FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2106890950> ?p ?o ?g. }

• W2106890950 endingPage "438" @default.
• W2106890950 startingPage "432" @default.
• W2106890950 abstract "No AccessJournal of UrologyReview article1 Feb 2006Targeting Death Receptors in Bladder, Prostate and Renal Cancer Hugh F. O’Kane, Chris J. Watson, Samuel R. Johnston, Istvan Petak, R. William, G. Watson, and Kate E. Williamson Hugh F. O’KaneHugh F. O’Kane Uro-oncology Group, Queen’s University Belfast, Belfast, United Kingdom More articles by this author , Chris J. WatsonChris J. Watson Uro-oncology Group, Queen’s University Belfast, Belfast, United Kingdom More articles by this author , Samuel R. JohnstonSamuel R. Johnston Uro-oncology Group, Queen’s University Belfast, Belfast, United Kingdom More articles by this author , Istvan PetakIstvan Petak Molecular Therapy Laboratory 1st Department of Pathology and Experimental Cancer Research and Rational Drug Design Laboratory Cooperative Research Center, Semmelweis University, Budapest, Hungary More articles by this author , R. WilliamR. William Department of Surgery, Mater Misericordiae University Hospital, Conway Institute, University College Dublin, Dublin, Ireland More articles by this author , G. WatsonG. Watson Department of Surgery, Mater Misericordiae University Hospital, Conway Institute, University College Dublin, Dublin, Ireland More articles by this author , and Kate E. WilliamsonKate E. Williamson Uro-oncology Group, Queen’s University Belfast, Belfast, United Kingdom More articles by this author View All Author Informationhttps://doi.org/10.1016/S0022-5347(05)00160-6AboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookLinked InTwitterEmail Abstract Purpose: We describe key components of normal and aberrant death receptor pathways, the association of these abnormalities with tumorigenesis in bladder, prostate and renal cancer, and their potential application in novel therapeutic strategies targeted toward patients with cancer. Materials and Methods: A MEDLINE literature search of the key words death receptors, TRAIL (tumor necrosis factor related apoptosis inducing ligand), FAS, bladder, prostate, renal and cancer was done to obtain information for review. A brief overview of the TRAIL and FAS death receptor pathways, and their relationship to apoptosis is described. Mechanisms that lead to nonfunction of these pathways and how they may contribute to tumorigenesis are linked. Current efforts to target death receptor pathways as a therapeutic strategy are highlighted. Results: Activation of tumor cell expressing death receptors by cytotoxic immune cells is the main mechanism by which the immune system eliminates malignant cells. Death receptor triggering induces a caspase cascade, leading to tumor cell apoptosis. Receptor gene mutation or hypermethylation, decoy receptor or splice variant over expression, and downstream inhibitor interference are examples of the ways that normal pathway functioning is lost in cancers of the bladder and prostate. Targeting death receptors directly through synthetic ligand administration and blocking downstream inhibitor molecules with siRNA or antisense oligonucleotides represent novel therapeutic strategies under development. Conclusions: Research into the death receptor pathways has demonstrated the key role that pathway aberrations have in the initiation and progression of malignancies of the bladder, prostate and kidney. This new understanding has resulted in exciting approaches to restore the functionality of these pathways as a novel therapeutic strategy. References 1 : Alteration of apoptotic regulatory molecules expression during carcinogenesis and tumor progression of renal cell carcinoma. Int J Urol2003; 10: 476. Google Scholar 2 : Decreased Fas expression in advanced-stage bladder cancer is not related to p53 status. Urology2004; 63: 392. Google Scholar 3 : p53 