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1. Arcaro A, Doepfner KT, Boller D, Guerreiro AS, Shalaby T, Jackson SP, Schoenwaelder SM, Delattre O, Grotzer MA, Fischer B: Novel role for insulin as an autocrine growth factor for malignant brain tumour cells. Biochem J; 2007 Aug 15;406(1):57-66
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  • [Title] Novel role for insulin as an autocrine growth factor for malignant brain tumour cells.
  • AT/RTs (atypical teratoid/rhabdoid tumours) of the CNS (central nervous system) are childhood malignancies associated with poor survival rates due to resistance to conventional treatments such as chemotherapy.
  • We characterized a panel of human AT/RT and MRT (malignant rhabdoid tumour) cell lines for expression of RTKs (receptor tyrosine kinases) and their involvement in tumour growth and survival.
  • When compared with normal brain tissue, AT/RT cell lines overexpressed the IR (insulin receptor) and the IGFIR (insulin-like growth factor-I receptor).
  • Pharmacological inhibitors, neutralizing antibodies, or RNAi (RNA interference) targeting the IR impaired the growth of AT/RT cell lines and induced apoptosis.
  • Inhibitors of the PI3K (phosphoinositide 3-kinase)/Akt pathway also impaired basal and insulin-stimulated AT/RT cell proliferation.
  • Experiments using RNAi and isoform-specific pharmacological inhibitors established a key role for the class I(A) PI3K p110alpha isoform in AT/RT cell growth and insulin signalling.
  • Taken together, our results reveal a novel role for autocrine signalling by insulin and the IR in growth and survival of malignant human CNS tumour cells via the PI3K/Akt pathway.
  • [MeSH-minor] Cell Line, Tumor. Cell Proliferation / drug effects. Child, Preschool. Chromosomal Proteins, Non-Histone / metabolism. Culture Media, Serum-Free. DNA-Binding Proteins / metabolism. Down-Regulation / drug effects. Down-Regulation / genetics. Enzyme Activation / drug effects. Female. Humans. Infant. Isoenzymes / metabolism. Male. Phosphatidylinositol 3-Kinases / metabolism. Proto-Oncogene Proteins c-akt / metabolism. RNA, Small Interfering / metabolism. Receptor, IGF Type 1 / metabolism. Receptor, Insulin / genetics. Receptor, Insulin / metabolism. Signal Transduction / drug effects. Transcription Factors / metabolism

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  • [Cites] Mol Cell Biol. 2006 Apr;26(7):2661-74 [16537910.001]
  • [Cites] Cancer Res. 2005 Nov 15;65(22):10123-7 [16287993.001]
  • [Cites] Cell. 2006 May 19;125(4):733-47 [16647110.001]
  • [Cites] Biosci Rep. 2006 Feb;26(1):7-17 [16779663.001]
  • [Cites] J Clin Invest. 2006 Jul;116(7):1761-6 [16823473.001]
  • [Cites] Drug News Perspect. 2006 Jun;19(5):261-72 [16941048.001]
  • [Cites] Science. 2006 Oct 13;314(5797):268-74 [16959974.001]
  • [Cites] Int J Cancer. 2006 Dec 1;119(11):2527-38 [16988940.001]
  • [Cites] Oncogene. 2007 Apr 5;26(16):2308-17 [17016438.001]
  • [Cites] Eur J Cancer. 2007 Jul;43(10):1581-9 [17446062.001]
  • [Cites] Annu Rev Cell Dev Biol. 2001;17:615-75 [11687500.001]
  • [Cites] Annu Rev Biochem. 2001;70:247-79 [11395408.001]
  • [Cites] Annu Rev Biochem. 2001;70:535-602 [11395417.001]
  • [Cites] Nature. 2002 Jan 24;415(6870):436-42 [11807556.001]
  • [Cites] Mol Cell Biol. 2002 Aug;22(16):5975-88 [12138206.001]
  • [Cites] Clin Cancer Res. 2002 Nov;8(11):3461-7 [12429635.001]
  • [Cites] J Immunol. 2003 Mar 1;170(5):2647-54 [12594293.001]
  • [Cites] Oncogene. 2003 Sep 29;22(42):6589-97 [14528284.001]
  • [Cites] Horm Metab Res. 2003 Nov-Dec;35(11-12):778-85 [14710358.001]
  • [Cites] Nat Rev Cancer. 2004 Feb;4(2):133-42 [14964309.001]
  • [Cites] Nature. 2004 Mar 25;428(6981):427-31 [15042091.001]
  • [Cites] Cancer Cell. 2004 Mar;5(3):231-9 [15050915.001]
  • [Cites] Am J Surg Pathol. 2004 May;28(5):644-50 [15105654.001]
  • [Cites] Science. 2004 Apr 23;304(5670):554 [15016963.001]
  • [Cites] Nat Rev Cancer. 2004 Jul;4(7):505-18 [15229476.001]
  • [Cites] J Clin Oncol. 2004 Jul 15;22(14):2877-84 [15254056.001]
  • [Cites] Cancer Res. 2004 Aug 1;64(15):5048-50 [15289301.001]
  • [Cites] Clin Cancer Res. 2004 Sep 1;10(17):5940-8 [15355927.001]
  • [Cites] Biochem J. 1990 Sep 1;270(2):397-400 [2205203.001]
  • [Cites] J Biol Chem. 1992 Jul 5;267(19):13488-97 [1618850.001]
  • [Cites] Annu Rev Biochem. 1992;61:307-30 [1323236.001]
  • [Cites] EMBO J. 1993 Nov;12(11):4251-9 [7901001.001]
  • [Cites] Endocrinology. 1995 Apr;136(4):1459-67 [7534700.001]
  • [Cites] Endocr Rev. 1995 Feb;16(1):3-34 [7758431.001]
  • [Cites] Genes Dev. 1996 Sep 1;10(17):2117-30 [8804307.001]
  • [Cites] EMBO J. 1996 Oct 1;15(19):5370-82 [8895581.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Apr 15;94(8):3777-82 [9108054.001]
  • [Cites] Trends Biochem Sci. 1997 Jul;22(7):267-72 [9255069.001]
  • [Cites] Nature. 1998 Jul 9;394(6689):203-6 [9671307.001]
  • [Cites] Cancer Res. 1999 Jan 1;59(1):74-9 [9892189.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Apr 13;96(8):4240-5 [10200246.001]
  • [Cites] Hum Mol Genet. 1999 Dec;8(13):2359-68 [10556283.001]
  • [Cites] Clin Cancer Res. 2000 Jul;6(7):2759-63 [10914721.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Dec 5;97(25):13796-800 [11095756.001]
  • [Cites] Pediatr Dev Pathol. 2001 Jan-Feb;4(1):23-31 [11200487.001]
  • [Cites] Mol Cell Biol. 2001 May;21(10):3598-603 [11313485.001]
  • [Cites] J Neurooncol. 2005 Dec;75(3):309-13 [16195799.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Dec 6;102(49):17745-50 [16301525.001]
  • [Cites] Oncogene. 2006 Feb 2;25(5):722-34 [16302003.001]
  • [Cites] Oncogene. 2006 Feb 16;25(7):1111-7 [16186793.001]
  • [Cites] Br J Cancer. 2006 Feb 27;94(4):465-8 [16450000.001]
  • [Cites] Mol Cell Biol. 1999 May;19(5):3278-88 [10207053.001]
  • [Cites] Oncogene. 1999 Apr 15;18(15):2471-9 [10229198.001]
  • [Cites] Mod Pathol. 1999 Apr;12(4):379-85 [10229502.001]
  • [Cites] Endocrinology. 2005 Feb;146(2):552-7 [15550513.001]
  • [Cites] J Pathol. 2005 Jan;205(2):145-53 [15641016.001]
  • [Cites] J Clin Oncol. 2005 Mar 1;23(7):1491-9 [15735125.001]
  • [Cites] Nat Med. 2005 May;11(5):507-14 [15834429.001]
  • [Cites] Cytokine Growth Factor Rev. 2005 Aug-Oct;16(4-5):421-39 [15936977.001]
  • [Cites] Blood. 2005 Aug 15;106(4):1432-40 [15878979.001]
  • [Cites] Nature. 2006 May 18;441(7091):366-70 [16625210.001]
  • (PMID = 17506723.001).
  • [ISSN] 1470-8728
  • [Journal-full-title] The Biochemical journal
  • [ISO-abbreviation] Biochem. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Chromosomal Proteins, Non-Histone; 0 / Culture Media, Serum-Free; 0 / DNA-Binding Proteins; 0 / Growth Substances; 0 / Insulin; 0 / Isoenzymes; 0 / RNA, Small Interfering; 0 / SMARCB1 protein, human; 0 / Transcription Factors; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / Receptor, IGF Type 1; EC 2.7.10.1 / Receptor, Insulin; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
  • [Other-IDs] NLM/ PMC1948991
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2. Engi H, Gyémánt N, Ohkoshi M, Amaral L, Molnár J: Modelling of tumour--host coexistence In vitro in the presence of serine protease inhibitors. In Vivo; 2009 Sep-Oct;23(5):711-5
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  • [Title] Modelling of tumour--host coexistence In vitro in the presence of serine protease inhibitors.
  • The activities of cell surface serine proteases are markedly enhanced in malignant tumours.
  • Proteolytic degradation of the extracellular matrix and basal membrane of normal cells is an important event for tumour cell growth and invasion.
  • Flow cytometry and differential staining demonstrated that in the mixed culture, the rate of tumor growth was dependent upon the presence of the feeder MRC5 lung fibroblasts and could be obviated by the additional presence of the inhibitors of serine proteases.
  • [MeSH-major] Allylglycine / analogs & derivatives. Antineoplastic Agents / pharmacology. Benzamidines / pharmacology. Breast Neoplasms / drug therapy. Gabexate / analogs & derivatives. Serine Endopeptidases / metabolism. Serine Proteinase Inhibitors / pharmacology
  • [MeSH-minor] Cell Line, Tumor. Cell Membrane / drug effects. Cell Membrane / enzymology. Cell Proliferation / drug effects. Cell Survival / drug effects. Coculture Techniques. Drug Screening Assays, Antitumor. Female. Fibroblasts / drug effects. Fibroblasts / enzymology. Fibroblasts / pathology. Flow Cytometry. Humans

