[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 100 of about 454
1. Chen M, Feuerstein MA, Levina E, Baghel PS, Carkner RD, Tanner MJ, Shtutman M, Vacherot F, Terry S, de la Taille A, Buttyan R: Hedgehog/Gli supports androgen signaling in androgen deprived and androgen independent prostate cancer cells. Mol Cancer; 2010 Apr 26;9:89
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hedgehog/Gli supports androgen signaling in androgen deprived and androgen independent prostate cancer cells.
  • BACKGROUND: Castration resistant prostate cancer (CRPC) develops as a consequence of hormone therapies used to deplete androgens in advanced prostate cancer patients.
  • CRPC cells are able to grow in a low androgen environment and this is associated with anomalous activity of their endogenous androgen receptor (AR) despite the low systemic androgen levels in the patients.
  • Therefore, the reactivated tumor cell androgen signaling pathway is thought to provide a target for control of CRPC.
  • Previously, we reported that Hedgehog (Hh) signaling was conditionally activated by androgen deprivation in androgen sensitive prostate cancer cells and here we studied the potential for cross-talk between Hh and androgen signaling activities in androgen deprived and androgen independent (AI) prostate cancer cells.
  • RESULTS: Treatment of a variety of androgen-deprived or AI prostate cancer cells with the Hh inhibitor, cyclopamine, resulted in dose-dependent modulation of the expression of genes that are regulated by androgen.
  • The effect of cyclopamine on endogenous androgen-regulated gene expression in androgen deprived and AI prostate cancer cells was consistent with the suppressive effects of cyclopamine on the expression of a reporter gene (luciferase) from two different androgen-dependent promoters.
  • Similarly, reduction of smoothened (Smo) expression with siRNA co-suppressed expression of androgen-inducible KLK2 and KLK3 in androgen deprived cells without affecting the expression of androgen receptor (AR) mRNA or protein.
  • Cyclopamine also prevented the outgrowth of AI cells from androgen growth-dependent parental LNCaP cells and suppressed the growth of an overt AI-LNCaP variant whereas supplemental androgen (R1881) restored growth to the AI cells in the presence of cyclopamine.
  • Conversely, overexpression of Gli1 or Gli2 in LNCaP cells enhanced AR-specific gene expression in the absence of androgen.
  • Overexpressed Gli1/Gli2 also enabled parental LNCaP cells to grow in androgen depleted medium.
  • CONCLUSIONS: Collectively, our results indicate that Hh/Gli signaling supports androgen signaling and AI growth in prostate cancer cells in a low androgen environment.
  • The finding that Gli2 co-immunoprecipitates with AR protein suggests that an interaction between these proteins might be the basis for Hedgehog/Gli support of androgen signaling under this condition.

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • Hazardous Substances Data Bank. CYCLOPAMINE .
  • 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 .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Biochem Biophys Res Commun. 2008 Aug 15;373(1):109-12 [18544338.001]
  • [Cites] N Engl J Med. 2009 Sep 17;361(12):1164-72 [19726763.001]
  • [Cites] Cancer Res. 2008 Aug 1;68(15):6407-15 [18676866.001]
  • [Cites] Clin Cancer Res. 2008 Sep 15;14(18):5769-77 [18794086.001]
  • [Cites] Genes Dev. 2008 Sep 15;22(18):2454-72 [18794343.001]
  • [Cites] Nat Rev Cancer. 2008 Oct;8(10):743-54 [18813320.001]
  • [Cites] Eur Urol. 2008 Dec;54(6):1333-43 [18262716.001]
  • [Cites] Mol Cell Endocrinol. 2008 Nov 25;295(1-2):115-20 [18782595.001]
  • [Cites] J Pathol. 2008 Dec;216(4):460-70 [18825689.001]
  • [Cites] J Biol Chem. 2001 Mar 9;276(10):6889-92 [11238441.001]
  • [Cites] J Natl Cancer Inst. 2001 Nov 21;93(22):1687-97 [11717329.001]
  • [Cites] Genes Dev. 2002 Jun 1;16(11):1433-40 [12050120.001]
  • [Cites] Curr Treat Options Oncol. 2002 Oct;3(5):437-46 [12194808.001]
  • [Cites] Genes Dev. 2002 Nov 1;16(21):2743-8 [12414725.001]
  • [Cites] Urol Clin North Am. 2003 May;30(2):219-26 [12735499.001]
  • [Cites] Cancer Res. 2003 Aug 1;63(15):4552-60 [12907631.001]
  • [Cites] Cancer Lett. 2004 Feb 20;204(2):145-57 [15013214.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Aug 24;101(34):12561-6 [15314219.001]
  • [Cites] Nature. 2004 Oct 7;431(7009):707-12 [15361885.001]
  • [Cites] Prostate. 2004 Dec 1;61(4):332-53 [15389811.001]
  • [Cites] Nature. 1980 Oct 30;287(5785):795-801 [6776413.001]
  • [Cites] Nature. 1988 Mar 24;332(6162):371-4 [2832761.001]
  • [Cites] Urol Clin North Am. 1991 Feb;18(1):1-13 [1899494.001]
  • [Cites] Science. 1996 Jun 14;272(5268):1668-71 [8658145.001]
  • [Cites] Cell. 1996 Jun 14;85(6):841-51 [8681379.001]
  • [Cites] Science. 1997 May 2;276(5313):817-21 [9115210.001]
  • [Cites] Ernst Schering Found Symp Proc. 2006;(5):181-217 [17939302.001]
  • [Cites] Cell Cycle. 2007 Oct 15;6(20):2458-63 [17726373.001]
  • [Cites] Gene Ther. 2008 Jan;15(2):126-35 [17989703.001]
  • [Cites] Blood. 2008 Jan 15;111(2):492-503 [17914027.001]
  • [Cites] Nature. 1998 Jan 1;391(6662):90-2 [9422511.001]
  • [Cites] Science. 1998 Jun 5;280(5369):1603-7 [9616123.001]
  • [Cites] J Virol. 1999 Apr;73(4):3258-63 [10074179.001]
  • [Cites] Cancer Res. 2005 Apr 15;65(8):2990-2 [15833820.001]
  • [Cites] Hum Mol Genet. 2005 Aug 1;14(15):2181-8 [15994174.001]
  • [Cites] J Cell Biochem. 2006 Oct 1;99(2):362-72 [16619264.001]
  • [Cites] J Urol. 2007 Mar;177(3):1179-85 [17296441.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 May 15;104(20):8455-60 [17494766.001]
  • [Cites] Science. 2007 Oct 5;318(5847):66-8 [17916724.001]
  • [Cites] Endocr Relat Cancer. 2008 Dec;15(4):841-9 [18667687.001]
  • [Cites] Cancer Res. 2008 Dec 1;68(23):9918-27 [19047173.001]
  • [Cites] Adv Cancer Res. 2008;101:29-43 [19055941.001]
  • [Cites] Dev Cell. 2008 Dec;15(6):801-12 [19081070.001]
  • [Cites] Cell Cycle. 2009 Jan 1;8(1):149-57 [19158486.001]
  • [Cites] Proc Natl Acad Sci U S A. 2009 Feb 24;106(8):2623-8 [19196978.001]
  • [Cites] Cancer Res. 2009 Mar 15;69(6):2305-13 [19244107.001]
  • [Cites] Dev Biol. 2009 May 1;329(1):96-103 [19268447.001]
  • [Cites] Clin Cancer Res. 2009 May 15;15(10):3251-5 [19447877.001]
  • [Cites] J Clin Oncol. 2009 Aug 10;27(23):3742-8 [19470933.001]
  • [Cites] Cancer Res. 2008 Jul 1;68(13):5469-77 [18593950.001]
  • (PMID = 20420697.001).
  • [ISSN] 1476-4598
  • [Journal-full-title] Molecular cancer
  • [ISO-abbreviation] Mol. Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA11618
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Androgens; 0 / GLI1 protein, human; 0 / Hedgehog Proteins; 0 / RNA, Small Interfering; 0 / Receptors, Androgen; 0 / Transcription Factors; 0 / Veratrum Alkaloids; ZH658AJ192 / cyclopamine
  • [Other-IDs] NLM/ PMC2873440
  •  go-up   go-down


