[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 11 of about 11
1. Wong NA, Brett L, Stewart M, Leitch A, Longley DB, Dunlop MG, Johnston PG, Lessells AM, Jodrell DI: Nuclear thymidylate synthase expression, p53 expression and 5FU response in colorectal carcinoma. Br J Cancer; 2001 Dec 14;85(12):1937-43
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Nuclear thymidylate synthase expression, p53 expression and 5FU response in colorectal carcinoma.
  • Nuclear expression of TS in human tissue in vivo has not been characterised and its clinicopathological correlates in malignancy are unknown.
  • 52 cases of primary colorectal carcinoma (CRC) and 24 cases of matched metastatic carcinoma were studied immunohistochemically using the monoclonal antibody TS106.
  • Strong nuclear immunostaining was seen in normal basal crypt colonocytes and germinal centre cells, and in a varying proportion of adenocarcinoma cells.
  • Higher TS nuclear expression also showed a significant association with poorer response to protracted venous infusional 5FU therapy.
  • There was no clear association between TS nuclear expression and Ki67 or p53 expression assessed immunohistochemically.
  • There was a strong positive correlation between TS nuclear expression in primary and metastatic CRC but the latter generally showed higher expression than matched primary tumour tissue.
  • [MeSH-major] Adenocarcinoma / genetics. Antimetabolites, Antineoplastic / therapeutic use. Cell Nucleus / enzymology. Colorectal Neoplasms / genetics. Enzyme Inhibitors / therapeutic use. Fluorouracil / therapeutic use. Neoplasm Proteins / biosynthesis. Thymidylate Synthase / biosynthesis. Tumor Suppressor Protein p53 / biosynthesis
  • [MeSH-minor] Adult. Aged. Cell Differentiation. Drug Resistance, Neoplasm / genetics. Enzyme Induction. Female. Gene Expression Profiling. Genes, p53. Humans. Ki-67 Antigen / biosynthesis. Ki-67 Antigen / genetics. Male. Middle Aged. Neoplasm Metastasis. RNA, Messenger / biosynthesis. RNA, Neoplasm / biosynthesis. Reproducibility of Results. Survival Analysis. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Colorectal Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. FLUOROURACIL .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Clin Cancer Res. 1998 May;4(5):1227-34 [9607581.001]
  • [Cites] Eur J Cancer. 2000 May;36(8):1038-42 [10885609.001]
  • [Cites] Anticancer Res. 1998 May-Jun;18(3A):1515-20 [9673363.001]
  • [Cites] J Pathol. 1998 Jun;185(2):123-9 [9713337.001]
  • [Cites] Oncology. 1998 Nov-Dec;55(6):564-8 [9778624.001]
  • [Cites] Clin Exp Pharmacol Physiol. 1998 Nov;25(11):887-95 [9807659.001]
  • [Cites] Cell Prolif. 1998 Jun-Aug;31(3-4):113-26 [9853425.001]
  • [Cites] Mol Cell Biol. 1999 Feb;19(2):1582-94 [9891091.001]
  • [Cites] Dis Esophagus. 1998 Oct;11(4):215-20 [10071801.001]
  • [Cites] Gastroenterology. 1999 Jul;117(1):123-31 [10381918.001]
  • [Cites] J Clin Oncol. 1999 Jun;17(6):1760-70 [10561213.001]
  • [Cites] Br J Cancer. 2000 Feb;82(3):560-7 [10682666.001]
  • [Cites] Clin Cancer Res. 2000 Mar;6(3):1063-72 [10741735.001]
  • [Cites] Clin Cancer Res. 2000 Apr;6(4):1322-7 [10778957.001]
  • [Cites] Lancet. 2000 May 20;355(9217):1745-50 [10832824.001]
  • [Cites] Gastroenterology. 2000 Oct;119(4):921-8 [11040179.001]
  • [Cites] Clin Cancer Res. 2000 Dec;6(12):4797-802 [11156237.001]
  • [Cites] Br J Cancer. 2001 Mar 2;84(5):600-3 [11237378.001]
  • [Cites] Arch Pathol Lab Med. 1985 Aug;109(8):716-21 [3893381.001]
  • [Cites] Cancer Res. 1990 Jul 1;50(13):3979-84 [2162250.001]
  • [Cites] Cancer Res. 1991 Dec 15;51(24):6668-76 [1720706.001]
  • [Cites] Cancer Res. 1992 Jan 1;52(1):108-16 [1727369.001]
  • [Cites] J Biol Chem. 1994 Mar 18;269(11):8341-7 [8132557.001]
  • [Cites] J Clin Oncol. 1994 Oct;12(10):2035-42 [7931471.001]
  • [Cites] J Clin Oncol. 1994 Dec;12(12):2640-7 [7989939.001]
  • [Cites] Cancer Res. 1995 Apr 1;55(7):1407-12 [7882343.001]
  • [Cites] Eur J Cancer. 1995 Jul-Aug;31A(7-8):1101-4 [7577000.001]
  • [Cites] Eur J Cancer. 1995 Jul-Aug;31A(7-8):1299-305 [7577040.001]
  • [Cites] Eur J Cancer. 1995 Jul-Aug;31A(7-8):1306-10 [7577041.001]
  • [Cites] Eur J Surg Oncol. 1996 Apr;22(2):182-5 [8608838.001]
  • [Cites] Nucleic Acids Res. 1996 Aug 15;24(16):3222-8 [8774904.001]
  • [Cites] Br J Cancer. 1997;75(6):903-9 [9062414.001]
  • [Cites] J Biol Chem. 1997 May 16;272(20):13281-5 [9148948.001]
  • [Cites] Exp Cell Res. 1997 Aug 1;234(2):270-6 [9260894.001]
  • [Cites] Int J Cancer. 1997 Sep 17;72(6):1137-41 [9378551.001]
  • [Cites] Cancer. 1998 Jan 1;82(1):70-7 [9428481.001]
  • [Cites] Eur J Cancer. 1997 Nov;33(13):2278-81 [9470819.001]
  • [Cites] Clin Cancer Res. 1998 May;4(5):1243-50 [9607583.001]
  • (PMID = 11747337.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Scotland
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Enzyme Inhibitors; 0 / Ki-67 Antigen; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Tumor Suppressor Protein p53; EC 2.1.1.45 / Thymidylate Synthase; U3P01618RT / Fluorouracil
  • [Other-IDs] NLM/ PMC2364004
  •  go-up   go-down