promotes selection for Fas-mediated apoptotic resistance. Cancer Res2000; 60: 4638. Google Scholar 4 : Androgen and the blocking of radiation-induced sensitization to Fas-mediated apoptosis through c-jun induction in prostate cancer cells. Int J Radiat Biol2003; 79: 451. Google Scholar 5 : Fas-dependent and -independent mechanisms of cell death following DNA damage in human colon carcinoma cells. Cancer Res2000; 60: 2643. Google Scholar 6 : Ionizing radiation enhances the therapeutic potential of TRAIL in prostate cancer in vitro and in vivo intracellular mechanisms. Prostate2004; 61: 35. Google Scholar 7 : Loss of heterozygosity at chromosome segments 8p22 and 8p11.2-21.1 in transitional-cell carcinoma of the urinary bladder. Int J Cancer2000; 86: 501. Google Scholar 8 : Physical mapping of chromosome 8p22 markers and their homozygous deletion in a metastatic prostate cancer. Genomics1996; 35: 46. Google Scholar 9 : Reduced response of prostate cancer cells to TRAIL is modulated by NFkappaB-mediated inhibition of caspases and Bid activation. Int J Oncol2002; 21: 111. Google Scholar 10 : Novel function of androgen receptor-associated protein 55/Hic-5 as a negative regulator of Smad3 signaling. J Biol Chem2005; 280: 5154. Google Scholar 11 : Structure of the human APO-1 gene. Eur J Immunol1994; 24: 3057. Google Scholar 12 : Human and mouse Fas (APO-1/CD95) death receptor genes each contain a p53-responsive element that is activated by p53 mutants unable to induce apoptosis. J Biol Chem2000; 275: 3867. Google Scholar 13 : Hypermethylation of the gene promoter and enhancer region can regulate Fas expression and sensitivity in colon carcinoma. Cell Death Differ2003; 10: 211. Google Scholar 14 : Hypermethylation of the tumor necrosis factor receptor superfamily 6 (APT1, Fas, CD95/Apo-1) gene promoter at rel/nuclear factor kappaB sites in prostatic carcinoma. Mol Carcinog2001; 32: 36. Google Scholar 15 : Aberrant methylation of trail decoy receptor genes is frequent in multiple tumor types. Int J Cancer2004; 109: 786. Google Scholar 16 : Alterations of Fas (APO-1/CD95) gene in transitional cell carcinomas of urinary bladder. Cancer Res1999; 59: 3068. Google Scholar 17 : Analysis of Fas gene mutations on laser capture microdissected specimens from renal cell carcinoma. Jpn J Cancer Res2002; 93: 1201. Google Scholar 18 : Fas gene mutations in prostatic intraepithelial neoplasia and concurrent carcinoma analysis of laser capture microdissected specimens. Lab Invest2001; 81: 283. Google Scholar 19 : Mutations of tumor necrosis factor-related apoptosis-inducing ligand receptor 1 (TRAIL-R1) and receptor 2 (TRAIL-R2) genes in metastatic breast cancers. Cancer Res2001; 61: 4942. Google Scholar 20 : Infrequent mutation of TRAIL receptor 2 (TRAIL-R2/DR5) in transitional cell carcinoma of the bladder with 8p21 loss of heterozygosity. Cancer Lett2005; 220: 137. Google Scholar 21 : Bladder cancer cells acquire competent mechanisms to escape Fas-mediated apoptosis and immune surveillance in the course of malignant transformation. Br J Cancer2001; 84: 1330. Google Scholar 22 : Transitional cell carcinoma expresses high levels of Fas ligand in vivo. BJU Int1999; 83: 698. Google Scholar 23 : Human urinary bladder transitional cell carcinomas acquire the functional Fas ligand during tumor progression. Am J Pathol2003; 162: 1139. Google Scholar 24 : Expression of fas ligand in metastatic prostatic carcinoma suggestive of possible clonal expansion of subpopulation with metastatic potential. Diagn Mol Pathol2001; 10: 236. Google Scholar 25 : Prognostic significance of serum soluble Fas level and its change during regression and progression of advanced prostate cancer. Endocr J2003; 50: 629. Google Scholar 26 : Significance of serum-soluble CD95 (Fas/APO-1) on prognosis in renal cell cancer patients. Br J Cancer1999; 80: 1648. Google Scholar 27 : Soluble Fas and Fas-ligand in