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  • (PMID = 19779105.001).
  • [ISSN] 0258-851X
  • [Journal-full-title] In vivo (Athens, Greece)
  • [ISO-abbreviation] In Vivo
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamidines; 0 / Serine Proteinase Inhibitors; 0 / ethyl N-allyl-N-(2-methyl-3-(4-(4-amidinophenoxycarbonyl)phenyl)propenoyl)aminoacetate methanesulfonate; 0FD207WKDU / camostat; 1069-48-3 / Allylglycine; 4V7M9137X9 / Gabexate; EC 3.4.21.- / Serine Endopeptidases
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3. Kuljaca S, Liu T, Tee AE, Haber M, Norris MD, Dwarte T, Marshall GM: Enhancing the anti-angiogenic action of histone deacetylase inhibitors. Mol Cancer; 2007;6:68
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  • BACKGROUND: Histone deacetylase inhibitors (HDACIs) have many effects on cancer cells, such as growth inhibition, induction of cell death, differentiation, and anti-angiogenesis, all with a wide therapeutic index.
  • RESULTS: Trichostatin A (TSA) and alpha-interferon (IFNalpha) were the most effective combination across a range of different cancer cell lines, while normal non-malignant cells did not respond in the same manner to the combination therapy.
  • There was a close correlation between absence of basal p21WAF1 expression and response to TSA and IFNalpha treatment.
  • Moreover, inhibition of p21WAF1 expression in a p21WAF1-expressing breast cancer cell line by a specific siRNA increased the cytotoxic effects of TSA and IFNalpha.
  • In vitro assays of endothelial cell function showed that TSA and IFNalpha decreased endothelial cell migration, invasion, and capillary tubule formation, without affecting endothelial cell viability.
  • Combination TSA and IFNalpha therapy markedly reduced tumour angiogenesis in neuroblastoma-bearing transgenic mice.
  • CONCLUSION: Our results indicate that combination TSA and IFNalpha therapy has potent co-operative cytotoxic and anti-angiogenic activity.
  • High basal p21WAF1 expression appears to be acting as a resistance factor to the combination therapy.
  • [MeSH-minor] Animals. Anoxia. Cell Movement. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. Drug Synergism. Humans. Hydroxamic Acids / pharmacology. Interferon-alpha / metabolism. Mice. Models, Biological. Neoplasm Invasiveness. Neoplasm Transplantation

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  • [Cites] Int J Oncol. 2004 Dec;25(6):1795-9 [15547719.001]
  • [Cites] Science. 1980 May 2;208(4443):516-8 [6154315.001]
  • [Cites] Cancer Res. 2004 Sep 15;64(18):6626-34 [15374977.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Aug 24;101(34):12664-9 [15314226.001]
  • [Cites] Nat Rev Cancer. 2004 May;4(5):335-48 [15122205.001]
  • [Cites] Clin Cancer Res. 2004 Mar 1;10(5):1813-25 [15014036.001]
  • [Cites] Nature. 2004 Feb 26;427(6977):787 [14985739.001]
  • [Cites] Mol Pharmacol. 2004 Mar;65(3):571-81 [14978235.001]
  • [Cites] Biochem Pharmacol. 2003 Sep 15;66(6):897-906 [12963476.001]
  • [Cites] Nat Rev Cancer. 2003 Jun;3(6):401-10 [12778130.001]
  • [Cites] J Biol Chem. 2003 May 23;278(21):18980-9 [12649266.001]
  • [Cites] J Natl Cancer Inst. 2003 Mar 19;95(6):437-48 [12644537.001]
  • [Cites] J Natl Cancer Inst. 2003 Mar 19;95(6):420-1 [12644529.001]
  • [Cites] Exp Cell Res. 2003 Jan 15;282(2):78-89 [12531694.001]
  • [Cites] Nat Rev Drug Discov. 2002 Apr;1(4):287-99 [12120280.001]
  • [Cites] Nat Rev Cancer. 2001 Dec;1(3):194-202 [11902574.001]
  • [Cites] Int J Cancer. 2002 Jan 20;97(3):290-6 [11774279.001]
  • [Cites] Int J Oncol. 2002 Jan;20(1):97-106 [11743648.001]
  • [Cites] Mol Pharmacol. 2001 Oct;60(4):828-37 [11562446.001]
  • [Cites] Clin Cancer Res. 2001 Sep;7(9):2840-53 [11555602.001]
  • [Cites] Neoplasia. 2001 Mar-Apr;3(2):154-64 [11420751.001]
  • [Cites] Nat Med. 2001 Apr;7(4):437-43 [11283670.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Aug 29;97(18):10014-9 [10954755.001]
  • [Cites] Mol Biol Cell. 2000 Jun;11(6):2069-83 [10848630.001]
  • [Cites] Clin Cancer Res. 2006 Jan 15;12(2):634-42 [16428510.001]
  • [Cites] Nat Clin Pract Oncol. 2005 Mar;2(3):150-7 [16264908.001]
  • [Cites] Br J Cancer. 2005 Aug 8;93(3):310-8 [16012519.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Jan 18;102(3):673-8 [15637150.001]
  • [Cites] Cancer Treat Rev. 2006 May;32(3):157-65 [16516391.001]
  • (PMID = 17958916.001).
  • [ISSN] 1476-4598
  • [Journal-full-title] Molecular cancer
  • [ISO-abbreviation] Mol. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / CDKN1A protein, human; 0 / Cdkn1a protein, mouse; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Enzyme Inhibitors; 0 / Histone Deacetylase Inhibitors; 0 / Hydroxamic Acids; 0 / Interferon-alpha; 3X2S926L3Z / trichostatin A
  • [Other-IDs] NLM/ PMC2173905
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4. Koon HK, Lo KW, Leung KN, Lung ML, Chang CC, Wong RN, Leung WN, Mak NK: Photodynamic therapy-mediated modulation of inflammatory cytokine production by Epstein-Barr virus-infected nasopharyngeal carcinoma cells. Cell Mol Immunol; 2010 Jul;7(4):323-6
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  • [Title] Photodynamic therapy-mediated modulation of inflammatory cytokine production by Epstein-Barr virus-infected nasopharyngeal carcinoma cells.
  • Nasopharyngeal carcinoma (NPC) is a malignant disease associated with Epstein-Barr virus (EBV) infection.
  • This study aims to examine the effects of EBV infection on the production of proinflammatory cytokines in NPC cells after the Zn-BC-AM photodynamic therapy (PDT) treatment.
  • Under the same experimental condition, HK-1-EBV cells produced a higher basal level of IL-1alpha (1561 pg/ml), IL-1beta (16.6 pg/ml) and IL-8 (422.9 pg/ml) than the HK-1 cells.
  • Our results suggest that Zn-BC-AM PDT might indirectly reduce tumour growth through the modulation of cytokine production.
  • [MeSH-major] Cytokines / biosynthesis. Epstein-Barr Virus Infections / immunology. Herpesvirus 4, Human / immunology. Inflammation Mediators / metabolism. Nasopharyngeal Neoplasms / drug therapy. Nasopharyngeal Neoplasms / virology. Photochemotherapy
  • [MeSH-minor] Cell Death / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Humans. Metalloporphyrins / pharmacology. Metalloporphyrins / therapeutic use. Photosensitizing Agents / pharmacology. Photosensitizing Agents / therapeutic use