2. Seidl H, Kreimer-Erlacher H, Bäck B, Soyer HP, Höfler G, Kerl H, Wolf P: Ultraviolet exposure as the main initiator of p53 mutations in basal cell carcinomas from psoralen and ultraviolet A-treated patients with psoriasis. J Invest Dermatol; 2001 Aug;117(2):365-70
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ultraviolet exposure as the main initiator of p53 mutations in basal cell carcinomas from psoralen and ultraviolet A-treated patients with psoriasis.
  • Basal cell carcinoma, the most frequent skin cancer in humans, is often linked to chronic sun exposure.
  • In psoralen and ultraviolet A-treated psoriatic patients, basal cell carcinomas may occur even more frequently; however, the exact etiology and mechanisms of tumorigenesis in psoriatic patients are unclear because psoralen and ultraviolet A is not only a carcinogen but also an immunosuppressor and because psoralen and ultraviolet A-treated psoriatic patients often have other (co)carcinogenic risk factors (e.g, therapeutic exposure to ultraviolet B, X-ray radiation, arsenic, tar, and/or chemotherapeutic agents such as methotrexate).
  • In this study, we analyzed the DNA of 13 basal cell carcinomas from five psoralen and ultraviolet A-treated psoriatic patients for mutations of the p53 tumor suppressor gene.
  • DNA sequencing revealed a total of 11 mis-sense, two non-sense, and four silent mutations in seven of the 13 basal cell carcinomas (54%).
  • Of the 13 total mis-sense or non-sense mutations, 12 (92%) occurred at dipyrimidine sites and nine (69%) were of the ultraviolet fingerprint type (eight C-->T transitions and one CC-->TT transition).
  • Thus, whether these mutations were induced by ultraviolet or psoralen and ultraviolet A was not clear.
  • In addition, two other mutations (15%) occurred at 5'-TpG sites, one (8%) occurred at a 5'-TpA site (the most frequent site of psoralen binding and mutagenesis in cell and murine studies), and one (8%) involved a G-->T transversion.
  • These results suggest that (i) the major initiator of p53 mutations in basal cell carcinoma in psoralen and ultraviolet A-treated psoriasis patients is environmental and/or therapeutic ultraviolet(B) exposure, and that (ii) psoralen and ultraviolet A itself causes only a smaller portion of p53 mutations in psoralen and ultraviolet A-associated basal cell carcinomas.
  • [MeSH-major] Carcinoma, Basal Cell / genetics. PUVA Therapy / adverse effects. Psoriasis / drug therapy. Skin Neoplasms / genetics. Tumor Suppressor Protein p53 / genetics. Ultraviolet Rays / adverse effects
  • [MeSH-minor] Adult. Aged. Female. Ficusin / adverse effects. Humans. Incidence. Male. Middle Aged. Photosensitizing Agents / adverse effects. Point Mutation / drug effects. Point Mutation / radiation effects. Polymorphism, Single-Stranded Conformational

  • Genetic Alliance. consumer health - Psoriasis.
  • MedlinePlus Health Information. consumer health - Psoriasis.
  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. PSORALEN .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [ErratumIn] J Invest Dermatol 2001 Dec;117(6):1688
  • (PMID = 11511317.001).
  • [ISSN] 0022-202X
  • [Journal-full-title] The Journal of investigative dermatology
  • [ISO-abbreviation] J. Invest. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Photosensitizing Agents; 0 / Tumor Suppressor Protein p53; KTZ7ZCN2EX / Ficusin
  •  go-up   go-down