bladder cancer in vitro and in vivo. Urol Oncol2001; 6: 163. Google Scholar 28 : Prognostic significance of serum osteoprotegerin levels in patients with bladder carcinoma. Cancer2004; 101: 1794. Google Scholar 29 : Serum osteoprotegerin (OPG) levels are associated with disease progression and response to androgen ablation in patients with prostate cancer. Prostate2004; 59: 304. Google Scholar 30 : Osteoprotegerin in prostate cancer bone metastasis. Cancer Res2005; 65: 1710. Google Scholar 31 : c-FLIP expression in bladder urothelial carcinomas its role in resistance to Fas-mediated apoptosis and clinicopathologic correlations. Urology2004; 63: 1198. Google Scholar 32 : High level of cFLIP correlates with resistance to death receptor-induced apoptosis in bladder carcinoma cells. Anticancer Res2003; 23: 1213. Google Scholar 33 : Persistent c-FLIP(L) expression is necessary and sufficient to maintain resistance to tumor necrosis factor-related apoptosis-inducing ligand-mediated apoptosis in prostate cancer. Cancer Res2004; 64: 7086. Google Scholar 34 : IL-4 protects tumor cells from anti-CD95 and chemotherapeutic agents via up-regulation of antiapoptotic proteins. J Immunol2004; 172: 5467. Google Scholar 35 : XIAP expression is an independent prognostic marker in clear-cell renal carcinomas. Hum Pathol2004; 35: 1022. Google Scholar 36 : Urine detection of survivin is a sensitive marker for the noninvasive diagnosis of bladder cancer. J Urol2004; 171: 626. Link, Google Scholar 37 : Elevated expression of inhibitor of apoptosis proteins in prostate cancer. Clin Cancer Res2003; 9: 4914. Google Scholar 38 : cIAP-2 block apoptotic events in bladder cancer cells. Anticancer Res2003; 23: 3311. Google Scholar 39 : Relationship of p53 and Bcl-2 to prognosis in muscle-invasive transitional cell carcinoma of the bladder. J Urol1996; 155: 1754. Link, Google Scholar 40 : Mutational spectra of PTEN/MMAC1 gene a tumor suppressor with lipid phosphatase activity. J Natl Cancer Inst1999; 91: 1922. Google Scholar 41 : Amiloride augments TRAIL-induced apoptotic death by inhibiting phosphorylation of kinases and phosphatases associated with the P13K-Akt pathway. Oncogene2005; 24: 355. Google Scholar 42 : Sensitization of cancer cells treated with cytotoxic drugs to fas-mediated cytotoxicity. J Natl Cancer Inst1997; 89: 783. Google Scholar 43 : Tumor necrosis factor-related apoptosis-inducing ligand-mediated apoptosis in androgen-independent prostate cancer cells. Cancer Res2000; 60: 2384. Google Scholar 44 : Safety and antitumor activity of recombinant soluble Apo2 ligand. J Clin Invest1999; 104: 155. Google Scholar 45 : TRAIL and its receptors as targets for cancer therapy. Cancer Sci2004; 95: 777. Google Scholar 46 : In vitro efficacy of Fas ligand gene therapy for the treatment of bladder cancer. Cancer Gene Ther2005; 12: 12. Google Scholar 47 : Tumor necrosis factor-related apoptosis-inducing ligand a novel mechanism for Bacillus Calmette-Guerin-induced antitumor activity. Cancer Res2004; 64: 3386. Google Scholar 48 : Downregulation of c-FLIP sensitizes DU145 prostate cancer cells to Fas-mediated apoptosis. Cancer Biol Ther2002; 1: 401. Google Scholar 49 : An antisense oligonucleotide to cIAP-1 sensitizes prostate cancer cells to fas and TNFalpha mediated apoptosis. Prostate2004; 59: 419. Google Scholar 50 : X-linked inhibitor of apoptosis protein inhibition induces apoptosis and enhances chemotherapy sensitivity in human prostate cancer cells. Mol Cancer Ther2004; 3: 699. Google Scholar 51 : Downregulation of Bcl-2 sensitises interferon-resistant renal cancer cells to Fas. Br J Cancer2004; 91: 164. Google Scholar 52 : Systematic in vitro evaluation of survivin directed antisense oligodeoxynucleotides in bladder cancer cells. J Urol2004; 171: 2471. Abstract, Google Scholar 53 : Reduction of the antiapoptotic protein cFLIP enhances the susceptibility of human renal cancer