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  • [Cites] Urology. 1990 Aug;36(2):167-71 [2117309.001]
  • [Cites] Proc Natl Acad Sci U S A. 1987 Sep;84(17):6262-6 [2819868.001]
  • [Cites] Cancer Res. 1993 Mar 1;53(5):1091-7 [8439953.001]
  • [Cites] Vitam Horm. 1997;53:27-63 [9197177.001]
  • [Cites] Cancer Res. 1999 Apr 1;59(7):1599-605 [10197635.001]
  • [Cites] Biochem Pharmacol. 2004 Dec 15;68(12):2387-96 [15548385.001]
  • [Cites] Neoplasia. 2006 Mar;8(3):173-80 [16611410.001]
  • [Cites] Cancer Lett. 2006 Apr 28;235(2):202-8 [15935550.001]
  • [Cites] J Virol. 2008 Apr;82(7):3679-88 [18234802.001]
  • [Cites] Lab Invest. 2000 Aug;80(8):1149-60 [10950106.001]
  • [Cites] Cancer Res. 2001 Jan 1;61(1):192-6 [11196160.001]
  • [Cites] J Pathol. 2001 Jun;194(2):145-51 [11400141.001]
  • [Cites] Clin Cancer Res. 2001 Jul;7(7):1946-51 [11448908.001]
  • [Cites] Int J Mol Med. 2002 Jul;10(1):73-6 [12060853.001]
  • [Cites] Br J Cancer. 2003 Jun 2;88(11):1772-9 [12771994.001]
  • [Cites] Cancer Res. 2003 Jul 1;63(13):3812-8 [12839978.001]
  • [Cites] Cancer Res. 2004 Sep 15;64(18):6579-87 [15374971.001]
  • [Cites] Br J Dermatol. 2004 Oct;151(4):776-83 [15491416.001]
  • [Cites] Int J Cancer. 1980 Aug;26(2):127-32 [6259064.001]
  • [Cites] J Immunol. 1981 Nov;127(5):1869-75 [6795263.001]
  • [Cites] Cancer Res. 1991 Apr 1;51(7):1823-8 [1825935.001]
  • (PMID = 20228836.001).
  • [ISSN] 2042-0226
  • [Journal-full-title] Cellular & molecular immunology
  • [ISO-abbreviation] Cell. Mol. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Cytokines; 0 / Inflammation Mediators; 0 / Metalloporphyrins; 0 / Photosensitizing Agents; 0 / Zn-BC-AM
  • [Other-IDs] NLM/ PMC4003233
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5. Uğraş S, Akpolat N, Er M, Yalçýnkaya I, Karaayvaz M: Primary composite tumour with bipartite differentiation of the esophagus. Acta Chir Belg; 2000 Feb;100(1):39-43
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  • [Title] Primary composite tumour with bipartite differentiation of the esophagus.
  • Primary small cell carcinoma of the esophagus is a rare tumour.
  • A primary composite tumour of the esophagus is even rarer and only four cases had been reported in the literature up to August 1998.
  • The definitive histogenesis of this tumour remains controversial in spite of the additional information provided by electron microscopy and immunohistochemistry.
  • In the presented case, histologically, the tumour tissue was composed of two malignant components: approximately 50% of a moderately differentiated squamous cell carcinoma, and approximately 50% of a small cell carcinoma.
  • A lot of morphological transition zones were observed between the squamous cell carcinoma components and the small cell carcinoma components in some areas in the squamous cell carcinoma component.
  • Histochemically and immunohistochemically, the small cell carcinoma cells demonstrated argyrophil granules, and Cytokeratin and Chromogranin A reactivity, but the squamous cell carcinoma cells demonstrated only Cytokeratin reactivity.
  • Negative reactivity for argentaffin granules, neuron-specific enolase and S-100 were observed in both the small cell carcinoma and the squamous cell carcinoma components.
  • Histological, histochemical and immunohistochemical findings suggest that a primary composite tumour of the esophagus may be derived from a totipotent primitive cell in the basal region of the squamous mucosa of the esophagus.
  • The patient received chemotherapy preoperatively but died one month after the initial diagnosis.
  • [MeSH-major] Carcinoma, Small Cell / pathology. Carcinoma, Squamous Cell / pathology. Esophageal Neoplasms / pathology
  • [MeSH-minor] Adult. Antineoplastic Agents / administration & dosage. Biopsy, Needle. Combined Modality Therapy. Esophagectomy. Esophagoscopy. Fatal Outcome. Humans. Immunohistochemistry. Male

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  • (PMID = 10776528.001).
  • [ISSN] 0001-5458
  • [Journal-full-title] Acta chirurgica Belgica
  • [ISO-abbreviation] Acta Chir. Belg.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] BELGIUM
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 25
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6. Micke P, Ostman A: Exploring the tumour environment: cancer-associated fibroblasts as targets in cancer therapy. Expert Opin Ther Targets; 2005 Dec;9(6):1217-33
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  • [Title] Exploring the tumour environment: cancer-associated fibroblasts as targets in cancer therapy.
  • Fibroblasts, often termed myofibroblasts or cancer-associated fibroblasts (CAFs), represent the most abundant cell type in the tumour stroma.
  • The demonstrated tumour-promoting capacities of CAFs has increased the interest to exploit them as drug targets for anticancer therapy.
  • Although single factors, such as platelet-derived growth factor, transforming growth factor-beta1, hepatocyte growth factor and matrix metalloproteinases have been identified as mediators in the fibroblast tumour interaction, the morphological and functional differences of CAFs compared with their normal counterparts are only incompletely understood.
  • Recently, novel global methods for gene expression profiling were applied to comprehensively characterise CAFs from breast, pancreas, colon and basal cell cancer in their in situ environment.
  • The analysis of different CAF preparations revealed regulated genes that were previously not described in the tumour-stroma context.
  • Additionally, besides a few striking overlaps, the comparison of the gene lists indicates a high level of heterogeneity in the expression pattern of CAFs from different tumour types.
  • Together, these studies emphasise the importance of cross-talk between stromal and malignant cells of the tumour.
  • It is likely that the continued characterisation of this interaction, and the molecular identification of key mediators, will provide insights into tumour biology and suggest novel therapeutic options.
  • [MeSH-minor] Animals. Cell Proliferation. Humans

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  • (PMID = 16300472.001).
  • [ISSN] 1744-7631
  • [Journal-full-title] Expert opinion on therapeutic targets
  • [ISO-abbreviation] Expert Opin. Ther. Targets
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 147
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7. Eros N, Karolyi Z, Kovács A, Matolcsy A, Barna T, Kelényi G: Large B-cell lymphoma of the leg in a patient with multiple malignant tumours. Acta Derm Venereol; 2003;83(5):354-7
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  • [Title] Large B-cell lymphoma of the leg in a patient with multiple malignant tumours.
  • A patient who had primary gastric B-cell non-Hodgkin's lymphoma, invasive ductal breast cancer and a basocellular carcinoma of the forehead in her medical history was studied.
  • Three years after polychemotherapy and irradiation of the breast cancer, a rapidly enlarging, ulcerated violaceous tumour developed on the patient's left leg.
  • The tumour was identified by the histopathological, immunohistochemical and immunoglobulin gene rearrangement analyses as a cutaneous large B-cell lymphoma.
  • Despite surgical excision, interferon-alpha2b treatment and chlorambucil + prednisone chemotherapy, a relapse occurred in the previously affected site, whereafter the patient received radiotherapy.
  • We discuss the clinical and histologic features and outcome of the large B-cell lymphoma of the leg, its coincidence with other diseases, and the uncommon occurrence of primary multiple malignant tumours.
  • [MeSH-major] Breast Neoplasms / complications. Carcinoma, Basal Cell / complications. Carcinoma, Ductal, Breast / complications. Lymphoma, B-Cell / complications. Skin Neoplasms / complications. Stomach Neoplasms / complications
  • [MeSH-minor] Aged. Combined Modality Therapy. Fatal Outcome. Female. Forehead. Humans. Leg Ulcer / etiology. Leg Ulcer / therapy