3. Herschkowitz JI, He X, Fan C, Perou CM: The functional loss of the retinoblastoma tumour suppressor is a common event in basal-like and luminal B breast carcinomas. Breast Cancer Res; 2008;10(5):R75
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The functional loss of the retinoblastoma tumour suppressor is a common event in basal-like and luminal B breast carcinomas.
  • One of these groups, the basal-like subtype, is poorly differentiated, highly metastatic, genomically unstable, and contains specific genetic alterations such as the loss of tumour protein 53 (TP53).
  • The loss of the retinoblastoma tumour suppressor encoded by the RB1 locus is a well-characterised occurrence in many tumour types; however, its role in breast cancer is less clear with many reports demonstrating a loss of heterozygosity that does not correlate with a loss of RB1 protein expression.
  • METHODS: We used gene expression analysis for tumour subtyping and polymorphic markers located at the RB1 locus to assess the frequency of loss of heterozygosity in 88 primary human breast carcinomas and their normal tissue genomic DNA samples.
  • RESULTS: RB1 loss of heterozygosity was observed at an overall frequency of 39%, with a high frequency in basal-like (72%) and luminal B (62%) tumours.
  • These tumours also concurrently showed low expression of RB1 mRNA. p16INK4a was highly expressed in basal-like tumours, presumably due to a previously reported feedback loop caused by RB1 loss.
  • An RB1 loss of heterozygosity signature was developed and shown to be highly prognostic, and was potentially a predictive marker of response to neoadjuvant chemotherapy.
  • CONCLUSIONS: These results suggest that the functional loss of RB1 is common in basal-like tumours, which may play a key role in dictating their aggressive biology and unique therapeutic responses.

  • Genetic Alliance. consumer health - Retinoblastoma.
  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • COS Scholar Universe. author profiles.
  • 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 .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cytogenet Cell Genet. 1992;60(3-4):190-3 [1354594.001]
  • [Cites] Cancer Res. 1992 May 15;52(10):2991-4 [1581913.001]
  • [Cites] Cancer Res. 1994 Nov 15;54(22):5816-20 [7954407.001]
  • [Cites] Cancer Res. 1994 Dec 1;54(23):6078-82 [7954450.001]
  • [Cites] Cell. 1995 May 5;81(3):323-30 [7736585.001]
  • [Cites] Nature. 1995 Jun 8;375(6531):503-6 [7777060.001]
  • [Cites] Am J Pathol. 1996 Jul;149(1):15-20 [8686738.001]
  • [Cites] Science. 1996 Dec 6;274(5293):1672-7 [8939849.001]
  • [Cites] Int J Cancer. 1998 Feb 20;79(1):71-5 [9495362.001]
  • [Cites] Oncogene. 1998 Jul 16;17(2):199-205 [9674704.001]
  • [Cites] Br J Cancer. 1998 Dec;78(12):1661-8 [9862580.001]
  • [Cites] Mol Med. 1998 Dec;4(12):807-22 [9990866.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Mar 16;96(6):2952-7 [10077618.001]
  • [Cites] N Engl J Med. 2004 Dec 30;351(27):2817-26 [15591335.001]
  • [Cites] Cancer Res. 2005 May 15;65(10):4059-66 [15899795.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Jun 14;102(24):8561-6 [15939874.001]
  • [Cites] Clin Chim Acta. 2005 Aug;358(1-2):75-80 [15921673.001]
  • [Cites] Clin Cancer Res. 2005 Aug 15;11(16):5678-85 [16115903.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Sep 20;102(38):13550-5 [16141321.001]
  • [Cites] Cancer Res. 2005 Oct 15;65(20):9155-8 [16230372.001]
  • [Cites] BMC Genet. 2005;6:53 [16269091.001]
  • [Cites] Mod Pathol. 2006 Feb;19(2):264-71 [16341146.001]
  • [Cites] Nat Rev Cancer. 2006 Feb;6(2):99-106 [16491069.001]
  • [Cites] Appl Immunohistochem Mol Morphol. 2006 Mar;14(1):63-70 [16540733.001]
  • [Cites] J Clin Oncol. 2006 Apr 10;24(11):1656-64 [16505416.001]
  • [Cites] BMC Genomics. 2006;7:96 [16643655.001]
  • [Cites] Breast Cancer Res. 2006;8(2):R23 [16626501.001]
  • [Cites] J Clin Oncol. 2006 Sep 10;24(26):4236-44 [16896004.001]
  • [Cites] Cancer Cell. 2006 Dec;10(6):529-41 [17157792.001]
  • [Cites] J Clin Invest. 2007 Jan;117(1):218-28 [17160137.001]
  • [Cites] Genes Dev. 2007 Jan 1;21(1):49-54 [17210787.001]
  • [Cites] Hum Pathol. 2007 Feb;38(2):197-204 [17234468.001]
  • [Cites] Mol Cancer. 2007;6:7 [17233903.001]
  • [Cites] Mol Diagn Ther. 2007;11(1):63-70 [17286451.001]
  • [Cites] Clin Cancer Res. 2007 Apr 15;13(8):2329-34 [17438091.001]
  • [Cites] Genome Biol. 2007;8(5):R76 [17493263.001]
  • [Cites] Nature. 2007 Aug 16;448(7155):811-5 [17700700.001]
  • [Cites] Clin Cancer Res. 2000 Jul;6(7):2777-87 [10914724.001]
  • [Cites] Nature. 2000 Aug 17;406(6797):747-52 [10963602.001]
  • [Cites] Mol Carcinog. 2000 Nov;29(3):151-8 [11108660.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Apr 24;98(9):5116-21 [11309499.001]
  • [Cites] Breast Cancer Res Treat. 2001 May;67(1):61-70 [11518467.001]
  • [Cites] Oncogene. 2007 Sep 20;26(43):6307-18 [17452985.001]
  • [Cites] Cancer Cell. 2007 Nov;12(5):479-91 [17996651.001]
  • [Cites] Clin Cancer Res. 2008 Apr 1;14(7):2199-209 [18381962.001]
  • [Cites] Hum Mol Genet. 2008 May 15;17(10):1363-72 [18211953.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Sep 11;98(19):10869-74 [11553815.001]
  • [Cites] Dis Markers. 2001;17(2):99-109 [11673656.001]
  • [Cites] Nat Genet. 2002 Jul;31(3):285-8 [12068296.001]
  • [Cites] Hum Mutat. 2002 Nov;20(5):408 [12402348.001]
  • [Cites] Virchows Arch. 2002 Dec;441(6):577-83 [12461615.001]
  • [Cites] N Engl J Med. 2002 Dec 19;347(25):1999-2009 [12490681.001]
  • [Cites] Am J Hum Genet. 2003 Feb;72(2):253-69 [12541220.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Jul 8;100(14):8418-23 [12829800.001]
  • [Cites] Cancer Res. 2004 Jan 1;64(1):64-71 [14729609.001]
  • [Cites] Cancer Cell. 2004 May;5(5):489-500 [15144956.001]
  • [Cites] Science. 1988 Jul 8;241(4862):218-21 [3388033.001]
  • [Cites] Science. 1988 Oct 14;242(4876):263-6 [3175651.001]
  • [Cites] Oncogene. 1989 Jun;4(6):725-9 [2543943.001]
  • [Cites] Oncogene. 1993 Aug;8(8):2127-33 [8336939.001]
  • (PMID = 18782450.001).
  • [ISSN] 1465-542X
  • [Journal-full-title] Breast cancer research : BCR
  • [ISO-abbreviation] Breast Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA058223; United States / NCI NIH HHS / CA / R01 CA101227
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CCND1 protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Retinoblastoma Protein; 136601-57-5 / Cyclin D1
  • [Other-IDs] NLM/ PMC2614508
  •  go-up   go-down