2. Shulman MJ, Benaim EA: Prognostic model of event-free survival for patients with androgen-independent prostate carcinoma. Cancer; 2005 Jun 1;103(11):2280-6
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic model of event-free survival for patients with androgen-independent prostate carcinoma.
  • BACKGROUND: The current study was conducted to develop a prognostic model of event-free survival (EFS) in men with androgen-independent prostate carcinoma (AIPC).
  • RESULTS: The final prognostic risk model included the presence of metastatic disease at the time of androgen-independent disease progression (P = 0.040), time to prostate-specific antigen (PSA) recurrence (P = 0.043), and PSA doubling time (P < 0.01).
  • Three highly independent risk groups were identified.
  • Patients who died of prostate carcinoma experienced significantly more clinical events than those who died of other causes (P < 0.01).
  • CONCLUSIONS: The prognostic model in the current study stratified patients into three highly significant and independent risk groups for EFS.
  • [MeSH-minor] Aged. Aged, 80 and over. Androgens / therapeutic use. Cohort Studies. Disease Progression. Disease-Free Survival. Humans. Male. Middle Aged. Neoplasm Staging. Prognosis. Prostate-Specific Antigen / metabolism. Prostatectomy. Retrospective Studies. Risk Factors. Survival Rate. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15844202.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; EC 3.4.21.77 / Prostate-Specific Antigen
  •  go-up   go-down


3. Pinto JT, Sinha R, Papp K, Facompre ND, Desai D, El-Bayoumy K: Differential effects of naturally occurring and synthetic organoselenium compounds on biomarkers in androgen responsive and androgen independent human prostate carcinoma cells. Int J Cancer; 2007 Apr 1;120(7):1410-7
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Differential effects of naturally occurring and synthetic organoselenium compounds on biomarkers in androgen responsive and androgen independent human prostate carcinoma cells.
  • Epidemiological studies and clinical trials show that selenium supplementation results in reduction of prostate cancer incidence; however, the form of selenium and mechanisms underlying protection remain largely unknown.
  • Toward this end, we compared the effects of naturally occurring selenomethionine (SM) and Se-methylselenocysteine (MSC) and synthetic 1,4-phenylenebis(methylene)selenocyanate (p-XSC) and p-xylylbis(methylselenide) p-XMS) organoselenium compounds in androgen responsive (AR) LNCaP and its androgen independent clone (AI) LNCaP C4-2 human prostate carcinoma cells on cell growth, secretion of prostate specific antigen (PSA), intracellular redox status and genomic profiles with emphasis on identifying redox sensitive genes.
  • Depending on the structure, organoselenium compounds exhibit differential effects on growth, PSA secretion, oxidative stress and selective gene responses in human prostate cancer cells and suggest the potential of developing novel organoselenium compounds as chemopreventive agents in models of human prostate cancer.
  • [MeSH-major] Androgens / pharmacology. Neoplasm Proteins / genetics. Neoplasms, Hormone-Dependent / pathology. Organoselenium Compounds / pharmacology. Prostate-Specific Antigen / metabolism. Prostatic Neoplasms / pathology
  • [MeSH-minor] Gene Expression Profiling. Gene Expression Regulation, Neoplastic / drug effects. Glutathione / metabolism. Humans. Male. Oligonucleotide Array Sequence Analysis. Oxidative Stress. RNA, Messenger / metabolism. Receptors, Androgen / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Tumor Cells, Cultured / drug effects

  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer Screening.
  • 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 .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2006 Wiley-Liss, Inc.
  • (PMID = 17205524.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA111842; United States / NCI NIH HHS / CA / CA29502; United States / NCI NIH HHS / CA / CA46589; United States / NCI NIH HHS / CA / CA89815
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Neoplasm Proteins; 0 / Organoselenium Compounds; 0 / RNA, Messenger; 0 / Receptors, Androgen; EC 3.4.21.77 / Prostate-Specific Antigen; GAN16C9B8O / Glutathione
  •  go-up   go-down


Advertisement
4. Li TQ, Feng CQ, Zou YG, Shi R, Liang S, Mao XM: [Literature-mining and bioinformatic analysis of androgen-independent prostate cancer-specific genes]. Zhonghua Nan Ke Xue; 2009 Dec;15(12):1102-7
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Literature-mining and bioinformatic analysis of androgen-independent prostate cancer-specific genes].
  • OBJECTIVE: To compare the differences of the gene expressions in androgen-independent and androgen-dependent prostate cancer (ADPC), gain a deeper insight into the molecular mechanism of androgen-independent prostate cancer (AIPC), and find effective means for its clinical diagnosis and treatment.
  • METHODS: Eats of genes highly-associated with prostate cancer were obtained by mining PubMed with the FACTA tool, and the specifically expressed genes in AIPC were analyzed with a set of bioinformatic tools including GATHER, PANTHER, STRING and ToppGene.
  • [MeSH-minor] Androgen Antagonists. Androgens / metabolism. Computational Biology. Data Mining. Gene Expression. Gene Regulatory Networks. Genes, Neoplasm. Humans. Male


5. Borden LS Jr, Clark PE, Lovato J, Hall MC, Stindt D, Harmon M, M Mohler R, Torti FM: Vinorelbine, doxorubicin, and prednisone in androgen-independent prostate cancer. Cancer; 2006 Sep 1;107(5):1093-100
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Vinorelbine, doxorubicin, and prednisone in androgen-independent prostate cancer.
  • BACKGROUND: Ultimately, patients with metastatic prostate cancer progress on androgen ablation therapy.
  • The investigation of new chemotherapeutic regimens for the treatment of androgen-independent prostate cancer (AIPC) is essential.
  • Endpoints included prostate-specific antigen (PSA) response and palliation, as measured by the Functional Assessment of Cancer Therapy-Prostate (FACT-P) instrument, the Brief Pain Inventory Scale, and a narcotic analgesic log.
  • [MeSH-minor] Aged. Aged, 80 and over. Drug Administration Schedule. Humans. Male. Middle Aged. Neoplasm Metastasis. Pain Measurement. Palliative Care. Prostate-Specific Antigen / analysis


6. Lebret T, Méjean A: [Management of metastatic androgeno-independent prostate cancer]. Prog Urol; 2008 Nov;18 Suppl 7:S343-8
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] [Management of metastatic androgeno-independent prostate cancer].
  • [Transliterated title] Prise en charge du cancer de prostate métastasé androgéno-indépendant.
  • After first line hormonal therapy (agonist LHRH), metastasic prostate cancer becomes androgen independent in a period of 18 months on average.
  • After this period and after having verified the castration by blood testosterone level, a few options are possible: either inhibit adrenal androgens by maximum androgen blockage (+anti androgens) or by specific adrenal androgen inhibitors.
  • [MeSH-minor] Androgens. Decision Trees. Drug Resistance, Neoplasm. Humans. Male

  • Genetic Alliance. consumer health - Prostate cancer.
  • Genetic Alliance. consumer health - Metastatic cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19070814.001).
  • [ISSN] 1166-7087
  • [Journal-full-title] Progrès en urologie : journal de l'Association française d'urologie et de la Société française d'urologie
  • [ISO-abbreviation] Prog. Urol.
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Androgens
  •  go-up   go-down