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  • (PMID = 14609103.001).
  • [ISSN] 0001-5555
  • [Journal-full-title] Acta dermato-venereologica
  • [ISO-abbreviation] Acta Derm. Venereol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Norway
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8. Serrels B, Serrels A, Mason SM, Baldeschi C, Ashton GH, Canel M, Mackintosh LJ, Doyle B, Green TP, Frame MC, Sansom OJ, Brunton VG: A novel Src kinase inhibitor reduces tumour formation in a skin carcinogenesis model. Carcinogenesis; 2009 Feb;30(2):249-57
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  • [Title] A novel Src kinase inhibitor reduces tumour formation in a skin carcinogenesis model.
  • The Src family tyrosine kinases are key modulators of cancer cell invasion and metastasis and a number of Src kinase inhibitors are currently in clinical development for the treatment of solid tumours.
  • We found that Src protein expression and activity was regulated during the normal hair cycle and was increased specifically during the proliferative anagen phase and also in response to the tumour promoter 12-O-tetradecanoylphorbol-13-acetate (TPA).
  • AZD0530, a selective Src inhibitor, prevented the TPA-induced proliferation of basal keratinocytes both in vivo and in vitro.
  • Moreover, treatment with AZD0530 reduced papilloma formation following the well-established 7,12-dimethylbenz(a)anthracene/TPA skin carcinogenesis protocol but did not inhibit the subsequent proliferation of the papillomas.
  • Furthermore, AZD0530 did not alter the malignant conversion of papillomas to squamous cell carcinoma suggesting a role for Src in early tumour development in the skin carcinogenesis model, rather than at later stages of tumour progression.
  • Src expression and activity were also seen in human actinic keratoses that are hyperproliferative pre-malignant skin lesions, indicating that Src may also play a role in the early stages of human skin tumour development.
  • [MeSH-major] Anticarcinogenic Agents / therapeutic use. Benzodioxoles / therapeutic use. Cell Transformation, Neoplastic / drug effects. Quinazolines / therapeutic use. Skin Neoplasms / prevention & control. src-Family Kinases / metabolism
  • [MeSH-minor] Adult. Aged. Animals. Carcinoma, Squamous Cell / metabolism. Cell Line, Tumor. Cell Proliferation / drug effects. Disease Models, Animal. Female. Humans. Keratinocytes / cytology. Keratinocytes / drug effects. Keratosis / metabolism. Male. Mice. Middle Aged. Papilloma / chemically induced. Papilloma / drug therapy. Precancerous Conditions / metabolism. Tetradecanoylphorbol Acetate

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  • (PMID = 19060248.001).
  • [ISSN] 1460-2180
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0601648; United Kingdom / Cancer Research UK / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Benzodioxoles; 0 / Quinazolines; 9KD24QGH76 / saracatinib; EC 2.7.10.2 / src-Family Kinases; NI40JAQ945 / Tetradecanoylphorbol Acetate
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9. Agnew KL, Ruchlemer R, Catovsky D, Matutes E, Bunker CB: Cutaneous findings in chronic lymphocytic leukaemia. Br J Dermatol; 2004 Jun;150(6):1129-35
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  • In 21 of these 41 complications there had been no prior immunosuppressive therapy.
  • There were 18 patients with 56 instances of basal cell carcinoma (BCC) or squamous cell carcinoma (SCC), and clinical atypia was more common with SCC than with BCC.
  • Other cutaneous findings included varicella zoster (n = 6), leukaemia cutis (n = 3), acute graft-versus-host disease (n = 5), cutaneous drug eruptions (n = 9), multiple warts (n = 3), herpes simplex (n = 3), cutaneous T-cell lymphoma (n = 2), eosinophilic folliculitis (n = 2), malignant melanoma (n = 2) and Merkel cell tumour (n = 2).
  • CONCLUSIONS: We have identified a range of dermatological conditions in CLL patients, with a tendency to atypical presentations.
  • The atypia was independent of prior chemotherapy.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Skin Diseases / pathology
  • [MeSH-minor] Acute Disease. Adult. Aged. Carcinoma, Basal Cell / complications. Carcinoma, Merkel Cell / complications. Carcinoma, Squamous Cell / complications. Chickenpox / complications. Drug Eruptions / complications. Female. Folliculitis / complications. Graft vs Host Disease. Herpes Simplex / complications. Humans. Lymphoma, T-Cell, Cutaneous / complications. Male. Melanoma / complications. Middle Aged. Retrospective Studies. Skin Neoplasms / complications. Warts / complications

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  • (PMID = 15214899.001).
  • [ISSN] 0007-0963
  • [Journal-full-title] The British journal of dermatology
  • [ISO-abbreviation] Br. J. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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10. Hassan HT: Ajoene (natural garlic compound): a new anti-leukaemia agent for AML therapy. Leuk Res; 2004 Jul;28(7):667-71
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  • [Title] Ajoene (natural garlic compound): a new anti-leukaemia agent for AML therapy.
  • Several garlic compounds including allicin and its corresponding sulfide inhibit the proliferation and induce apoptosis of several human non-leukaemia malignant cells including breast, bladder, colorectal, hepatic, prostate cancer, lymphoma and skin tumour cell lines.
  • Recently, topic application of ajoene has produced significant clinical response in patients with skin basal cell carcinoma.
  • More significantly, ajoene profoundly enhanced the apoptotic effect of the two chemotherapeutic drugs: cytarabine and fludarabine in human CD34-positive resistant myeloid leukaemia cells through enhancing their bcl-2 inhibitory and caspase-3 activation activities.
  • Studies have shown the anti-proliferation activity of ajoene to be associated with a block in the G2/M phase of cell cycle in human myeloid leukaemia cells.
  • Since acute myeloid leukaemia (AML) is a heterogeneous malignant disease in which disease progression at the level of CD34-positive cells has a major impact on resistance to chemotherapy and relapse and the inability to undergo apoptosis is a crucial mechanism of multi-drug resistance in AML patients.
  • The recent findings of the potent enhancing activity of ajoene on chemotherapy-induced apoptosis in CD34-positive resistant human myeloid leukaemia cells suggest a novel promising role for the treatment of refractory and/or relapsed AML patients as well as elderly AML patients.
  • [MeSH-major] Disulfides / therapeutic use. Garlic. Leukemia, Myeloid / drug therapy. Plant Extracts / therapeutic use
  • [MeSH-minor] Acute Disease. Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Drug Resistance, Neoplasm. Drug Synergism. Humans

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  • (PMID = 15158086.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Editorial; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Disulfides; 0 / Plant Extracts; 99A0041VG8 / ajoene
  • [Number-of-references] 66
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11. Sánchez-Muñoz A, Pérez-Ruiz E, Jiménez B, Ribelles N, Márquez A, García-Ríos I, Alba Conejo E: Targeted therapy of metastatic breast cancer. Clin Transl Oncol; 2009 Oct;11(10):643-50
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  • [Title] Targeted therapy of metastatic breast cancer.
  • Breast cancer is a heterogeneous disease characterised by a dysregulation of multiple pathways related to cell differentiation, cell cycle control, apoptosis, angiogenesis and development of metastasis.
  • Acting against these pathways provides therapeutic targets for new targeted biologic therapies, which, in the future, might constitute a key for fighting cancer.
  • New targeted biologic therapies will block essential functions of cancer cells and tumour stroma.
  • A growing number of therapy options, alone or in combination with background treatments (chemotherapy, hormone therapy, radiotherapy), will allow oncologists a better adaptation of treatment to patients and disease characteristics.
  • In addition, there are other therapy classes under evaluation, including novel antiEGFR or antiHER2 therapies; agents fighting other tyrosine kinases, including the Src and the insulinlike growth factor receptor; agents interfering critically relevant pathways, such as PI3K/AKT/mTOR inhibitors; and agents promoting apoptosis, such as PARP inhibitors (for particular breast cancer subtypes, such as basal-like, or breast cancer with BRCA mutations) and others.
  • The better selectivity against malignant cells of these therapies, when compared to conventional chemotherapy, gives, a priori, at least two advantages to biologic treatments: fewer side effects and a more individualised treatment of cancer depending on the tumour's molecular characteristics.
  • Unsolved questions remain, such as appropriate patient selection based on the expression of the therapeutic target in the tumour, the study of the efficacy of the drug in not so extensively pretreated populations and with a greater chance of response, the use of new pharmacodynamic models to help to define new response predicting factors for a specific new biologic therapy, the combined and rational use of different biologic therapies having different molecular targets and fighting the same target through a complementary mechanism of action that might improve clinical efficacy.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Breast Neoplasms / drug therapy. Enzyme Inhibitors / therapeutic use


12. Oliver P: Topical photodynamic therapy: an introduction for nurses. Br J Nurs; 2006 Aug 10-Sep 13;15(15):811-3
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  • [Title] Topical photodynamic therapy: an introduction for nurses.
  • Topical photodynamic therapy (PDT) is one of several effective treatments for pre-malignant and malignant non-pigmented skin cancers.
  • The treatment is non-invasive and can be administered by nurses in a clinical setting.
  • The treatment results in the elimination of tumour cells while leaving the healthy skin unharmed.
  • [MeSH-major] Carcinoma, Basal Cell / drug therapy. Carcinoma, Squamous Cell / drug therapy. Photochemotherapy / methods. Precancerous Conditions / drug therapy. Skin Neoplasms / drug therapy
  • [MeSH-minor] Age Distribution. Aged. Aminolevulinic Acid / analogs & derivatives. Aminolevulinic Acid / therapeutic use. Bowen's Disease / drug therapy. Decision Making, Organizational. Great Britain / epidemiology. Humans. Incidence. Keratosis / drug therapy. Leadership. Nurse's Role. Patient Selection. Population Surveillance. Registries

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  • (PMID = 16936603.001).
  • [ISSN] 0966-0461
  • [Journal-full-title] British journal of nursing (Mark Allen Publishing)
  • [ISO-abbreviation] Br J Nurs
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / methyl 5-aminolevulinate; 88755TAZ87 / Aminolevulinic Acid
  • [Number-of-references] 10
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13. Katsimbri PP, Bamias AT, Froudarakis ME, Peponis IA, Constantopoulos SH, Pavlidis NA: Endobronchial metastases secondary to solid tumors: report of eight cases and review of the literature. Lung Cancer; 2000 May;28(2):163-70