Advertisement
4. Watson S, Serrate C, Vignot S: [Sonic Hedgehog signaling pathway: from embryology to molecular targeted therapies]. Bull Cancer; 2010 Dec;97(12):1477-83
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Sonic Hedgehog signaling pathway: from embryology to molecular targeted therapies].
  • During the past few years its implication in carcinogenesis has become clear and today it is acknowledged that this pathway plays a role in the malignant transformation of multiple cell types, either owing to the mutation of some of its components or to its erratic activation.
  • New molecular targeted therapies that inhibit the pathway have shown their unquestionable efficiency in several tumours -among which basal cell carcinoma, medulloblastoma, or pancreatic adenocarcinoma.
  • The assessment of these inhibitors in other types of tumours is currently underway with promising results, suggesting that the Sonic hedgehog signalling pathway may become one of the therapeutic targets of the future.
  • [MeSH-major] Embryonic Development / physiology. Hedgehog Proteins / antagonists & inhibitors. Hedgehog Proteins / physiology. Molecular Targeted Therapy / methods. Neoplasms / drug therapy. Neoplasms / genetics
  • [MeSH-minor] Anilides / therapeutic use. Animals. Carcinoma, Basal Cell / drug therapy. Carcinoma, Basal Cell / genetics. Cerebellar Neoplasms / genetics. Embryonic Induction / physiology. Humans. Lung Neoplasms / genetics. Medulloblastoma / genetics. Mutation / physiology. Neoplastic Stem Cells / physiology. Pancreatic Neoplasms / genetics. Patient Selection. Pyridines / therapeutic use. Receptors, Cell Surface / physiology. Signal Transduction / drug effects. Signal Transduction / physiology. Skin Neoplasms / drug therapy. Skin Neoplasms / genetics. Small Cell Lung Carcinoma / genetics