7. Aragon-Ching JB, Gillespie J, Price DK, Chuaqui R, Rodriguez-Canales J, Steinberg SM, Dahut WL, Figg WD: Lack of prognostic significance of prostate biopsies in metastatic androgen independent prostate cancer. BJU Int; 2007 Dec;100(6):1245-8
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Lack of prognostic significance of prostate biopsies in metastatic androgen independent prostate cancer.
  • OBJECTIVE: To assess the significance of viable tumour in the prostate of patients with metastatic androgen-independent prostate cancer (AIPC).
  • PATIENTS AND METHODS: We evaluated the clinicopathological features, including follow-up, of 40 men with metastatic AIPC who had a transrectal biopsy of the prostate.
  • RESULTS: Prostate biopsies (median three cores per biopsy) showed viable tumour in 19 of 40 patients (48%).
  • CONCLUSIONS: Taking prostate biopsies at the time of documented metastatic AIPC yielded tumour in about half the patients.
  • A previous history of RT was not associated with a negative prostate biopsy; the latter appears to have no influence on the prognosis.
  • [MeSH-major] Androgens / metabolism. Neoplasms, Hormone-Dependent / pathology. Prostate / pathology. Prostatic Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antineoplastic Agents / therapeutic use. Biopsy, Needle. Follow-Up Studies. Humans. Male. Middle Aged. Neoplasm Metastasis. Prognosis. Prostate-Specific Antigen / blood

  • Genetic Alliance. consumer health - Prostate cancer.
  • Genetic Alliance. consumer health - Metastatic cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17850370.001).
  • [ISSN] 1464-410X
  • [Journal-full-title] BJU international
  • [ISO-abbreviation] BJU Int.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Intramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Androgens; 0 / Antineoplastic Agents; EC 3.4.21.77 / Prostate-Specific Antigen
  •  go-up   go-down


8. Vanquelef E, Hélesbeux JJ, Duval O, Debiton E, Barthomeuf C, Jarry C, Forfar I, Richomme P: Synthesis and PC3 androgen-independent prostate cells antiproliferative effect of fagaronine derivatives. J Enzyme Inhib Med Chem; 2007 Oct;22(5):647-54
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] Synthesis and PC3 androgen-independent prostate cells antiproliferative effect of fagaronine derivatives.
  • Fagaronine derivatives syntheses were optimized and their effect on PC3 androgen-independent prostate cell line was evaluated.
  • [MeSH-minor] Benzophenanthridines. Cell Line, Tumor. Drug Resistance, Neoplasm / drug effects. Drug Screening Assays, Antitumor. Humans. Hydrogen-Ion Concentration / drug effects. Male. Molecular Structure

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18035833.001).
  • [ISSN] 1475-6366
  • [Journal-full-title] Journal of enzyme inhibition and medicinal chemistry
  • [ISO-abbreviation] J Enzyme Inhib Med Chem
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Alkaloids; 0 / Androgens; 0 / Antineoplastic Agents; 0 / Benzophenanthridines; 0 / Phenanthridines; 41758-44-5 / fagaronine
  •  go-up   go-down


9. Schnadig ID, Beer TM: Optimal timing of chemotherapy in androgen independent prostate cancer. Urol Oncol; 2009 Jan-Feb;27(1):97-100
Hazardous Substances Data Bank. DOCETAXEL .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Optimal timing of chemotherapy in androgen independent prostate cancer.
  • PURPOSE: To interpret available docetaxel clinical trial data in order to define optimal timing of the initiation of chemotherapy in androgen independent prostate cancer (AIPC).
  • Studies that test the efficacy of chemotherapy early in the natural history of prostate cancer are under way or are planned.
  • [MeSH-minor] Androgens / metabolism. Antineoplastic Agents, Hormonal / therapeutic use. Chemotherapy, Adjuvant / methods. Clinical Trials as Topic. Humans. Male. Neoplasm Metastasis. Quality of Life. Taxoids / therapeutic use

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19111808.001).
  • [ISSN] 1078-1439
  • [Journal-full-title] Urologic oncology
  • [ISO-abbreviation] Urol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Antineoplastic Agents; 0 / Antineoplastic Agents, Hormonal; 0 / Taxoids; 15H5577CQD / docetaxel
  • [Number-of-references] 16
  •  go-up   go-down


10. Gustavsson H, Welén K, Damber JE: Transition of an androgen-dependent human prostate cancer cell line into an androgen-independent subline is associated with increased angiogenesis. Prostate; 2005 Mar 1;62(4):364-73
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Transition of an androgen-dependent human prostate cancer cell line into an androgen-independent subline is associated with increased angiogenesis.
  • BACKGROUND: Androgen-independent prostate cancer is today an incurable disease, but increased understanding of the mechanisms for the transition into an androgen-independent state may increase the possibilities for more efficient strategies in the future.
  • METHODS: An androgen-independent subline, LNCaP-19, to the androgen-dependent prostate cancer cell line LNCaP was developed in vitro under standard culture conditions.
  • The characteristics of LNCaP-19 regarding androgen responsiveness, PSA, and VEGF secretion was studied in vitro.
  • RESULTS: LNCaP-19 grows equally well in dextran-charcoal stripped FBS (DCC-FBS) as in normal FBS, and rapidly gives rise to tumors in both intact and castrated mice, indicating a true androgen-independent growth.
  • The PSA secretion from LNCaP-19 cells was lower than from LNCaP cells, while the VEGF level was comparable to the secretion from LNCaP cells without androgen stimulation.
  • CONCLUSIONS: LNCaP-19 shows characteristics resembling those of androgen-independent prostate cancer.
  • An increased MVD and changed vessel morphology in the tumor, makes it an interesting model system for studies regarding angiogenesis in the context of the acquisition of androgen independence.
  • [MeSH-minor] Drug Resistance, Neoplasm. Humans. Male. Tumor Cells, Cultured


11. Bai Q, Chen F, Qi J, Chen JH, Wang YX: [Relationship between HER-2/neu over-expression and androgen independent prostate cancer]. Zhonghua Nan Ke Xue; 2007 May;13(5):414-6
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Relationship between HER-2/neu over-expression and androgen independent prostate cancer].
  • OBJECTIVE: To detect HER-2/neu expression in prostate cancer tissues of both androgen dependent and independent groups and to evaluate the role of HER-2/neu in androgen independent prostate cancer.
  • METHODS: Immunohistochemical assay was used in the detection of HER-2/neu in the prostate cancer samples from 30 cases of androgen dependent cancer and 24 cases of androgen independent cancer.
  • RESULTS: The rates of HER-2/neu over-expression were 10% and 33% in the androgen dependent group and the androgen independent group, significantly higher in the Gleason score >7 group and the clinical stage > T2 group than in the -7 group and the > T2 group (14.29% vs. 26.92%, 34.62% vs. 7.14%, P < 0.01).
  • CONCLUSION: The rate of HER-2/neu over-expression is high in androgen independent prostate cancer and is correlated with the tumor stage and Gleason score.
  • [MeSH-minor] Humans. Immunohistochemistry. Male. Neoplasm Staging

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17569256.001).
  • [ISSN] 1009-3591
  • [Journal-full-title] Zhonghua nan ke xue = National journal of andrology
  • [ISO-abbreviation] Zhonghua Nan Ke Xue
  • [Language] chi
  • [Publication-type] Controlled Clinical Trial; English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Androgens; EC 2.7.10.1 / Receptor, ErbB-2
  •  go-up   go-down


12. Li Y, Wang L, Zhang M, Melamed J, Liu X, Reiter R, Wei J, Peng Y, Zou X, Pellicer A, Garabedian MJ, Ferrari A, Lee P: LEF1 in androgen-independent prostate cancer: regulation of androgen receptor expression, prostate cancer growth, and invasion. Cancer Res; 2009 Apr 15;69(8):3332-8
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] LEF1 in androgen-independent prostate cancer: regulation of androgen receptor expression, prostate cancer growth, and invasion.
  • A major obstacle in treating prostate cancer is the development of androgen-independent disease.
  • In this study, we examined LEF1 expression in androgen-independent cancer as well as its regulation of androgen receptor (AR) expression, prostate cancer growth, and invasion in androgen-independent prostate cancer cells.
  • Affymetrix microarray analysis of LNCaP and LNCaP-AI (androgen-independent variant LNCaP) cells revealed 100-fold increases in LEF1 expression in LNCaP-AI cells.
  • Thus, we identified LEF1 as a potential marker for androgen-independent disease and as a key regulator of AR expression and prostate cancer growth and invasion.
  • LEF1 is highly expressed in androgen-independent prostate cancer, potentially serving as a marker for androgen-independent disease.