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  • Endobronchial metastases (EBM) secondaries to extrapulmonary solid malignant tumors are rare.
  • Since 1990 we have treated eight patients with EBM secondary to renal adenocarcinoma (three cases), colon adenocarcinoma (two cases), gastric adenocarcinoma (one case), bladder carcinoma (one case) and basal cell carcinoma (one case).
  • The median interval from the diagnosis of the primary tumour was 41 months.
  • Five patients were treated with external radiotherapy with symptomatic improvement while two patients had chemotherapy and one patient underwent surgical resection of the metastasis.
  • Systemic treatment was used in six cases with no significant effect on EBM.
  • Local treatment may result in symptomatic improvement but prognosis is generally poor averaging 1-2 years in most series.
  • [MeSH-minor] Adult. Aged. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Colonic Neoplasms / pathology. Diagnosis, Differential. Female. Humans. Kidney Neoplasms / pathology. Male. Middle Aged. Prognosis. Stomach Neoplasms / pathology. Survival Analysis. Urinary Bladder Neoplasms / pathology

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  • [CommentIn] Lung Cancer. 2001 Feb-Mar;31(2-3):351-2 [11305261.001]
  • (PMID = 10717334.001).
  • [ISSN] 0169-5002
  • [Journal-full-title] Lung cancer (Amsterdam, Netherlands)
  • [ISO-abbreviation] Lung Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] IRELAND
  • [Number-of-references] 26
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14. Tomassetti P, Salomone T, Migliori M, Campana D, Corinaldesi R: Optimal treatment of Zollinger-Ellison syndrome and related conditions in elderly patients. Drugs Aging; 2003;20(14):1019-34
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  • [Title] Optimal treatment of Zollinger-Ellison syndrome and related conditions in elderly patients.
  • Zollinger-Ellison syndrome is characterised by refractory peptic ulcer disease, severe diarrhoea and gastric acid hypersecretion associated with an islet-cell tumour of the pancreas (gastrinoma).
  • Zollinger-Ellison syndrome is sporadic in 62-80% of cases and in 20-38% of cases is associated with multiple endocrine neoplasia type 1 (MEN 1).
  • The diagnosis of Zollinger-Ellison syndrome is certain when the plasma gastrin is >1000 pg/mL and the basal acid output is >15 mEq/h in patients with an intact stomach, >5 mEq/h in gastrectomised patients, or when this hypergastrinemia is associated with a pH <2.
  • The treatment is based on control of gastric acid hypersecretion and of the malignant tumour and its possible metastases.
  • Proton pump inhibitors are the most effective antisecretory drugs and can be administered in the elderly at high dosages without drug-related adverse effects.
  • As an initial therapy, daily dosages of omeprazole 80-100 mg or pantoprazole 40-160 mg are employed.
  • In long-term treatment the doses can be greatly reduced once effective control of the gastric output has been established.
  • Intravenous proton pump inhibitors may be administered when patients cannot take oral therapy, particularly in acute conditions.
  • When liver metastases are also present, their debulking may improve symptoms and survival, and facilitate medical treatment.
  • Chemotherapy is not the therapy of choice in patients with gastrinomas and is indicated only in those with malignant progressive disease; interferon alpha, embolisation and chemoembolisation are not advisable for the elderly.
  • The treatment of elderly Zollinger-Ellison syndrome patients, similarly to all elderly oncological patients, should be based on the use of comprehensive geriatric assessment.
  • This will enable the clinician to define the functional status of the elderly person, to decide whether the patient can tolerate surgery and/or the stress of antineoplastic therapy, and finally, to determine whether this patient can tolerate an aggressive treatment for Zollinger-Ellison syndrome or whether the only possible choice is palliative relief of symptoms.
  • [MeSH-major] Geriatrics. Helicobacter pylori. Histamine H2 Antagonists / therapeutic use. Proton Pump Inhibitors. Zollinger-Ellison Syndrome
  • [MeSH-minor] Aged. Carcinoid Tumor / complications. Helicobacter Infections / complications. Humans. Multiple Endocrine Neoplasia Type 1 / complications