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 21220225.001).
  • [ISSN] 1769-6917
  • [Journal-full-title] Bulletin du cancer
  • [ISO-abbreviation] Bull Cancer
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Anilides; 0 / Hedgehog Proteins; 0 / HhAntag691; 0 / Pyridines; 0 / Receptors, Cell Surface; 0 / patched receptors
  •  go-up   go-down


5. Ljuca D, Fatusić Z, Iljazović E, Ahmetović B: Monitoring of chemotherapy successfulness of platina/taxol chemotherapy protocol by using determination of serum urokinase plasminogen activator (uPA) and soluble urokinase plasminogen activator receptor (suPAR) in patients with ovarian carcinoma FIGO II and III stage. Bosn J Basic Med Sci; 2007 May;7(2):111-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Monitoring of chemotherapy successfulness of platina/taxol chemotherapy protocol by using determination of serum urokinase plasminogen activator (uPA) and soluble urokinase plasminogen activator receptor (suPAR) in patients with ovarian carcinoma FIGO II and III stage.
  • In about 70% of cases, ovarian carcinoma has been diagnosed at an advanced stage.
  • Invasion and metastasis of solid tumors request protease activity resulting in basal membrane destruction and surrounding matrix.
  • In that process, urokinase plasminogen activator (uPA) and its receptor, urokinase plasminogen activator receptor (suPAR) play a key role, that via plasmin activation lead to basal membrane and matrix degradation in surrounding of the tumor, enable to its invasion and metastasis.
  • Their serum concentrations in ovarian cancer patients may help in good monitoring of remission or progression during chemotherapy treatment.
  • In late 1950s and ear1y 1960s, when it was found out that malignant ovarian tumors were chemosensitive, their chemotherapy treatment has begun.
  • In the beginning it was used only mono-therapy, and by discovering new cytostatics it was replaced by poly-chemotherapy.
  • Now days, in the therapy of advanced stages of ovarian carcinoma combination of cisplatine or carboplatine with paclitaxel is considering as standard treatment.
  • Aim of this study was to determine serum uPA, suPAR and CEA in FIGO II and III patients with different histological type (serous, mucinous, clear cell tumor) before and after PT chemotherapy protocol during following three cycles.
  • In this prospective study we have analyzed 17 patients with ovarian carcinoma, those have been after surgery treated by chemotherapy.
  • Results of this study have shown that uPA, suPAR and CEA met criteria for prognostic markers for monitoring of successfulness of platina/taxol chemotherapy protocol for serous, mucinous and clear cell tumor FIGO II and III stage of ovarian carcinoma.
  • In case of PT chemotherapy protocol suPAR was better prognostic marker for monitoring of chemotherapy successfulness (Pearson coefficient 0,9 do 1,0; p<0,00l) than uPA (Pearson coefficient between 0,86 and 0,92; p<0,02) and CEA (Pearson coefficient 0,5 do 0,89; p<0,04).

  • MedlinePlus Health Information. consumer health - Ovarian Cancer.
  • Hazardous Substances Data Bank. CIS-DIAMINEDICHLOROPLATINUM .
  • Hazardous Substances Data Bank. TAXOL .
  • Hazardous Substances Data Bank. CARBOPLATIN .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17489744.001).
  • [ISSN] 1512-8601
  • [Journal-full-title] Bosnian journal of basic medical sciences
  • [ISO-abbreviation] Bosn J Basic Med Sci
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] Bosnia and Herzegovina
  • [Chemical-registry-number] 0 / PLAUR protein, human; 0 / Receptors, Cell Surface; 0 / Receptors, Urokinase Plasminogen Activator; BG3F62OND5 / Carboplatin; EC 3.4.21.73 / Urokinase-Type Plasminogen Activator; P88XT4IS4D / Paclitaxel; Q20Q21Q62J / Cisplatin
  •  go-up   go-down


6. Prignano F, Lotti T, Spallanzani A, Berti S, de Giorgi V, Moretti S: Sequential effects of photodynamic treatment of basal cell carcinoma. J Cutan Pathol; 2009 Apr;36(4):409-16
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Sequential effects of photodynamic treatment of basal cell carcinoma.
  • BACKGROUND: Photodynamic therapy (PDT) of superficial basal cell carcinoma (SBCC) acts as a biological response modifier or killing target cells, but sequential biological effects have not been reported in depth in humans.
  • At baseline, SBCC cells expressed stem cell factor in all cases, and granulocyte-monocyte colony-stimulating factor, basic fibroblastic growth factor, interleukin (IL)-8 and vascular endothelial growth factor in most cases.
  • CONCLUSIONS: We show a clear time-dependent profile of apoptotic markers and inflammatory infiltrate composition in SBCC after ALA-PDT.
  • [MeSH-major] Aminolevulinic Acid / therapeutic use. Carcinoma, Basal Cell / drug therapy. Photosensitizing Agents / therapeutic use. Skin Neoplasms / drug therapy
  • [MeSH-minor] Apoptosis / drug effects. Cytokines / drug effects. Humans. Immunohistochemistry. In Situ Nick-End Labeling. Inflammation / chemically induced. Inflammation / immunology. Inflammation / pathology. Microscopy, Electron, Transmission. Photochemotherapy