cells to TRAIL apoptosis. Cancer Immunol Immunother2005; 54: 499. Google Scholar 54 : Inhibitor of apoptosis proteins: translating basic knowledge into clinical practice. Cancer Res2004; 64: 7183. Google Scholar 55 : HGS-ETR1, a fully human TRAIL-receptor 1 monoclonal antibody, induces cell death in multiple tumour types in vitro and in vivo. Br J Cancer2005; 92: 1430. Google Scholar 56 : An antibody against DR4 (TRAIL-R1) in combination with doxorubicin selectively kills malignant but not normal prostate cells. Cancer Biol Ther2003; 2: 283. Google Scholar 57 : Induction and regulation of tumor necrosis factor-related apoptosis-inducing ligand/Apo-2 ligand-mediated apoptosis in renal cell carcinoma. Cancer Res2002; 62: 3093. Google Scholar 58 : The proteasome inhibitor bortezomib sensitizes cells to killing by death receptor ligand TRAIL via BH3-only proteins Bik and Bim. Mol Cancer Ther2005; 4: 443. Google Scholar 59 : Doxorubicin sensitizes human bladder carcinoma cells to Fas-mediated cytotoxicity. Cancer1997; 79: 1180. Google Scholar 60 : Quantification and characterization of the bystander effect in prostate cancer cells following adenovirus-mediated FasL expression. Cancer Gene Ther2003; 10: 330. Google Scholar © 2006 by American Urological AssociationFiguresReferencesRelatedDetailsCited byAtala A (2018) Re: TRAIL-Coated Leukocytes that Kill Cancer Cells in the CirculationJournal of Urology, VOL. 192, NO. 4, (1293-1295), Online publication date: 1-Oct-2014.Buttyan R and Mian B (2018) Molecularly Targeted Therapies for Renal Cell Cancer: TRAIL Research AdvancesJournal of Urology, VOL. 177, NO. 5, (1606-1606), Online publication date: 1-May-2007. Volume 175Issue 2February 2006Page: 432-438 Advertisement Copyright & Permissions© 2006 by American Urological AssociationKeywordskidney neoplasmsimmune systemprostate neoplasmsapoptosisbladder neoplasmsMetricsAuthor Information Hugh F. O’Kane Uro-oncology Group, Queen’s University Belfast, Belfast, United Kingdom More articles by this author Chris J. Watson Uro-oncology Group, Queen’s University Belfast, Belfast, United Kingdom More articles by this author Samuel R. Johnston Uro-oncology Group, Queen’s University Belfast, Belfast, United Kingdom More articles by this author Istvan Petak Molecular Therapy Laboratory 1st Department of Pathology and Experimental Cancer Research and Rational Drug Design Laboratory Cooperative Research Center, Semmelweis University, Budapest, Hungary More articles by this author R. William Department of Surgery, Mater Misericordiae University Hospital, Conway Institute, University College Dublin, Dublin, Ireland More articles by this author G. Watson Department of Surgery, Mater Misericordiae University Hospital, Conway Institute, University College Dublin, Dublin, Ireland More articles by this author Kate E. Williamson Uro-oncology Group, Queen’s University Belfast, Belfast, United Kingdom More articles by this author Expand All Advertisement PDF downloadLoading ..." @default.
• W2106890950 created "2016-06-24" @default.
• W2106890950 creator A5046324422 @default.
• W2106890950 creator A5047619380 @default.
• W2106890950 creator A5052868080 @default.
• W2106890950 creator A5054331050 @default.
• W2106890950 creator A5067683587 @default.
• W2106890950 creator A5081711830 @default.
• W2106890950 creator A5088923903 @default.
• W2106890950 date "2006-02-01" @default.
• W2106890950 modified "2023-10-18" @default.
• W2106890950 title "Targeting Death Receptors in Bladder, Prostate and Renal Cancer" @default.
• W2106890950 cites W1511895445 @default.
• W2106890950 cites W1599411566 @default.
• W2106890950 cites W1911504906 @default.
• W2106890950 cites W1920968130 @default.
• W2106890950 cites W1951460484 @default.
• W2106890950 cites W1967992429 @default.
• W2106890950 cites W1969803481 @default.
• W2106890950 cites W1973198032 @default.
• W2106890950 cites W1974144614 @default.