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  • [Cites] Am J Gastroenterol. 1998 Sep;93(9):1468-71 [9732927.001]
  • [Cites] Lancet. 1968 Oct 26;2(7574):895-8 [4176152.001]
  • [Cites] Ann Surg. 1964 Sep;160:512-30 [14206854.001]
  • [Cites] N Engl J Med. 1987 Nov 5;317(19):1200-9 [3309661.001]
  • [Cites] Curr Gastroenterol Rep. 2000 Dec;2(6):482-93 [11079051.001]
  • [Cites] Semin Oncol. 1987 Sep;14(3):343-53 [2820064.001]
  • [Cites] Aliment Pharmacol Ther. 2001 Nov;15(11):1795-806 [11683694.001]
  • [Cites] Gut. 1985 May;26(5):438-44 [2860052.001]
  • [Cites] Recenti Prog Med. 2000 Apr;91(4):191-210 [10804753.001]
  • [Cites] Aliment Pharmacol Ther. 1994 Feb;8(1):87-93 [8186351.001]
  • [Cites] Hum Pathol. 1975 Jan;6(1):47-76 [45919.001]
  • [Cites] Gastroenterology. 1983 Jan;84(1):108-13 [6128284.001]
  • [Cites] J Am Pharm Assoc (Wash). 2000 Jan-Feb;40(1):52-62; quiz 121-3 [10665250.001]
  • [Cites] Surg Clin North Am. 1974 Apr;54(2):395-407 [4361607.001]
  • [Cites] J Intern Med. 1995 Sep;238(3):269-80 [7673858.001]
  • [Cites] Medicine (Baltimore). 2001 May;80(3):189-222 [11388095.001]
  • [Cites] Am J Surg Pathol. 1997 Sep;21(9):1075-82 [9298884.001]
  • [Cites] Eur J Cancer. 2003 May;39(7):870-80 [12706355.001]
  • [Cites] Ann Surg. 1994 Sep;220(3):320-8; discussion 328-30 [7916560.001]
  • [Cites] Gastroenterology. 1970 May;58(5):609-15 [5444164.001]
  • [Cites] N Engl J Med. 1975 Jun 26;292(26):1377-84 [1138166.001]
  • [Cites] N Engl J Med. 1986 May 15;314(20):1287-93 [2871488.001]
  • [Cites] Aliment Pharmacol Ther. 2000 May;14(5):557-60 [10792118.001]
  • [Cites] Gastroenterology. 1991 Oct;101(4):943-7 [1889718.001]
  • [Cites] Postgrad Med. 1998 Jul;104(1):155-8, 163-4 [9676569.001]
  • [Cites] N Engl J Med. 1980 Nov 20;303(21):1189-94 [6252466.001]
  • [Cites] Medicine (Baltimore). 2000 Nov;79(6):379-411 [11144036.001]
  • [Cites] Drugs. 2001;61(15):2327-56 [11772142.001]
  • [Cites] Gastroenterology. 1993 Oct;105(4):1179-83 [8405864.001]
  • [Cites] World J Surg. 1993 Jul-Aug;17(4):489-97 [8103251.001]
  • [Cites] N Engl J Med. 1999 Aug 26;341(9):635-44 [10460814.001]
  • [Cites] J Surg Oncol. 1977;9(5):419-24 [201809.001]
  • [Cites] Surgery. 1989 Dec;106(6):1081-5; discussion 1085-6 [2573955.001]
  • [Cites] Radiology. 1983 Oct;149(1):79-83 [6611956.001]
  • [Cites] Gastroenterology. 1990 Oct;99(4):943-50 [1697548.001]
  • [Cites] Am J Med. 1984 Nov 19;77(5B):90-105 [6150641.001]
  • [Cites] Gut. 1973 May;14(5):369-73 [4197748.001]
  • [Cites] Drugs. 1991 Jul;42(1):138-70 [1718683.001]
  • [Cites] Gastroenterology. 1997 Jan;112(1):84-91 [8978346.001]
  • [Cites] Digestion. 2000;62(2-3):73-81 [11025353.001]
  • [Cites] Cancer. 2002 Jan 15;94(2):331-43 [11900219.001]
  • [Cites] Aliment Pharmacol Ther. 1996 Feb;10(1):61-71 [8871445.001]
  • [Cites] N Engl J Med. 2000 Aug 24;343 (8):551-4 [10954763.001]
  • [Cites] Int J Clin Pract. 2002 Mar;56(2):132-9 [11926700.001]
  • [Cites] Eur J Clin Invest. 1988 Aug;18(4):360-8 [3139421.001]
  • [Cites] Curr Opin Oncol. 1998 Jan;10(1):58-65 [9466486.001]
  • [Cites] Gut. 1996 Mar;38(3):430-8 [8675099.001]
  • [Cites] Henry Ford Hosp Med J. 1992;40(3-4):195-8 [1362404.001]
  • [Cites] Gastroenterology. 1977 Apr;72(4 Pt.2):788-92 [838237.001]
  • [Cites] J Clin Oncol. 1998 Mar;16(3):1040-53 [9508189.001]
  • [Cites] Eur J Clin Invest. 1993 May;23(5):296-301 [8354336.001]
  • [Cites] Am J Med. 1989 Nov;87(5):528-36 [2573280.001]
  • [Cites] Gastroenterology. 2000 Apr;118(4):696-704 [10734021.001]
  • [Cites] Gut. 1992 Sep;33(9):1275-9 [1358767.001]
  • [Cites] Microsc Res Tech. 2000 Mar 15;48(6):339-48 [10738315.001]
  • [Cites] Scand J Gastroenterol Suppl. 1989;166:95-100; discussion 111-3 [2574912.001]
  • [Cites] Cancer. 2001 Sep 1;92(5):1101-7 [11571721.001]
  • [Cites] Aliment Pharmacol Ther. 2001 Jan;15(1):87-103 [11136282.001]
  • [Cites] J Gastroenterol. 2000;35(10):735-41 [11063216.001]
  • [Cites] World J Surg. 1996 Feb;20(2):168-72 [8661813.001]
  • [Cites] Am J Med. 1998 May;104(5):422-30 [9626024.001]
  • [Cites] Gastroenterology. 1978 Feb;74(2 Pt 2):453-8 [620913.001]
  • [Cites] Gastroenterology. 1973 Jul;65(1):140-65 [4354624.001]
  • [Cites] Drugs. 2003;63(1):101-33 [12487624.001]
  • [Cites] Dig Dis Sci. 1984 Apr;29(4):363-6 [6705649.001]
  • [Cites] Am J Med. 1994 Nov;97(5):436-44 [7977432.001]
  • [Cites] Drugs. 1999 Oct;58(4):725-42 [10551440.001]
  • [Cites] Scand J Gastroenterol Suppl. 1979;53:79-91 [290036.001]
  • [Cites] Langenbecks Arch Surg. 2002 Mar;386(8):558-69 [11914931.001]
  • [Cites] Am J Gastroenterol. 2001 Dec;96(12):3274-80 [11774936.001]
  • [Cites] J Intern Med. 1998 Jun;243(6):495-500 [9681848.001]
  • [Cites] Ann Intern Med. 1973 Jul;79(1):108-18 [4352784.001]
  • [Cites] Clin Pharmacokinet. 2001;40(2):145-50 [11286324.001]
  • [Cites] J Clin Oncol. 1999 Feb;17(2):615-30 [10080607.001]
  • [Cites] Gastroenterology. 1989 Oct;97(4):827-36 [2777040.001]
  • [Cites] Digestion. 2000;62 Suppl 1:73-8 [10940691.001]
  • [Cites] Gastroenterol Clin Biol. 1994;18(8-9):695-701 [7875436.001]
  • [Cites] Radiology. 1976 Jan;118(1):63-4 [1244675.001]
  • [Cites] Pancreas. 1988;3(2):145-52 [2897687.001]
  • [Cites] World J Surg. 1993 Jul-Aug;17(4):468-80 [8362529.001]
  • [Cites] Dig Dis Sci. 1993 Feb;38(2):245-56 [8425437.001]
  • [Cites] J Clin Oncol. 1997 Jun;15(6):2420-31 [9196158.001]
  • [Cites] Gastroenterology. 1975 Feb;68(2):222-30 [1116670.001]
  • [Cites] Aliment Pharmacol Ther. 1996 Aug;10(4):507-22 [8853754.001]
  • [Cites] Am J Med. 1986 Oct 24;81(4B):49-59 [2877575.001]
  • [Cites] J Clin Invest. 1978 Feb;61(2):308-13 [621275.001]
  • [Cites] Am J Clin Pathol. 2000 Sep;114(3):419-25 [10989643.001]
  • [Cites] Cancer Treat Rep. 1987 Mar;71(3):305-7 [2434226.001]
  • [Cites] Gut. 1988 Jun;29(6):838-42 [2898423.001]
  • [Cites] Surgery. 1992 Dec;112(6):1048-56; discussion 1056-8 [1360710.001]
  • [Cites] World J Surg. 1993 Jul-Aug;17(4):455-62 [8103249.001]
  • [Cites] Gastroenterology. 1986 Nov;91(5):1179-85 [3758610.001]
  • [Cites] Digestion. 2000;62 Suppl 1:84-91 [10940693.001]
  • [Cites] Gastroenterology. 1985 Apr;88(4):1026-33 [2857672.001]
  • [Cites] Rev Rhum Ed Fr. 1994 Jun;61(6):453-5 [7833871.001]
  • [Cites] Gastroenterology. 2002 Jul;123(1):68-85 [12105835.001]
  • [Cites] Expert Opin Pharmacother. 2001 Oct;2(10):1663-70 [11825309.001]
  • [Cites] Gastroenterology. 1988 Jun;94(6):1326-34 [2966088.001]
  • [Cites] Curr Opin Oncol. 2000 Jul;12(4):368-77 [10888424.001]
  • [Cites] Drugs. 2002;62(10):1503-38 [12093317.001]
  • [Cites] Gastroenterology. 1995 Jun;108(6):1637-49 [7768367.001]
  • [Cites] Ann Intern Med. 1983 Jan;98(1):59-75 [6336642.001]
  • [Cites] Cancer. 1987 May 1;59(9):1654-60 [2435403.001]
  • [Cites] Eur J Nucl Med. 2001 Apr;28(4):426-34 [11357492.001]
  • [Cites] Aliment Pharmacol Ther. 1988 Feb;2(1):13-32 [2979229.001]
  • [Cites] Ann Intern Med. 1989 Nov 1;111(9):713-22 [2572194.001]
  • [Cites] Dig Dis Sci. 1991 Apr;36(4):394-404 [2007355.001]
  • [Cites] J Intern Med. 1998 Jun;243(6):477-88 [9681846.001]
  • [Cites] Gastroenterology. 1993 Apr;104(4):994-1006 [7681798.001]
  • [Cites] Surgery. 1986 Aug;100(2):437-44 [2426819.001]
  • [Cites] Nature. 1981 Mar 12;290(5802):159-61 [6259537.001]
  • [Cites] Aliment Pharmacol Ther. 1993 Dec;7(6):597-610 [8161665.001]
  • [Cites] Surgery. 1988 Dec;104(6):1054-63 [2904182.001]
  • [Cites] Drugs. 1996 Mar;51(3):460-82 [8882382.001]
  • [Cites] CA Cancer J Clin. 1989 Jul-Aug;39(4):231-47 [2503237.001]
  • [Cites] Crit Care Med. 2002 Jun;30(6 Suppl):S356-61 [12072661.001]
  • [Cites] Clin Nucl Med. 1986 Nov;11(11):799-800 [3791791.001]
  • [Cites] Regul Pept. 1993 Sep 22;47(3):307-18 [8234912.001]
  • [Cites] Am J Surg Pathol. 1995;19 Suppl 1:S1-7 [7762735.001]
  • [Cites] Gastroenterology. 1985 Apr;88(4):939-44 [3972233.001]
  • [Cites] Gastroenterology. 1992 Nov;103(5):1498-508 [1426868.001]
  • [Cites] Clin Endocrinol Metab. 1979 Jul;8(2):433-46 [383324.001]
  • [Cites] J Clin Gastroenterol. 2000 Jan;30(1):29-33 [10636207.001]
  • [Cites] Gut. 1988 Jan;29(1):75-80 [3343017.001]
  • [Cites] Gastroenterology. 1988 Feb;94(2):294-9 [3335308.001]
  • [Cites] N Engl J Med. 1975 Jun 19;292(25):1324-34 [236515.001]
  • (PMID = 14651442.001).
  • [ISSN] 1170-229X
  • [Journal-full-title] Drugs & aging
  • [ISO-abbreviation] Drugs Aging
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] New Zealand
  • [Chemical-registry-number] 0 / Histamine H2 Antagonists; 0 / Proton Pump Inhibitors
  • [Number-of-references] 143
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15. Venuti A, Salani D, Cirilli A, Simeone P, Muller A, Flamini S, Padley R, Bagnato A: Endothelin receptor blockade inhibits the growth of human papillomavirus-associated cervical carcinoma. Clin Sci (Lond); 2002 Aug;103 Suppl 48:310S-313S
MedlinePlus Health Information. consumer health - Cervical Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Human papillomaviruses (HPVs) are associated with cervical cancer and interact with growth factors that may enhance malignant transformation of cervical carcinoma cells.
  • Endothelin-1 (ET-1) is released from HPV-transfected keratinocytes and induces increased growth response in these cell lines in comparison with normal cells.
  • HPV-positive cancer cells secrete ET-1 and express mRNA for ET-1 and its receptors, whereas HPV-negative carcinoma cell lines express only the ET(B) receptor (ET(B)R) mRNA and do not secrete ET-1.
  • In HPV-positive cancer cells, ET(A)R mediates the ET-1-induced mitogenic effect and sustains the basal growth rate of unstimulated cervical tumour cells.
  • Therefore, ET-1 may be involved in the neoplastic growth of HPV-associated cervical carcinoma, where the increased ET-1 autocrine loop can be targeted for antitumour therapy.
  • In HPV-positive cancer cells ABT-627 strongly inhibited the proliferation induced by ET-1 and substantially reduced the basal growth rate of unstimulated cervical tumour cells, whereas the ET(B)R antagonist had no effect.
  • These results demonstrate that ET-1 participates in the progression of neoplastic growth in HPV-associated carcinoma, in which ET(A)R expression is increased and could be targeted for antitumour therapy.
  • In conclusion, an ET-1 autocrine loop is involved in tumour cell proliferation via ET(A)R, and ABT-627 is effective in controlling proliferation of cervical carcinoma cells.
  • [MeSH-major] Endothelin Receptor Antagonists. Peptides, Cyclic / therapeutic use. Pyrrolidines / therapeutic use. Uterine Cervical Neoplasms / drug therapy
  • [MeSH-minor] Cell Division / drug effects. Endothelin-1 / metabolism. Female. Humans. Papillomaviridae. Receptor, Endothelin A. Tumor Cells, Cultured

