0.72 to 1.03).
  • CONCLUSION: Women in this study who received tamoxifen, especially younger women (i.e., <50 years), had a reduced incidence of clinically detected benign breast disease and underwent fewer breast biopsies.
  • [MeSH-major] Anticarcinogenic Agents / therapeutic use. Biopsy / statistics & numerical data. Breast Diseases / drug therapy. Breast Neoplasms / prevention & control. Estrogen Receptor Modulators / therapeutic use. Tamoxifen / therapeutic use
  • [MeSH-minor] Adult. Age Factors. Cell Transformation, Neoplastic / drug effects. Female. Humans. Middle Aged. Risk Assessment. Risk Factors

  • Genetic Alliance. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Biopsy.
  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Breast Diseases.
  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • Hazardous Substances Data Bank. TAMOXIFEN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12591986.001).
  • [ISSN] 0027-8874
  • [Journal-full-title] Journal of the National Cancer Institute
  • [ISO-abbreviation] J. Natl. Cancer Inst.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / U10 CA 37377; United States / NCI NIH HHS / CA / U10 CA 69974
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Estrogen Receptor Modulators; 094ZI81Y45 / Tamoxifen
  •  go-up   go-down


20. Muratovska A, Zhou C, He S, Goodyer P, Eccles MR: Paired-Box genes are frequently expressed in cancer and often required for cancer cell survival. Oncogene; 2003 Sep 11;22(39):7989-97
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] Paired-Box genes are frequently expressed in cancer and often required for cancer cell survival.
  • Although PAX genes are primarily expressed in the embryo, constitutive expression promotes tissue hyperplasia.
  • We analysed the pattern and requirement for PAX gene expression in a panel of common cancer cell lines.
  • Very frequent PAX gene expression was identified in tumor cell lines, including lymphoma, breast, ovarian, lung, and colon cancer.
  • In addition, the PAX2 gene was frequently expressed in a panel of 406 common primary tumor tissues.
  • Apoptosis was rapidly induced in ovarian and bladder cancer cell lines following RNA interference to silence PAX2 expression, despite concomitant TP53 and/or HRAS mutations.
  • [MeSH-major] DNA-Binding Proteins / genetics. Gene Expression Regulation, Neoplastic. Neoplasms / genetics. Neoplasms / pathology. Nuclear Proteins. Transcription Factors / genetics
  • [MeSH-minor] Apoptosis / genetics. Cell Survival / genetics. Eye Proteins. Female. Genes, ras. Homeodomain Proteins / genetics. Humans. Male. Melanoma / drug therapy. Melanoma / genetics. Melanoma / pathology. Mutation. Oligonucleotides, Antisense / pharmacology. Ovarian Neoplasms / genetics. Ovarian Neoplasms / pathology. PAX2 Transcription Factor. PAX9 Transcription Factor. Paired Box Transcription Factors. Repressor Proteins. Trans-Activators / genetics. Tumor Cells, Cultured. Tumor Suppressor Protein p53 / genetics. Urinary Bladder Neoplasms / genetics. Urinary Bladder Neoplasms / pathology

  • Genetics Home Reference. consumer health - PAX2 gene.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12970747.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [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] 0 / DNA-Binding Proteins; 0 / Eye Proteins; 0 / Homeodomain Proteins; 0 / Nuclear Proteins; 0 / Oligonucleotides, Antisense; 0 / PAX2 Transcription Factor; 0 / PAX2 protein, human; 0 / PAX3 protein, human; 0 / PAX6 protein; 0 / PAX8 protein, human; 0 / PAX9 Transcription Factor; 0 / PAX9 protein, human; 0 / Paired Box Transcription Factors; 0 / Repressor Proteins; 0 / Trans-Activators; 0 / Transcription Factors; 0 / Tumor Suppressor Protein p53; 138016-91-8 / Pax3 protein, mouse
  •  go-up   go-down


21. Masuelli L, Focaccetti C, Cereda V, Lista F, Vitolo D, Trono P, Gallo P, Amici A, Monaci P, Mattei M, Modesti M, Forni G, Kraus MH, Muraro R, Modesti A, Bei R: Gene-specific inhibition of breast carcinoma in BALB-neuT mice by active immunization with rat Neu or human ErbB receptors. Int J Oncol; 2007 Feb;30(2):381-92
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] Gene-specific inhibition of breast carcinoma in BALB-neuT mice by active immunization with rat Neu or human ErbB receptors.
  • The outcome of neu-mediated tumorigenesis was compared following vaccination with isogeneic normal rat ErbB2/Neu (LTR-Neu) or xenogeneic human ErbB receptors (LTR-EGFR, LTR-ErbB2, LTR-ErbB3 and LTR-ErbB4), each recombinantly expressed in an NIH3T3 murine cell background.
  • Vaccination using rat LTR-Neu at the stage of atypical hyperplasia potently inhibited neu-mediated mammary tumorigenesis.
  • Furthermore, a T cell response specific for peptide epitopes of rat Neu was elicited in spleen cells of mice immunized with LTR-Neu and was remotely detectable for discrete peptides upon vaccination with LTR-ErbB2 and LTR-EGFR.
  • [MeSH-major] Breast Neoplasms / drug therapy. Breast Neoplasms / genetics. Gene Expression Regulation, Neoplastic. Genes, erbB-2. Receptor, ErbB-2 / biosynthesis
  • [MeSH-minor] Animals. Apoptosis. Cancer Vaccines. Disease-Free Survival. Epitopes / chemistry. Humans. Lymphocytes, Tumor-Infiltrating / cytology. Mice. Mice, Inbred BALB C. Mice, Transgenic. NIH 3T3 Cells. Rats. Time Factors. Transgenes


22. Murray AR, Kisin ER, Kommineni C, Vallyathan V, Castranova V, Shvedova AA: Pro/antioxidant status and AP-1 transcription factor in murine skin following topical exposure to cumene hydroperoxide. Carcinogenesis; 2007 Jul;28(7):1582-8
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.
  • Organic peroxides, widely used in the chemical and pharmaceutical industries, can act as skin tumor promoters and cause epidermal hyperplasia.
  • The present study evaluated the effect of cumene hydroperoxide (Cum-OOH) on the induction of activator protein-1 (AP-1), which is linked to the expression of genes regulating cell proliferation, growth and transformation.
  • The present study used JB6 P+ mouse epidermal cells and AP-1-luciferase reporter transgenic mice to identify whether exposure to Cum-OOH caused activation of AP-1, oxidative stress, depletion of antioxidants and tumor formation during two-stage carcinogenesis.
  • [MeSH-major] Benzene Derivatives / toxicity. Cell Transformation, Neoplastic / drug effects. Oxidative Stress. Papilloma / drug therapy. Skin Neoplasms / metabolism. Transcription Factor AP-1 / metabolism
  • [MeSH-minor] 9,10-Dimethyl-1,2-benzanthracene / toxicity. Animals. Cell Line. Cell Proliferation / drug effects. Female. Gene Expression Regulation, Neoplastic / drug effects. Glutathione / metabolism. Mice. Mice, Transgenic. Oxidation-Reduction. Skin / drug effects. Skin / metabolism. Tetradecanoylphorbol Acetate / toxicity






Advertisement