  • MedlinePlus Health Information. consumer health - Skin 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 = 19278425.001).
  • [ISSN] 1600-0560
  • [Journal-full-title] Journal of cutaneous pathology
  • [ISO-abbreviation] J. Cutan. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Cytokines; 0 / Photosensitizing Agents; 88755TAZ87 / Aminolevulinic Acid
  •  go-up   go-down


7. Jadotte YT, Sarkissian NA, Kadire H, Lambert WC: CASE REPORT Superficial Spreading Basal Cell Carcinoma of the Face: A Surgical Challenge. Eplasty; 2010;10:e46
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] CASE REPORT Superficial Spreading Basal Cell Carcinoma of the Face: A Surgical Challenge.
  • OBJECTIVE: We present the case of a white man with a facial nodule suspicious for basal cell carcinoma.
  • METHODS: Biopsy revealed clusters of basaloid tumor cells with peripheral palisading, consistent with a superficial spreading variant of basal cell carcinoma.
  • RESULTS: The patient was treated with Mohs micrographic surgery, with clear margins achieved after the second stage of excision.
  • However, since it was a superficial spreading basal cell carcinoma, this was followed by topical imiquimod treatment.
  • CONCLUSION: Topical chemotherapy with imiquimod or 5-fluorouracil may be valuable alternatives or adjuncts, given the increased likelihood of recurrence after surgical excision of superficial spreading basal cell carcinoma.
  • Mohs surgery is of limited value in the management of superficial spreading basal cell carcinoma because it characteristically shows areas of uninvolved skin between tumor nests.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Br J Dermatol. 2003 Feb;148(2):195-202 [12588368.001]
  • [Cites] J Invest Dermatol. 2003 Jun;120(6):1087-93 [12787139.001]
  • [Cites] Br J Dermatol. 2004 Jul;151(1):141-7 [15270883.001]
  • [Cites] J Am Acad Dermatol. 2005 Mar;52(3 Pt 1):468-73 [15761425.001]
  • [Cites] J Am Acad Dermatol. 2005 Sep;53(3):445-51 [16112351.001]
  • [Cites] Dermatol Surg. 2009 Sep;35(9):1349-54 [19500127.001]
  • [Cites] Br J Nurs. 2009 Jan 8-21;18(1):8-16 [19127226.001]
  • [Cites] J Chin Med Assoc. 2006 Aug;69(8):364-71 [16970272.001]
  • [Cites] Cochrane Database Syst Rev. 2007;(1):CD003412 [17253489.001]
  • [Cites] Drugs. 2007;67(6):915-34 [17428108.001]
  • [Cites] Acta Clin Croat. 2008 Mar;47(1):25-30 [18714644.001]
  • [Cites] Int J Dermatol. 2008 Oct;47(10):1015-8 [18986346.001]
  • [Cites] Br J Dermatol. 2006 Aug;155(2):401-7 [16882181.001]
  • (PMID = 20596236.001).
  • [ISSN] 1937-5719
  • [Journal-full-title] Eplasty
  • [ISO-abbreviation] Eplasty
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2890390
  •  go-up   go-down


8. Palayoor ST, Burgos MA, Shoaibi A, Tofilon PJ, Coleman CN: Effect of radiation and ibuprofen on normoxic renal carcinoma cells overexpressing hypoxia-inducible factors by loss of von Hippel-Lindau tumor suppressor gene function. Clin Cancer Res; 2004 Jun 15;10(12 Pt 1):4158-64
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of radiation and ibuprofen on normoxic renal carcinoma cells overexpressing hypoxia-inducible factors by loss of von Hippel-Lindau tumor suppressor gene function.
  • PURPOSE: Tumor hypoxia is a major limiting factor for radiation therapy.
  • Hypoxia-inducible factors (HIFs) are overexpressed in several human cancers and are considered prognostic markers and potential targets for cancer therapy.
  • EXPERIMENTAL DESIGN: Renal clear cell carcinoma (RCC) cell lines overexpressing HIFs under normoxic conditions because of inactivation of von Hippel-Lindau tumor suppressor gene function (VHL-ve) and their matched pairs in which overexpression of HIFs was abolished by expression of functional VHL (VHL+ve) were irradiated.
  • The effect of ibuprofen on radiosensitization and HIF and VHL proteins was compared in RCC matched-pair cell lines.
  • RESULTS: The data showed only small differences in the radiosensitivity between the cells overexpressing HIFs and cells with basal HIF levels.
  • Ibuprofen inhibited HIFs in VHL+ve cells expressing basal levels of HIFs.
  • [MeSH-major] Carcinoma / drug therapy. Carcinoma / radiotherapy. Ibuprofen / pharmacology. Kidney Neoplasms / drug therapy. Kidney Neoplasms / radiotherapy. Trans-Activators / physiology. Transcription Factors / physiology. Tumor Suppressor Proteins / physiology. Ubiquitin-Protein Ligases / physiology
  • [MeSH-minor] Anti-Inflammatory Agents, Non-Steroidal / pharmacology. Basic Helix-Loop-Helix Transcription Factors. Blotting, Western. Cell Line. Cell Survival. Dose-Response Relationship, Drug. Dose-Response Relationship, Radiation. Enzyme-Linked Immunosorbent Assay. Humans. Hypoxia-Inducible Factor 1, alpha Subunit. Immunoblotting. Mutation. Oxygen / metabolism. Prognosis. Radiation Tolerance. Time Factors. Transfection. Up-Regulation. Vascular Endothelial Growth Factor A / metabolism. Von Hippel-Lindau Tumor Suppressor Protein