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Oncogene. 2006 Jun 8;25(24):3436-44 [16474850.001]
  • [Cites] J Cell Biochem. 2006 Oct 1;99(2):402-10 [16741972.001]
  • [Cites] J Mol Endocrinol. 2006 Oct;37(2):283-300 [17032745.001]
  • [Cites] Nat Clin Pract Oncol. 2007 Apr;4(4):236-44 [17392714.001]
  • [Cites] Endocrinology. 2007 Sep;148(9):4334-43 [17540719.001]
  • [Cites] Cancer Res. 2008 Feb 15;68(4):1128-35 [18281488.001]
  • [Cites] BMC Cell Biol. 2008;9:4 [18218096.001]
  • [Cites] J Androl. 2008 Mar-Apr;29(2):207-12 [17916567.001]
  • [Cites] Cancer Res. 2008 Apr 15;68(8):2678-88 [18413735.001]
  • [Cites] J Cell Mol Med. 2008 Dec;12(6B):2790-8 [18266956.001]
  • [Cites] Cancer Res. 1999 Nov 1;59(21):5483-7 [10554023.001]
  • [Cites] Genes Dev. 2000 Aug 1;14(15):1837-51 [10921899.001]
  • [Cites] Cancer Res. 2000 Sep 1;60(17):4709-13 [10987273.001]
  • [Cites] J Natl Cancer Inst. 2000 Dec 6;92(23):1918-25 [11106683.001]
  • [Cites] Cancer Res. 2000 Dec 15;60(24):6841-5 [11156376.001]
  • [Cites] Biochem Biophys Res Commun. 2001 Apr 27;283(1):179-87 [11322786.001]
  • [Cites] Cancer Res. 2001 May 1;61(9):3550-5 [11325816.001]
  • [Cites] Cancer Res. 2001 Jun 1;61(11):4315-9 [11389051.001]
  • [Cites] J Urol. 2001 Oct;166(4):1514-9 [11547123.001]
  • [Cites] Cancer Res. 2001 Oct 15;61(20):7544-51 [11606392.001]
  • [Cites] Nat Rev Cancer. 2001 Oct;1(1):34-45 [11900250.001]
  • [Cites] Biol Chem. 2002 Feb;383(2):255-61 [11934263.001]
  • [Cites] J Biol Chem. 2002 Jun 7;277(23):20702-10 [11916967.001]
  • [Cites] J Cancer Res Clin Oncol. 2003 Apr;129(4):199-221 [12707770.001]
  • [Cites] Br J Cancer. 2003 Oct 20;89(8):1566-73 [14562033.001]
  • [Cites] Nat Med. 2004 Jan;10(1):33-9 [14702632.001]
  • [Cites] Oncogene. 2004 Jul 1;23(30):5175-84 [15156193.001]
  • [Cites] Proc Natl Acad Sci U S A. 1992 Jul 15;89(14):6319-23 [1631125.001]
  • [Cites] Cancer Res. 1994 Mar 15;54(6):1566-73 [7511045.001]
  • [Cites] Cancer Res. 1994 Jun 1;54(11):2861-4 [8187068.001]
  • [Cites] J Biol Chem. 1994 Oct 14;269(41):25655-9 [7929269.001]
  • [Cites] Cell Growth Differ. 1994 Nov;5(11):1243-51 [7848925.001]
  • [Cites] N Engl J Med. 1995 May 25;332(21):1393-8 [7723794.001]
  • [Cites] Nat Genet. 1995 Apr;9(4):401-6 [7795646.001]
  • [Cites] Mol Cell Endocrinol. 1996 May 17;119(1):83-93 [8793857.001]
  • [Cites] Oncol Res. 1995;7(10-11):545-58 [8866667.001]
  • [Cites] Cancer Res. 1997 Jan 15;57(2):314-9 [9000575.001]
  • [Cites] Cancer Res. 1998 Oct 15;58(20):4640-5 [9788616.001]
  • [Cites] Cancer Res. 1999 Jan 15;59(2):279-84 [9927031.001]
  • [Cites] J Biol Chem. 1999 Mar 19;274(12):7777-83 [10075669.001]
  • [Cites] Nat Med. 1999 Mar;5(3):280-5 [10086382.001]
  • [Cites] J Cell Physiol. 1999 Jun;179(3):336-46 [10228952.001]
  • [Cites] Endocrinology. 1999 Sep;140(9):4056-64 [10465276.001]
  • [Cites] Biochim Biophys Acta. 1999 Oct 29;1424(2-3):M23-37 [10528152.001]
  • [Cites] Cell Res. 2005 Jan;15(1):28-32 [15686623.001]
  • [Cites] Nature. 2005 Apr 14;434(7035):843-50 [15829953.001]
  • [Cites] Prostate Cancer Prostatic Dis. 2005;8(2):119-26 [15809669.001]
  • [Cites] Mol Endocrinol. 2005 Jul;19(7):1792-802 [15731171.001]
  • [Cites] Endocr Rev. 2005 Dec;26(7):898-915 [16126938.001]
  • [Cites] Exp Cell Res. 2006 Apr 1;312(6):831-43 [16413016.001]
  • [Cites] Clin Cancer Res. 2006 Mar 15;12(6):1665-71 [16551847.001]
  • (PMID = 19351848.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK058024; United States / NCRR NIH HHS / RR / UL1 RR025741; United States / NIDDK NIH HHS / DK / DK058024
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / LEF1 protein, human; 0 / Lymphoid Enhancer-Binding Factor 1; 0 / RNA, Messenger; 0 / Receptors, Androgen
  • [Other-IDs] NLM/ NIHMS97236; NLM/ PMC3182465
  •  go-up   go-down


13. Guan XX, Chen LB: [Current opinions on the treatment of androgen-independent prostate cancer]. Zhonghua Nan Ke Xue; 2006 Nov;12(11):1021-5
MedlinePlus Health Information. consumer health - Prostate Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Current opinions on the treatment of androgen-independent prostate cancer].
  • Prostate cancer is a most common malignant neoplasm in males.
  • Patients with recurrent prostate cancer may be treated with androgen deprivation strategies, but most cases will eventually develop into androgen-independent prostate cancer (AIPC).
  • Molecular mechanisms underlying the development of androgen-independent prostate cancer (AIPC) are poorly understood.