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  • (PMID = 12193111.001).
  • [ISSN] 0143-5221
  • [Journal-full-title] Clinical science (London, England : 1979)
  • [ISO-abbreviation] Clin. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Endothelin Receptor Antagonists; 0 / Endothelin-1; 0 / Peptides, Cyclic; 0 / Pyrrolidines; 0 / Receptor, Endothelin A; 136553-81-6 / cyclo(Trp-Asp-Pro-Val-Leu); V6D7VK2215 / atrasentan
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16. Phillips D: Light relief: photochemistry and medicine. Photochem Photobiol Sci; 2010 Dec;9(12):1589-96

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Photomedicine as a 'modern' subject began in the late 1880's, and currently encompasses the effects of light upon the skin, diagnostic uses of light, therapies using non-laser light, and the use of lasers.
  • Effects of light on the skin include production of Vitamin D, tanning, ageing of the skin, and the skin cancers basal cell and squamous cell carcinomas, and malignant melanoma.
  • Diagnostic uses of light include luminescence [photo and chemi] in immunoassays, fluorescence in cell sorting, and the various forms of fluorescence microscopy, including confocal, fluorescence lifetime imaging [FLIM], and single molecule.
  • Therapies include the PUVA treatment of psoriasis and vitiligo, blue light curing of neonatal jaundice, and photoinactivation of microbes.
  • Laser treatments include ablative corrective eye surgery, general 'bloodless' surgery, and, of most importance photochemically, the various treatments using sensitisers and laser light known as photodynamic therapy, PDT.
  • We concentrate here on discussion of future developments in PDT, concluding that the main advance will be through targeted PDT, in which the tissue to be destroyed receives the photosensitiser in a highly selective fashion.
  • Strategies to achieve this highlighted here are the use of monoclonal antibody fragments selected for tumour cell targets, and two-photon spatial selection.
  • [MeSH-minor] Antibodies, Monoclonal / chemistry. Humans. Lasers. Photochemotherapy. Photosensitizing Agents / chemistry. Skin Diseases / diagnosis. Skin Diseases / drug therapy. Skin Neoplasms / diagnosis. Skin Neoplasms / drug therapy

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  • (PMID = 21082123.001).
  • [ISSN] 1474-9092
  • [Journal-full-title] Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology
  • [ISO-abbreviation] Photochem. Photobiol. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Photosensitizing Agents
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17. Juarranz A, Jaén P, Sanz-Rodríguez F, Cuevas J, González S: Photodynamic therapy of cancer. Basic principles and applications. Clin Transl Oncol; 2008 Mar;10(3):148-54
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Photodynamic therapy of cancer. Basic principles and applications.
  • Photodynamic therapy (PDT) is a minimally invasive therapeutic modality approved for clinical treatment of several types of cancer and non-oncological disorders.
  • In PDT, a compound with photosensitising properties (photosensitiser, PS) is selectively accumulated in malignant tissues.
  • The subsequent activation of the PS by visible light, preferentially in the red region of the visible spectrum (lambda>or=600 nm), where tissues are more permeable to light, generates reactive oxygen species, mainly singlet oxygen ((1)O(2)), responsible for cytotoxicity of neoplastic cells and tumour regression.
  • There are three main mechanisms described by which (1)O(2) contributes to the destruction of tumours by PDT: direct cellular damage, vascular shutdown and activation of immune response against tumour cells.
  • The advantages of PDT over other conventional cancer treatments are its low systemic toxicity and its ability to selectively destroy tumours accessible to light.
  • Therefore, PDT is being used for the treatment of endoscopically accessible tumours such as lung, bladder, gastrointestinal and gynaecological neoplasms, and also in dermatology for the treatment of non-melanoma skin cancers (basal cell carcinoma) and precancerous diseases (actinic keratosis).
  • [MeSH-major] Neoplasms / drug therapy. Photochemotherapy / methods. Photosensitizing Agents / therapeutic use

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  • [Cites] Clin Exp Pharmacol Physiol. 2006 May-Jun;33(5-6):551-6 [16700893.001]
  • [Cites] Curr Med Chem Anticancer Agents. 2002 Jul;2(4):465-75 [12678731.001]
  • [Cites] Photochem Photobiol Sci. 2007 Dec;6(12):1234-45 [18046478.001]
  • [Cites] J Urol. 2004 Jan;171(1):135-8 [14665861.001]
  • [Cites] Adv Drug Deliv Rev. 2004 Jan 13;56(1):77-94 [14706446.001]
  • [Cites] Autophagy. 2006 Oct-Dec;2(4):289-90 [16921269.001]
  • [Cites] Nat Rev Cancer. 2006 Jul;6(7):535-45 [16794636.001]
  • [Cites] J Am Acad Dermatol. 2002 Aug;47(2):258-62 [12140473.001]
  • [Cites] Photochem Photobiol. 2001 Mar;73(3):283-9 [11281025.001]
  • [Cites] Nat Rev Cancer. 2003 May;3(5):380-7 [12724736.001]
  • [Cites] Biochim Biophys Acta. 2007 Sep;1776(1):86-107 [17693025.001]
  • [Cites] Photochem Photobiol. 1996 Dec;64(6):994-1000 [8972644.001]
  • [Cites] Lasers Surg Med. 2006 Jun;38(5):516-21 [16607618.001]
  • [Cites] Adv Exp Med Biol. 1985;193:213-27 [2937264.001]
  • [Cites] Curr Med Chem. 2007;14(9):997-1026 [17439399.001]
  • [Cites] Expert Opin Drug Deliv. 2005 May;2(3):477-87 [16296769.001]
  • [Cites] Br J Dermatol. 2002 Apr;146 Suppl 61:1-6 [11966724.001]
  • [Cites] Expert Opin Pharmacother. 2001 Feb;2(2):351-61 [11336591.001]
  • [Cites] Dermatol Clin. 2007 Jan;25(1):89-94 [17126746.001]
  • [Cites] Lancet. 2005 Jan 15-21;365(9455):241-52 [15652607.001]
  • [Cites] Nat Rev Cancer. 2005 Jun;5(6):423-35 [15928673.001]
  • [Cites] Br J Dermatol. 2006 Apr;154(4):740-2 [16536820.001]
  • [Cites] Cancer Res. 1997 Apr 15;57(8):1481-6 [9108449.001]
  • [Cites] Int J Biochem Cell Biol. 2006;38(12):2183-95 [16931106.001]
  • [Cites] Eur J Dermatol. 2006 Jul-Aug;16(4):340-8 [16935788.001]
  • [Cites] J Photochem Photobiol B. 1990 Jun;6(1-2):143-8 [2121931.001]
  • [Cites] Arch Dermatol Res. 2002 Jul;294(5):237-42 [12115027.001]
  • [Cites] J Natl Cancer Inst. 1998 Jun 17;90(12):889-905 [9637138.001]
  • [Cites] Mol Pharmacol. 2001 Aug;60(2):290-301 [11455016.001]
  • [Cites] J Cell Physiol. 2005 Oct;205(1):86-96 [15880654.001]
  • [Cites] J Med Chem. 2004 Jul 29;47(16):3897-915 [15267226.001]
  • [Cites] Photochem Photobiol. 1991 Apr;53(4):549-53 [1830395.001]
  • [Cites] Photochem Photobiol Sci. 2002 Nov;1(11):837-40 [12659521.001]
  • [Cites] Acta Derm Venereol. 2005;85(5):424-8 [16159735.001]
  • [Cites] Lasers Surg Med. 2006 Jun;38(5):522-31 [16671102.001]
  • [Cites] Photochem Photobiol Sci. 2002 Jan;1(1):1-21 [12659143.001]
  • (PMID = 18321817.001).
  • [ISSN] 1699-048X
  • [Journal-full-title] Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico
  • [ISO-abbreviation] Clin Transl Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Photosensitizing Agents
  • [Number-of-references] 37
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18. Lichtlen P, Schaffner W: The "metal transcription factor" MTF-1: biological facts and medical implications. Swiss Med Wkly; 2001 Dec 1;131(45-46):647-52
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Metallothioneins (MTs) are a class of small, cysteine-rich proteins that have an important function in heavy metal metabolism and detoxification and in the management of various forms of cell stress.
  • Several lines of evidence suggest a role for metallothioneins in therapy resistance of malignant tumours, regulation of blood pressure and protection against some neurological diseases.
  • Basal and heavy metal-induced expression of the stress-inducible metallothionein-I and -II genes and some other stress-regulated genes depends on the zinc-finger transcription factor MTF-1.
  • Under pathological conditions, MTF-1 seems to be involved in clinically important processes such as tumour angiogenesis and drug resistance.