  • MedlinePlus Health Information. consumer health - Kidney Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. IBUPROFEN .
  • Hazardous Substances Data Bank. OXYGEN .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15217953.001).
  • [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] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Trans-Activators; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 0 / Vascular Endothelial Growth Factor A; 0 / endothelial PAS domain-containing protein 1; EC 6.3.2.19 / Ubiquitin-Protein Ligases; EC 6.3.2.19 / VHL protein, human; EC 6.3.2.19 / Von Hippel-Lindau Tumor Suppressor Protein; S88TT14065 / Oxygen; WK2XYI10QM / Ibuprofen
  •  go-up   go-down


9. Fayter D, Corbett M, Heirs M, Fox D, Eastwood A: A systematic review of photodynamic therapy in the treatment of pre-cancerous skin conditions, Barrett's oesophagus and cancers of the biliary tract, brain, head and neck, lung, oesophagus and skin. Health Technol Assess; 2010 Jul;14(37):1-288
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A systematic review of photodynamic therapy in the treatment of pre-cancerous skin conditions, Barrett's oesophagus and cancers of the biliary tract, brain, head and neck, lung, oesophagus and skin.
  • BACKGROUND: Photodynamic therapy (PDT) is the use of a light-sensitive drug, in combination with light of a visible wavelength, to destroy target cells.
  • PDT is used either as a primary treatment or as an adjunctive treatment.
  • It is fairly well accepted in clinical practice for some types of skin cancer but has yet to be fully explored as a treatment for other forms of cancer.
  • OBJECTIVE: To systematically review the clinical effectiveness and safety of PDT in the treatment of Barrett's oesophagus, pre-cancerous skin conditions and the following cancers: biliary tract, brain, head and neck, lung, oesophageal and skin.
  • STUDY DESIGNS: Randomised controlled trials (RCTs) in skin conditions and Barrett's oesophagus, non-randomised trials for all other sites.
  • PARTICIPANTS: People with Barrett's oesophagus, pre-cancerous skin conditions or primary cancer in the following sites: biliary tract, brain, head and neck, lung, oesophageal and skin.
  • INTERVENTION: Any type of PDT for either curative or palliative treatment.
  • COMPARATORS: Any comparator including differing applications of PDT treatments (relevant comparators varied according to the condition).
  • For actinic keratosis (AK), the only clear evidence of effectiveness was that PDT appeared to be superior to placebo.
  • For basal cell carcinoma (BCC), PDT may result in similar lesion response rates to surgery or cryotherapy but with better cosmetic outcomes.
  • CONCLUSIONS: Evidence of effectiveness was found for PDT in the treatment of AK and nodular BCC in relation to placebo, and possibly for treating Barrett's oesophagus.
  • However, the effectiveness of PDT in relation to other treatments is not yet apparent.
  • [MeSH-major] Neoplasms / drug therapy. Photochemotherapy / methods. Precancerous Conditions / drug therapy
  • [MeSH-minor] Barrett Esophagus / drug therapy. Barrett Esophagus / mortality. Biliary Tract Neoplasms / drug therapy. Biliary Tract Neoplasms / mortality. Brain Neoplasms / drug therapy. Brain Neoplasms / mortality. Clinical Trials as Topic. Esophageal Neoplasms / drug therapy. Esophageal Neoplasms / mortality. Head and Neck Neoplasms / drug therapy. Head and Neck Neoplasms / mortality. Humans. Lung Neoplasms / drug therapy. Lung Neoplasms / mortality. Quality of Life. Skin Neoplasms / drug therapy. Skin Neoplasms / mortality

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • PubMed Health. PubMed Health .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20663420.001).
  • [ISSN] 2046-4924
  • [Journal-full-title] Health technology assessment (Winchester, England)
  • [ISO-abbreviation] Health Technol Assess
  • [Language] eng
  • [Publication-type] Journal Article; Meta-Analysis; Review
  • [Publication-country] England
  •  go-up   go-down