  • Genetic Alliance. consumer health - Prostate cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17146932.001).
  • [ISSN] 1009-3591
  • [Journal-full-title] Zhonghua nan ke xue = National journal of andrology
  • [ISO-abbreviation] Zhonghua Nan Ke Xue
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Androgens; 0 / Antineoplastic Agents, Hormonal
  • [Number-of-references] 21
  •  go-up   go-down


14. Mohler JL: Castration-recurrent prostate cancer is not androgen-independent. Adv Exp Med Biol; 2008;617:223-34
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Castration-recurrent prostate cancer is not androgen-independent.
  • An American man is diagnosed with prostate cancer (PC) every 3 min and dies from the disease every 17 min.
  • Although androgen receptor (AR) expression is diminished following androgen deprivation therapy (ADT) that induces clinical remission in most patients, castration-recurrent PC expresses levels of AR protein similar to those found in androgen-stimulated PC and benign prostate.
  • This observation suggests that the AR may be as important for growth regulation in castration-recurrent PC, as it is in androgen-stimulated PC and benign hyperplasia.
  • Castration-recurrent PC tissue has levels of testosterone (T) similar to androgen-stimulated benign prostate and levels of dihydrotestosterone (DHT), the most active androgen for AR activation that are approximately 10% of androgen-stimulated benign prostate.
  • These levels of tissue androgens appear capable of activating the AR since prostate-specific antigen (PSA), the classic androgen-regulated gene, is expressed at similar tissue levels in castration-recurrent and androgen-stimulated PC.
  • These startling findings suggest a paradigm shift; PC that recurs during ADT is not androgen-independent.
  • [MeSH-major] Androgens / pharmacology. Neoplasm Recurrence, Local / etiology. Neoplasms, Hormone-Dependent / etiology. Orchiectomy. Prostatic Neoplasms / drug therapy. Receptors, Androgen / physiology

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18497046.001).
  • [ISSN] 0065-2598
  • [Journal-full-title] Advances in experimental medicine and biology
  • [ISO-abbreviation] Adv. Exp. Med. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Receptors, Androgen
  • [Number-of-references] 55
  •  go-up   go-down


15. Ishikura N, Kawata H, Nishimoto A, Nakamura R, Ishii N, Aoki Y: Establishment and characterization of an androgen receptor-dependent, androgen-independent human prostate cancer cell line, LNCaP-CS10. Prostate; 2010 Apr 1;70(5):457-66
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Establishment and characterization of an androgen receptor-dependent, androgen-independent human prostate cancer cell line, LNCaP-CS10.
  • BACKGROUND: Hormone refractoriness is a lethal event for advanced prostate cancer patients, but the mechanisms of the disease are not well elucidated, especially for the so-called "outlaw" pathways of androgen receptor (AR)-dependent, androgen-independent hormone-refractory prostate cancer.
  • METHODS: Androgen-dependent prostate cancer LNCaP cells were treated with bicalutamide under an androgen-depleted condition to obtain refractory cells.
  • In the obtained cell line, LNCaP-CS10, we analyzed the effects of androgen and bicalutamide on cell growth and prostate-specific antigen (PSA) production.
  • RESULTS: In LNCaP-CS10, cell growth and PSA production were found under an androgen-depleted condition and were induced by both R1881 and bicalutamide.
  • Knocking down AR by siRNAs did suppress the growth and PSA production of LNCaP-CS10 cells in the androgen-depleted condition.
  • CONCLUSIONS: We have generated a bicalutamide-resistant and androgen-independent prostate cancer cell line, LNCaP-CS10, with outlaw activation both in vitro and in vivo.
  • The LNCaP-CS10 cell line is beneficial for elucidating outlaw pathway mechanisms and evaluating the efficacy of new therapeutics for hormone-refractory prostate cancer.
  • [MeSH-major] Anilides / pharmacology. Nitriles / pharmacology. Prostatic Neoplasms / pathology. Receptors, Androgen / physiology. Tosyl Compounds / pharmacology
  • [MeSH-minor] Animals. Cell Line, Tumor. Drug Resistance, Neoplasm. Humans. Male. Mice. Mice, SCID. Prostate-Specific Antigen / blood. Receptors, Interleukin-6 / physiology


16. Chuu CP, Hiipakka RA, Fukuchi J, Kokontis JM, Liao S: Androgen causes growth suppression and reversion of androgen-independent prostate cancer xenografts to an androgen-stimulated phenotype in athymic mice. Cancer Res; 2005 Mar 15;65(6):2082-4
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Androgen causes growth suppression and reversion of androgen-independent prostate cancer xenografts to an androgen-stimulated phenotype in athymic mice.
  • Most prostate cancer patients develop androgen-independent recurrent prostate tumors a few years after androgen ablation therapy.
  • Previously, we reported that androgen suppresses the growth of androgen-independent LNCaP prostate tumor cells both in vitro and in vivo.
  • In cell culture, androgen receptor (AR)-rich androgen-independent LNCaP 104-R1 cells adapt to growth suppression by androgen and then their growth is androgen stimulated.
  • Because maintaining androgen dependency of prostate tumor cells should prolong the usefulness of androgen ablation therapy, we determined if androgen-independent prostate tumors would revert to an androgen-stimulated phenotype in vivo upon androgen treatment.
  • Growth of the LNCaP 104-R1 tumors was suppressed by androgen, but tumors then adapted to suppression by androgen and growth became androgen stimulated.
  • Tumor AR and prostate-specific antigen mRNA and protein were initially high in 104-R1 tumors but decreased during adaptation.
  • Subsequent removal of androgen decreased the serum prostate-specific antigen level further and stopped the growth of the adapted tumors.
  • Because androgen caused growth suppression and then reversion of androgen-independent tumors to an androgen-stimulated phenotype and because the growth of androgen-stimulated tumors could be restrained by androgen ablation, these results suggest a novel therapy for AR-positive androgen-independent prostate cancer.


17. Yang Q, Titus MA, Fung KM, Lin HK: 5alpha-androstane-3alpha,17beta-diol supports human prostate cancer cell survival and proliferation through androgen receptor-independent signaling pathways: implication of androgen-independent prostate cancer progression. J Cell Biochem; 2008 Aug 1;104(5):1612-24
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 5alpha-androstane-3alpha,17beta-diol supports human prostate cancer cell survival and proliferation through androgen receptor-independent signaling pathways: implication of androgen-independent prostate cancer progression.
  • Androgen and androgen receptor (AR) are involved in growth of normal prostate and development of prostatic diseases including prostate cancer.
  • Androgen deprivation therapy is used for treating advanced prostate cancer.
  • Unfortunately, the majority of patients with prostate cancer eventually advance to androgen-independent states and no longer respond to the therapy.
  • In addition to the potent androgens, 5alpha-androstane-3alpha,17beta-diol (3alpha-diol), reduced from 5alpha-DHT through 3alpha-hydroxysteroid dehydrogenases (3alpha-HSDs), activated signaling may represent a novel pathway responsible for the progression to androgen-independent prostate cancer.
  • Androgen sensitive human prostate cancer LNCaP cells were used to compare 5alpha-DHT and 3alpha-diol activated androgenic effects.
  • More significantly, 3alpha-diol, but not 5alpha-DHT, supported AR-silenced LNCaP cells and AR negative prostate cancer PC-3 cell proliferation.
  • 3alpha-diol-activated androgenic effects in prostate cells cannot be attributed to the accumulation of 5alpha-DHT, since 5alpha-DHT formation was not detected following 3alpha-diol administration.
  • Potential accumulation of 3alpha-diol, as a result of elevated 3alpha-HSD expression in cancerous prostate, may continue to support prostate cancer growth in the presence of androgen deprivation.
  • Future therapeutic strategies for treating advanced prostate cancer might need to target reductive 3alpha-HSD to block intraprostatic 3alpha-diol accumulation.
  • [MeSH-minor] Apoptosis / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Cell Survival / drug effects. Cytoplasm / drug effects. Dihydrotestosterone / pharmacology. Disease Progression. Drug Screening Assays, Antitumor. Gene Expression Regulation, Neoplastic / drug effects. Genes, Neoplasm. Humans. Male. Models, Biological. Phosphorylation / drug effects. Proto-Oncogene Proteins c-akt / metabolism. RNA, Small Interfering / metabolism. Receptors, Androgen / metabolism. Time Factors. beta Catenin / metabolism