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  • (PMID = 11835113.001).
  • [ISSN] 1424-7860
  • [Journal-full-title] Swiss medical weekly
  • [ISO-abbreviation] Swiss Med Wkly
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Metals, Heavy; 0 / Trans-Activators; 0 / Transcription Factors; 0 / transcription factor MTF-1; 9038-94-2 / Metallothionein
  • [Number-of-references] 54
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19. Chuan Y, Pang ST, Bergh A, Norstedt G, Pousette A: Androgens induce CD-9 in human prostate tissue. Int J Androl; 2005 Oct;28(5):291-6
MedlinePlus Health Information. consumer health - Prostate Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Androgens induce CD-9 in human prostate tissue.
  • Based on microarray analyses of LNCaP and LNCaP-r prostatic cell-lines we tentatively identified CD-9 as an androgen sensitive protein.
  • Using Western blot, RT-PCR and immunohistochemistry the expression of CD-9 was analysed in LNCaP cells stimulated during increasing time by the synthetic androgen R1881 and also in 88 specimens of human prostate cancer tissues.
  • CD-9 was immunolocalized in human prostate tissue sections representing non-malignant tissue as well as tumour areas.
  • In non-malignant glands CD-9 immunoreactivity was observed at the apical and lateral cell borders of luminal epithelial cells.
  • Basal epithelial cells were largely unstained.
  • In tumour areas CD-9 staining intensity was variable and apparently not related to primary Gleason grade.
  • In prostate tissue from a patient under androgen ablation therapy no staining was observed in luminal epithelial cells or in the tumour areas, but some staining was observed in basal epithelial cells.
  • These and earlier studies using other tissues indicate that CD-9 and its cellular localization could have an important role in prostate cancer cell development.
  • [MeSH-major] Androgens / pharmacology. Antigens, CD / biosynthesis. Membrane Glycoproteins / biosynthesis. Metribolone / pharmacology. Prostate / drug effects. Prostate / metabolism. Prostatic Neoplasms / metabolism
  • [MeSH-minor] Antigens, CD9. Blotting, Western. Cell Line, Tumor. Gene Expression Regulation / drug effects. Humans. Male. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16128989.001).
  • [ISSN] 0105-6263
  • [Journal-full-title] International journal of andrology
  • [ISO-abbreviation] Int. J. Androl.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Androgens; 0 / Antigens, CD; 0 / Antigens, CD9; 0 / CD9 protein, human; 0 / Membrane Glycoproteins; 2C323EGI97 / Metribolone
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20. Apalla Z, Sotiriou E, Chovarda E, Lefaki I, Devliotou-Panagiotidou D, Ioannides D: Skin cancer: preventive photodynamic therapy in patients with face and scalp cancerization. A randomized placebo-controlled study. Br J Dermatol; 2010 Jan;162(1):171-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Skin cancer: preventive photodynamic therapy in patients with face and scalp cancerization. A randomized placebo-controlled study.
  • Background Patients with a previous medical history of nonmelanoma skin cancers (NMSCs) often develop multiple or recurrent malignant lesions around the site of the primary tumour.
  • This finding led to the field cancerization theory, which suggests that the entire epithelial surface of the regional skin has an increased risk for the development of malignant lesions.
  • Objectives We sought to investigate whether field-photodynamic therapy (PDT) of extreme photodamaged skin would prevent new NMSCs, in comparison with a control area receiving placebo-PDT, in patients with clinical and histological signs of field cancerization.
  • Methods Forty-five patients, previously diagnosed as having NMSCs of the face or scalp, with actinic keratoses symmetrically distributed over the same regions, were randomized for field treatment with 20% aminolaevulinic acid (ALA)-PDT on one side and placebo-PDT on the other.
  • Results A significant delay in the mean time of appearance and a reduction in the total number of new lesions were observed in the field-PDT protocol, when compared with the control.
  • Conclusions The results obtained showed that field therapy with ALA-PDT confers a significant preventive potential against the formation of new NMSCs in patients with field changes.
  • [MeSH-major] Facial Neoplasms / prevention & control. Head and Neck Neoplasms / drug therapy. Neoplasms, Second Primary / prevention & control. Photochemotherapy. Scalp. Skin Neoplasms / prevention & control
  • [MeSH-minor] Aged. Aged, 80 and over. Aminolevulinic Acid / therapeutic use. Carcinoma, Basal Cell / drug therapy. Carcinoma, Squamous Cell / drug therapy. Female. Humans. Keratosis, Actinic / drug therapy. Male. Middle Aged. Photosensitizing Agents / therapeutic use

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  • (PMID = 19863513.001).
  • [ISSN] 1365-2133
  • [Journal-full-title] The British journal of dermatology
  • [ISO-abbreviation] Br. J. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article; Randomized Controlled Trial
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Photosensitizing Agents; 88755TAZ87 / Aminolevulinic Acid
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21. Jirásková M, Jirásek L, Stork J, Vosmík F, Jirsa M: [Photodynamic diagnosis and therapy in dermatology. Experience with use of TPPS4 in skin diseases]. Cas Lek Cesk; 2003 Aug;142(8):493-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Photodynamic diagnosis and therapy in dermatology. Experience with use of TPPS4 in skin diseases].
  • [Transliterated title] Fotodynamická diagnostika a terapie v dermatologii. Zkusenosti s aplikací TPPS4 u nĕkterých kozních afekcí.
  • BACKGROUND: Some skin lesions e.g. basal cell carcinomas are sometimes difficult to remove completely and frequent relapses can develop after their imperfect removal.
  • In case the patient refuses to undergo a radical surgical intervention, more painful alternative like cryotherapy comes into consideration as a method of tumour destruction.
  • Not even such a procedure does guarantee complete destruction of all tumour cells.
  • During the last years new diagnostics and therapeutic methods like photodynamic diagnostic and photodynamic therapy have been developed and they became subjects of our interest.
  • CONCLUSIONS: PDD and PDT were used for diagnostics and treatment of different dermatoses (basal cell carcinomas, malignant melanoma metastases, verrucae vulgares, keratoacanthomas, solitary lesions of T lymphoma--mycosis fungoides, m.
  • Authors do not consider the PDT to be the only and miraculous method relevant to treatment of all skin tumours or other skin diseases.
  • They are of the opinion that this technique, when properly used, can extend the scale of therapeutic methods.
  • [MeSH-major] Photochemotherapy. Photosensitizing Agents / therapeutic use. Porphyrins / therapeutic use. Skin Diseases / drug therapy
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Humans. Male. Middle Aged. Skin Neoplasms / diagnosis. Skin Neoplasms / drug therapy

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  • (PMID = 14626566.001).
  • [ISSN] 0008-7335
  • [Journal-full-title] Casopís lékar̆ů c̆eských
  • [ISO-abbreviation] Cas. Lek. Cesk.
  • [Language] cze
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Czech Republic
  • [Chemical-registry-number] 0 / Photosensitizing Agents; 0 / Porphyrins; 35218-75-8 / tetraphenylporphine sulfonate
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22. Hayashi I, Harada T, Muraoka M, Ishii M: Malignant proliferating trichilemmal tumour and CAV (cisplatin, adriamycin, vindesine) treatment. Br J Dermatol; 2004 Jan;150(1):156-7
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  • [Title] Malignant proliferating trichilemmal tumour and CAV (cisplatin, adriamycin, vindesine) treatment.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Basal Cell / drug therapy. Hair Follicle. Head and Neck Neoplasms / drug therapy. Skin Neoplasms / drug therapy

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  • (PMID = 14746636.001).
  • [ISSN] 0007-0963
  • [Journal-full-title] The British journal of dermatology
  • [ISO-abbreviation] Br. J. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
  • [Chemical-registry-number] 80168379AG / Doxorubicin; Q20Q21Q62J / Cisplatin; RSA8KO39WH / Vindesine
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