• W2106890950 cites W1974912213 @default.
• W2106890950 cites W1976457595 @default.
• W2106890950 cites W1977602802 @default.
• W2106890950 cites W1981861078 @default.
• W2106890950 cites W1983390331 @default.
• W2106890950 cites W1990291291 @default.
• W2106890950 cites W1993691675 @default.
• W2106890950 cites W1996848161 @default.
• W2106890950 cites W1997888702 @default.
• W2106890950 cites W1999134519 @default.
• W2106890950 cites W2004952453 @default.
• W2106890950 cites W2005808869 @default.
• W2106890950 cites W2008277835 @default.
• W2106890950 cites W2012904619 @default.
• W2106890950 cites W2020311145 @default.
• W2106890950 cites W2022923458 @default.
• W2106890950 cites W2023040267 @default.
• W2106890950 cites W2024590240 @default.
• W2106890950 cites W2028512857 @default.
• W2106890950 cites W2031084877 @default.
• W2106890950 cites W2031107713 @default.
• W2106890950 cites W2031848351 @default.
• W2106890950 cites W2034518007 @default.
• W2106890950 cites W2057829457 @default.
• W2106890950 cites W2059337995 @default.
• W2106890950 cites W2061945098 @default.
• W2106890950 cites W2062194863 @default.
• W2106890950 cites W2074494405 @default.
• W2106890950 cites W2076536275 @default.
• W2106890950 cites W2080607227 @default.
• W2106890950 cites W2083458436 @default.
• W2106890950 cites W2087359605 @default.
• W2106890950 cites W2089909138 @default.
• W2106890950 cites W2092362867 @default.
• W2106890950 cites W2106284224 @default.
• W2106890950 cites W2122522737 @default.
• W2106890950 cites W2154063020 @default.
• W2106890950 cites W2171486499 @default.
• W2106890950 cites W2330823925 @default.
• W2106890950 cites W4255137433 @default.
• W2106890950 cites W4302360388 @default.
• W2106890950 doi "https://doi.org/10.1016/s0022-5347(05)00160-6" @default.
• W2106890950 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/16406966" @default.
• W2106890950 hasPublicationYear "2006" @default.
• W2106890950 type Work @default.
• W2106890950 sameAs 2106890950 @default.
• W2106890950 citedByCount "44" @default.
• W2106890950 countsByYear W21068909502012 @default.
• W2106890950 countsByYear W21068909502013 @default.
• W2106890950 countsByYear W21068909502014 @default.
• W2106890950 countsByYear W21068909502015 @default.
• W2106890950 countsByYear W21068909502016 @default.
• W2106890950 countsByYear W21068909502017 @default.
• W2106890950 countsByYear W21068909502018 @default.
• W2106890950 countsByYear W21068909502019 @default.
• W2106890950 crossrefType "journal-article" @default.
• W2106890950 hasAuthorship W2106890950A5046324422 @default.
• W2106890950 hasAuthorship W2106890950A5047619380 @default.
• W2106890950 hasAuthorship W2106890950A5052868080 @default.
• W2106890950 hasAuthorship W2106890950A5054331050 @default.
• W2106890950 hasAuthorship W2106890950A5067683587 @default.
• W2106890950 hasAuthorship W2106890950A5081711830 @default.
• W2106890950 hasAuthorship W2106890950A5088923903 @default.
• W2106890950 hasConcept C121608353 @default.
• W2106890950 hasConcept C126322002 @default.
• W2106890950 hasConcept C126894567 @default.
• W2106890950 hasConcept C143998085 @default.
• W2106890950 hasConcept C170493617 @default.
• W2106890950 hasConcept C2776235491 @default.
• W2106890950 hasConcept C2780192828 @default.
• W2106890950 hasConcept C2780352672 @default.
• W2106890950 hasConcept C71924100 @default.
• W2106890950 hasConceptScore W2106890950C121608353 @default.
• W2106890950 hasConceptScore W2106890950C126322002 @default.
• W2106890950 hasConceptScore W2106890950C126894567 @default.
• W2106890950 hasConceptScore W2106890950C143998085 @default.
• W2106890950 hasConceptScore W2106890950C170493617 @default.

• next