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • 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 = 18320593.001).
  • [ISSN] 1097-4644
  • [Journal-full-title] Journal of cellular biochemistry
  • [ISO-abbreviation] J. Cell. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AR protein, human; 0 / RNA, Small Interfering; 0 / Receptors, Androgen; 0 / beta Catenin; 08J2K08A3Y / Dihydrotestosterone; 25126-76-5 / Androstane-3,17-diol; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
  •  go-up   go-down


18. Kikugawa T, Kinugasa Y, Shiraishi K, Nanba D, Nakashiro K, Tanji N, Yokoyama M, Higashiyama S: PLZF regulates Pbx1 transcription and Pbx1-HoxC8 complex leads to androgen-independent prostate cancer proliferation. Prostate; 2006 Jul 1;66(10):1092-9
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] PLZF regulates Pbx1 transcription and Pbx1-HoxC8 complex leads to androgen-independent prostate cancer proliferation.
  • BACKGROUND: Promyelocytic leukemia zinc finger (PLZF) protein, a transcriptional repressor and negative regulator of the cell cycle, has been characterized as a prostatic androgen-responsive gene.
  • DU145 cells show androgen-independent growth and lack PLZF gene expression.
  • Androgen receptor (AR)-expressing DU145 cells recovered androgen-dependent PLZF expression and subsequent repression of Pbx1 expression.
  • Immunoprecipitation of Pbx1 in DU145 cells revealed a Pbx1-HoxC8 heterocomplex. siRNAs for Pbx1 and HoxC8 knocked downexpression of each, and this suppressed androgen-independent cell growth.
  • CONCLUSIONS: Androgen-independent cell line DU145 cells lack PLZF gene expression, resulting in the upregulation of Pbx1 and HoxC8 expression.
  • The Pbx1-HoxC8 heterocomplex may lead to androgen-independent growth in prostate cancer.
  • [MeSH-minor] Blotting, Western. Cell Cycle / genetics. Cell Cycle / physiology. Cell Line, Tumor. Cell Proliferation. DNA, Neoplasm / analysis. DNA, Neoplasm / genetics. Down-Regulation. Gene Expression Profiling. Gene Expression Regulation, Neoplastic / drug effects. Gene Expression Regulation, Neoplastic / physiology. Genes, Tumor Suppressor / physiology. Humans. Kruppel-Like Transcription Factors. Male. Oligonucleotide Array Sequence Analysis. Protein Binding. RNA, Small Interfering / pharmacology. Reverse Transcriptase Polymerase Chain Reaction. Transcription, Genetic / physiology. Transfection

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2005 Wiley-Liss, Inc.
  • (PMID = 16637071.001).
  • [ISSN] 0270-4137
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / DNA, Neoplasm; 0 / DNA-Binding Proteins; 0 / HOXC8 protein, human; 0 / Homeodomain Proteins; 0 / Kruppel-Like Transcription Factors; 0 / Proto-Oncogene Proteins; 0 / RNA, Small Interfering; 0 / Transcription Factors; 0 / pbx1 protein, human; 147855-37-6 / ZBTB16 protein, human
  •  go-up   go-down


19. Li Y, Li CX, Ye H, Chen F, Melamed J, Peng Y, Liu J, Wang Z, Tsou HC, Wei J, Walden P, Garabedian MJ, Lee P: Decrease in stromal androgen receptor associates with androgen-independent disease and promotes prostate cancer cell proliferation and invasion. J Cell Mol Med; 2008 Dec;12(6B):2790-8
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Decrease in stromal androgen receptor associates with androgen-independent disease and promotes prostate cancer cell proliferation and invasion.
  • Androgen receptor (AR) is expressed in both stromal and epithelial cells of the prostate.
  • The majority of studies on AR expression and function in prostate cancer is focused on malignant epithelial cells rather than stromal cells.
  • In this study, we examined the levels of stromal AR in androgen-dependent and -independent prostate cancer and the function of stromal AR in prostate cancer growth and invasion.
  • We showed that stromal AR levels were decreased in the areas surrounding cancerous tissue, especially in androgen-independent cancer.
  • Using two telomerase-immortalized human stromal cell lines, one AR-positive and the other AR-negative, we demonstrated that stromal cells lacking AR stimulated cell proliferation of co-cultured prostate cancer cells in vitro and enhanced tumour growth in vivo when co-injected with PC3 epithelial cells in nude mice.
  • In contrast, stromal cells expressing AR suppressed prostate cancer growth in vitro and in vivo.
  • These results indicate a negative regulation of prostate cancer growth and invasion by stromal AR.
  • This provides potentially new mechanistic insights into the failure of androgen ablation therapy, and the reactivation of stromal AR could be a novel therapeutic approach for treating hormone refractory prostate cancer.

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18266956.001).
  • [ISSN] 1582-1838
  • [Journal-full-title] Journal of cellular and molecular medicine
  • [ISO-abbreviation] J. Cell. Mol. Med.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA083639; United States / NCI NIH HHS / CA / R01 CA131183; United States / NIDDK NIH HHS / DK / R01 DK058024; United States / NIDDK NIH HHS / DK / DK058024
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AR protein, human; 0 / Androgens; 0 / Receptors, Androgen; EC 2.7.7.49 / TERT protein, human; EC 2.7.7.49 / Telomerase
  • [Other-IDs] NLM/ PMC3828892
  •  go-up   go-down


20. Chau CH, Permenter MG, Steinberg SM, Retter AS, Dahut WL, Price DK, Figg WD: Polymorphism in the hypoxia-inducible factor 1alpha gene may confer susceptibility to androgen-independent prostate cancer. Cancer Biol Ther; 2005 Nov;4(11):1222-5
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Polymorphism in the hypoxia-inducible factor 1alpha gene may confer susceptibility to androgen-independent prostate cancer.
  • The role of this transcription factor in prostate cancer development and its transition to a metastatic and androgen refractory state remains to be elucidated.
  • Previous reports have identified the existence of single nucleotide polymorphisms (SNPs) in the oxygen-dependent degradation domain of the HIF-1alpha gene in renal cell carcinoma, head and neck squamous cell carcinoma, and androgen-independent prostate cancer (AIPC).
  • Studies in prostate cancer, however, are variable and limited in the number of cases assessed.
  • [MeSH-minor] Case-Control Studies. DNA, Neoplasm / analysis. DNA, Neoplasm / genetics. Disease Susceptibility. Humans. Male

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16205110.001).
  • [ISSN] 1538-4047
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / DNA, Neoplasm; 0 / Hypoxia-Inducible Factor 1
  •  go-up   go-down


21. Zhu X, Ning JY, You JF, Wang JL, Cui XL, Fang WG, Zheng J: [Biological implications of the inhibition of survivin by RNA interference in human androgen-independent prostate carcinoma with highly metastatic potential]. Zhonghua Bing Li Xue Za Zhi; 2006 Sep;35(9):549-54
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] [Biological implications of the inhibition of survivin by RNA interference in human androgen-independent prostate carcinoma with highly metastatic potential].
  • OBJECTIVE: To determine the expression level of survivin in androgen-independent prostate carcinoma, and to investigate the biological role of survivin in invasion and metastasis of androgen-independent prostate carcinoma.
  • The biological effects were observed, including anchorage-independent growth, in vitro invasion by soft agar colony formation and Boyden chamber assay, and also in vivo tumorigenesis in nude mice.
  • The growth of tumor cells was retarded by anchorage-independent growth assay.
  • CONCLUSIONS: Survivin expression is high in androgen-independent prostate cancer cells and likely may be related to the apoptosis, growth and invasion of the tumor cells.
  • Targeting the survivin pathway by RNA interference appears to be a promising approach for clinical treatment of androgen-independent prostate cancer.
  • [MeSH-major] Microtubule-Associated Proteins / genetics. Neoplasm Proteins / genetics. Prostatic Neoplasms / pathology. RNA Interference
  • [MeSH-minor] Androgens / metabolism. Animals. Apoptosis. Blotting, Western. Caspase 3 / metabolism. Cell Cycle. Cell Line. Cell Line, Tumor. Cell Proliferation. Female. Gene Expression Regulation, Neoplastic. Green Fluorescent Proteins / genetics. Green Fluorescent Proteins / metabolism. Humans. Inhibitor of Apoptosis Proteins. Male. Mice. Mice, Inbred BALB C. Mice, Nude. NIH 3T3 Cells. Neoplasm Metastasis. Neoplasm Transplantation. Transfection. Transplantation, Heterologous