10. Gao Y, Lin LP, Zhu CH, Chen Y, Hou YT, Ding J: Growth arrest induced by C75, A fatty acid synthase inhibitor, was partially modulated by p38 MAPK but not by p53 in human hepatocellular carcinoma. Cancer Biol Ther; 2006 Aug;5(8):978-85
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Growth arrest induced by C75, A fatty acid synthase inhibitor, was partially modulated by p38 MAPK but not by p53 in human hepatocellular carcinoma.
  • In this study, we reveal that C75 is a cell cycle arrest inducer and explore the potential mechanisms for this effect in hepatocellular carcinoma (HCC) cell lines with abundant FAS expression: HepG2 and SMMC7721 cells with wt-p53, and Hep3B cells with null p53.
  • The results showed FAS protein expression and basal activity levels were higher in HepG2 cells than in the other two HCC cell lines.
  • Treatment with C75 inhibited FAS activity within 30 min of administration and induced G(2) phase arrest accompanied by p53 overexpression in HepG2 and SMMC7721 cells.
  • However, we observed a clear correlation between p38 MAPK activation triggered by C75 and the induction of cell cycle arrest in all three HCC cells.
  • Furthermore, treatment with the p38 MAPK inhibitor SB203580 reduced p38 MAPK activity and cell cycle arrest, and also partially restored cyclin A, cyclin B1, cyclin D1 and p21 protein levels.
  • Collectively, it was p38 MAPK but not p53 involved in C75-mediated tumor cell growth arrest in HCC cells.
  • [MeSH-major] 4-Butyrolactone / analogs & derivatives. Carcinoma, Hepatocellular / metabolism. Fatty Acid Synthases / antagonists & inhibitors. G2 Phase / drug effects. Liver Neoplasms / metabolism. Tumor Suppressor Protein p53 / metabolism. p38 Mitogen-Activated Protein Kinases / metabolism
  • [MeSH-minor] Antigens, CD95 / metabolism. Blotting, Western. Cell Proliferation. Cyclin A / metabolism. Cyclin B / metabolism. Cyclin B1. Cyclin D1 / metabolism. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. Flow Cytometry. Humans. Immunoprecipitation. Plasmids / genetics. RNA, Small Interfering / pharmacology. Tumor Cells, Cultured

  • MedlinePlus Health Information. consumer health - Liver Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. BUTYROLACTONE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • 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
  • [CommentIn] Cancer Biol Ther. 2006 Aug;5(8):986-7 [16998303.001]
  • (PMID = 16855382.001).
  • [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 / 4-methylene-2-octyl-5-oxofuran-3-carboxylic acid; 0 / Antigens, CD95; 0 / CCNB1 protein, human; 0 / Cyclin A; 0 / Cyclin B; 0 / Cyclin B1; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / RNA, Small Interfering; 0 / Tumor Suppressor Protein p53; 136601-57-5 / Cyclin D1; EC 2.3.1.85 / Fatty Acid Synthases; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; OL659KIY4X / 4-Butyrolactone
  •  go-up   go-down


11. Shore RE: Radiation-induced skin cancer in humans. Med Pediatr Oncol; 2001 May;36(5):549-54
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Radiation-induced skin cancer in humans.
  • The principal epidemiologic studies of ionizing radiation and skin cancer have all shown that radiation causes basal cell carcinoma but have not found dose-related excesses of squamous cell carcinoma or malignant melanoma.
  • The Japanese atomic bomb study indicates that doses of radiation under about 1 Gy confer less risk per unit dose than higher doses do.
  • All available studies show that skin cancer risk is greater from radiation exposure at young ages than at older ages.
  • Finding few excess skin cancers among irradiated African-Americans as compared to Caucasians with a comparable dose indicates that skin susceptibility to ultraviolet exposure modifies the excess risk from ionizing radiation.
  • Available evidence indicates that the excess risk of skin cancer lasts for 45 years or more following irradiation.
  • Several studies indicate a risk of nonmelanoma skin cancer (NMSC) following cancer therapy; however, most of the studies reporting on NMSC have not distinguished between patients who received radiotherapy versus chemotherapy.
  • It is not clear from the studies how much, if any, of the excess melanoma risk is attributable to radiotherapy.
  • [MeSH-major] Neoplasms, Radiation-Induced / epidemiology. Skin Neoplasms / epidemiology
  • [MeSH-minor] Carcinoma, Basal Cell / epidemiology. Carcinoma, Squamous Cell / epidemiology. Humans. Melanoma / epidemiology. Risk Factors

  • Genetic Alliance. consumer health - Radiation induced cancer.
  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • COS Scholar Universe. author profiles.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2001 Wiley-Liss, Inc.
  • (PMID = 11340610.001).
  • [ISSN] 0098-1532
  • [Journal-full-title] Medical and pediatric oncology
  • [ISO-abbreviation] Med. Pediatr. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA43175; United States / NIEHS NIH HHS / ES / ES-00260; United States / NCI NIH HHS / CA / P30CA16087
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] United States
  • [Number-of-references] 48
  •  go-up   go-down






Advertisement