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17134550.001).
  • [ISSN] 0529-5807
  • [Journal-full-title] Zhonghua bing li xue za zhi = Chinese journal of pathology
  • [ISO-abbreviation] Zhonghua Bing Li Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Androgens; 0 / BIRC5 protein, human; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 147336-22-9 / Green Fluorescent Proteins; EC 3.4.22.- / Caspase 3
  •  go-up   go-down


22. Seaton A, Scullin P, Maxwell PJ, Wilson C, Pettigrew J, Gallagher R, O'Sullivan JM, Johnston PG, Waugh DJ: Interleukin-8 signaling promotes androgen-independent proliferation of prostate cancer cells via induction of androgen receptor expression and activation. Carcinogenesis; 2008 Jun;29(6):1148-56
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Interleukin-8 signaling promotes androgen-independent proliferation of prostate cancer cells via induction of androgen receptor expression and activation.
  • The aim of our study was to assess the importance of the CXC chemokine and interleukin (IL)-8 in promoting the transition of prostate cancer (CaP) to the androgen-independent state.
  • Stimulation of the androgen-dependent cell lines, LNCaP and 22Rv1, with exogenous recombinant human interleukin-8 (rh-IL-8) increased androgen receptor (AR) gene expression at the messenger RNA (mRNA) and protein level, assessed by quantitative polymerase chain reaction and immunoblotting, respectively.
  • Using an androgen response element-luciferase construct, we demonstrated that rh-IL-8 treatment also resulted in increased AR transcriptional activity in both these cell lines, and a subsequent upregulation of prostate-specific antigen and cyclin-dependent kinase 2 mRNA transcript levels in LNCaP cells.
  • Our data show that IL-8 signaling increases AR expression and promotes ligand-independent activation of this receptor in two androgen-dependent cell lines, describing two mechanisms by which this chemokine may assist in promoting the transition of CaP to the androgen-independent state.
  • [MeSH-major] Drug Resistance, Neoplasm / physiology. Interleukin-8 / metabolism. Prostatic Neoplasms / metabolism. Receptors, Androgen / metabolism. Signal Transduction / physiology
  • [MeSH-minor] Androgen Antagonists / pharmacology. Anilides / pharmacology. Antineoplastic Agents, Hormonal / pharmacology. Blotting, Western. Cell Line, Tumor. Cell Proliferation / drug effects. Flow Cytometry. Humans. Male. Nitriles / pharmacology. RNA, Small Interfering. Receptors, Interleukin-8B / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Tosyl Compounds / pharmacology. Transfection

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. BICALUTAMIDE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18487223.001).
  • [ISSN] 1460-2180
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Anilides; 0 / Antineoplastic Agents, Hormonal; 0 / Interleukin-8; 0 / Nitriles; 0 / RNA, Small Interfering; 0 / Receptors, Androgen; 0 / Receptors, Interleukin-8B; 0 / Tosyl Compounds; A0Z3NAU9DP / bicalutamide
  •  go-up   go-down


23. Kalmadi S, Raghavan D: Evolving perspectives of the role of novel agents in androgen-independent prostate cancer. Indian J Urol; 2008 Jul;24(3):303-8

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Evolving perspectives of the role of novel agents in androgen-independent prostate cancer.
  • Metastatic androgen-independent prostate cancer presents an intriguing clinical challenge, with a subtle interaction between hormone-responsive and refractory tumor cell elements.
  • The treatment of advanced prostate carcinoma, which had remained stagnant for several decades following the understanding of the link between androgenic stimulation and carcinogenesis, has now started to make steady headway with chemotherapy and targeted approaches.
  • Metastatic prostate cancer is almost always treated with initial androgen deprivation, in various forms.
  • However, despite such treatment androgen-independent prostate cancer cells eventually emerge and progress to threaten life.
  • The therapeutic objectives for treatment of metastatic prostate cancer are to maintain the quality of life and prolong survival.
  • The out-dated nihilistic dogma of deferring chemotherapy until the most advanced stages in advanced prostate cancer is now falling by the wayside with the development of newer effective, tolerable agents.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Clin Oncol. 1999 Aug;17(8):2506-13 [10561316.001]
  • [Cites] Endocrinology. 1993 May;132(5):1952-60 [7682937.001]
  • [Cites] Cancer. 1992 Jul 1;70(1 Suppl):254-68 [1350941.001]
  • [Cites] CA Cancer J Clin. 1972 Jul-Aug;22(4):232-40 [4625049.001]
  • [Cites] N Engl J Med. 1971 Nov 18;285(21):1182-6 [4938153.001]
  • [Cites] N Engl J Med. 2004 Oct 7;351(15):1513-20 [15470214.001]
  • [Cites] N Engl J Med. 2004 Oct 7;351(15):1502-12 [15470213.001]
  • [Cites] Br J Cancer. 2004 Sep 13;91(6):1003-4 [15475939.001]
  • [Cites] J Clin Oncol. 2004 Jul 1;22(13):2532-9 [15226321.001]
  • [Cites] Cancer. 2003 Dec 1;98(11):2362-7 [14635070.001]
  • [Cites] J Urol. 2002 Dec;168(6):2439-43 [12441935.001]
  • [Cites] J Urol. 2003 Oct;170(4 Pt 1):1363-9 [14501770.001]
  • [Cites] J Clin Oncol. 2002 Jul 15;20(14):3072-80 [12118020.001]
  • [Cites] J Natl Cancer Inst. 2000 Sep 6;92(17):1367-9 [10974062.001]
  • [Cites] J Natl Cancer Inst. 2000 Feb 2;92(3):205-16 [10655437.001]
  • [Cites] J Clin Oncol. 1999 Nov;17(11):3461-7 [10550143.001]
  • [Cites] Drugs Today (Barc). 2007 Feb;43(2):85-95 [17353946.001]
  • [Cites] Urology. 2006 Aug;68(2):244-8 [16904427.001]
  • [Cites] Hematol Oncol Clin North Am. 2006 Aug;20(4):965-83, xi [16861126.001]
  • [Cites] J Natl Cancer Inst. 2006 Apr 19;98(8):516-21 [16622120.001]
  • [Cites] J Urol. 2005 Nov;174(5):1808-13; discussion 1813 [16217292.001]
  • [Cites] Oncology. 2005;68(1):2-9 [15741753.001]
  • [Cites] J Clin Oncol. 2005 Mar 1;23(7):1439-46 [15735119.001]
  • [Cites] J Clin Oncol. 1996 Jun;14(6):1756-64 [8656243.001]
  • [Cites] Cancer Res. 1996 Feb 15;56(4):663-8 [8630991.001]
  • [Cites] Semin Oncol. 1994 Oct;21(5):613-9 [7939752.001]
  • (PMID = 19468458.001).
  • [ISSN] 0970-1591
  • [Journal-full-title] Indian journal of urology : IJU : journal of the Urological Society of India
  • [ISO-abbreviation] Indian J Urol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Other-IDs] NLM/ PMC2684340
  • [Keywords] NOTNLM ; Prostate neoplasm / bio-markers / chemotherapy / quality of life
  •  go-up   go-down


24. Deo DD, Rao AP, Bose SS, Ouhtit A, Baliga SB, Rao SA, Trock BJ, Thouta R, Raj MH, Rao PN: Differential effects of leptin on the invasive potential of androgen-dependent and -independent prostate carcinoma cells. J Biomed Biotechnol; 2008;2008:163902
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Differential effects of leptin on the invasive potential of androgen-dependent and -independent prostate carcinoma cells.
  • Obesity has been linked with an increased risk of prostate cancer.
  • The rationale of the study was to determine the impact of leptin on the metastatic potential of androgen-sensitive (LNCaP) cells as well as androgen-insensitive (PC-3 and DU-145) cells.
  • At a concentration of 200 nm, LNCaP cells showed a significant increase (20% above control; P < .0001) in cellular proliferation without any effect on androgen-insensitive cells.
  • Furthermore, exposure to leptin caused a significant (P < .01 to P < .0001) dose-dependent decrease in migration and invasion of PC3 and Du-145 prostate carcinoma cell lines.
  • At the molecular level, exposure of androgen-independent prostate cancer cells to leptin stimulates the phosphorylation of MAPK at early time point as well as the transcription factor STAT3, suggesting the activation of the intracellular signaling cascade upon leptin binding to its cognate receptor.
  • Taken together, these results suggest that leptin mediates the invasive potential of prostate carcinoma cells, and that this effect is dependent on their androgen sensitivity.

  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Surg Res. 2004 Feb;116(2):337-49 [15013374.001]
  • [Cites] J Biol Chem. 2003 Oct 24;278(43):42660-7 [12902351.001]
  • [Cites] Science. 1995 Jul 28;269(5223):540-3 [7624776.001]
  • [Cites] Science. 1995 Jul 28;269(5223):546-9 [7624778.001]
  • [Cites] Bioessays. 1996 Feb;18(2):95-8 [8851041.001]
  • [Cites] J Biol Chem. 1997 Mar 7;272(10):6093-6 [9102398.001]
  • [Cites] Int J Urol. 1998 Mar;5(2):134-7 [9559838.001]
  • [Cites] Science. 1998 Sep 11;281(5383):1683-6 [9733517.001]
  • [Cites] Lipids. 1998 Nov;33(11):1055-9 [9870899.001]
  • [Cites] Am J Surg. 2004 Nov;188(5):560-5 [15546570.001]
  • [Cites] J Urol. 2005 Mar;173(3):773-6 [15711267.001]
  • [Cites] Clin Cancer Res. 2005 Oct 1;11(19 Pt 1):6889-94 [16203779.001]
  • [Cites] Biochem Biophys Res Commun. 2006 Feb 24;340(4):1158-66 [16403434.001]
  • [Cites] Endocr Relat Cancer. 2006 Jun;13(2):629-40 [16728588.001]
  • [Cites] Pathol Oncol Res. 2006;12(2):69-72 [16799705.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2006 Jul;15(7):1331-5 [16835332.001]
  • [Cites] Free Radic Biol Med. 2007 Jan 15;42(2):299-310 [17189835.001]
  • [Cites] Prostate. 2000 Feb 15;42(3):239-42 [10639195.001]
  • [Cites] J Biol Chem. 2000 May 12;275(19):14563-72 [10799542.001]
  • [Cites] FASEB J. 2000 Nov;14(14):2329-38 [11053255.001]
  • [Cites] Prostate. 2001 Jan 1;46(1):62-7 [11170133.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Mar;86(3):1341-5 [11238530.001]
  • [Cites] Cancer Res. 2001 Apr 15;61(8):3276-80 [11309279.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2001 Apr;10(4):345-53 [11319175.001]
  • [Cites] J Natl Cancer Inst. 2001 May 16;93(10):783-9 [11353789.001]
  • [Cites] Cancer Causes Control. 2001 Sep;12(7):627-33 [11552710.001]
  • [Cites] Urology. 2001 Nov;58(5):723-8 [11711349.001]
  • [Cites] Clin Cancer Res. 2002 Apr;8(4):945-54 [11948098.001]
  • [Cites] N Engl J Med. 2003 Apr 24;348(17):1625-38 [12711737.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2003 May;12(5):474-5 [12750247.001]
  • [Cites] J Surg Res. 2004 May 1;118(1):71-82 [15093720.001]
  • (PMID = 18584049.001).
  • [ISSN] 1110-7251
  • [Journal-full-title] Journal of biomedicine & biotechnology
  • [ISO-abbreviation] J. Biomed. Biotechnol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA 918858
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Leptin
  • [Other-IDs] NLM/ PMC2435597
  •  go-up   go-down


25. Mishra DK, Chen Z, Wu Y, Sarkissyan M, Koeffler HP, Vadgama JV: Global methylation pattern of genes in androgen-sensitive and androgen-independent prostate cancer cells. Mol Cancer Ther; 2010 Jan;9(1):33-45
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Global methylation pattern of genes in androgen-sensitive and androgen-independent prostate cancer cells.
  • We have characterized the promoter methylation profile of 82 genes in three prostate cancer cell lines (LNCaP, PC3, and DU145) and two normal prostate cell lines (RWPE1 and RWPE2).
  • We analyzed methylation profile in normal (RWPE1) versus cancerous cells and androgen receptor (AR)-sensitive (LNCaP) versus AR-negative cells (DU145 and PC3).
  • Our study shows that >50% of the genes were hypermethylated in prostate cancer cells compared with 13% in normal cell lines.
  • Relative methylation pattern shows that most of these genes were methylated from 5-fold to >10-fold compared with the normal prostate cells.
  • In summary, our study identified candidate genes that are methylated in prostate cancer.

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. DOCETAXEL .
  • Hazardous Substances Data Bank. AZACITIDINE .
  • 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 .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cancer Res. 2001 Apr 15;61(8):3225-9 [11309270.001]
  • [Cites] Cancer Res. 2000 Nov 15;60(22):6236-42 [11103776.001]
  • [Cites] Clin Cancer Res. 2002 Feb;8(2):514-9 [11839671.001]
  • [Cites] Am J Pathol. 2002 Apr;160(4):1207-14 [11943705.001]
  • [Cites] Nat Rev Cancer. 2002 Mar;2(3):210-9 [11990857.001]
  • [Cites] Nat Rev Genet. 2002 Jun;3(6):415-28 [12042769.001]
  • [Cites] Oncogene. 2002 Aug 12;21(35):5427-40 [12154405.001]
  • [Cites] Int J Cancer. 2003 Sep 1;106(3):382-7 [12845678.001]
  • [Cites] N Engl J Med. 2003 Nov 20;349(21):2042-54 [14627790.001]
  • [Cites] J Pathol. 2004 Feb;202(2):233-40 [14743506.001]
  • [Cites] Int J Mol Med. 2004 Mar;13(3):413-7 [14767572.001]
  • [Cites] Cancer Res. 2004 Mar 15;64(6):1975-86 [15026333.001]
  • [Cites] J Clin Pathol. 2004 Aug;57(8):872-6 [15280411.001]
  • [Cites] Int J Cancer. 2004 Dec 10;112(5):840-5 [15386391.001]
  • [Cites] Nucleic Acids Res. 1980 Oct 24;8(20):4777-90 [7443525.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Sep 3;93(18):9821-6 [8790415.001]
  • [Cites] Cancer. 1997 Apr 1;79(7):1370-80 [9083160.001]
  • [Cites] Nat Genet. 1999 Feb;21(2):163-7 [9988266.001]
  • [Cites] Clin Cancer Res. 2004 Dec 15;10(24):8472-8 [15623627.001]
  • [Cites] Carcinogenesis. 2005 Feb;26(2):471-9 [15485992.001]
  • [Cites] JAMA. 2005 Sep 14;294(10):1255-9 [16160134.001]
  • [Cites] Clin Cancer Res. 2005 Sep 15;11(18):6582-8 [16166436.001]
  • [Cites] Neoplasia. 2005 Aug;7(8):748-60 [16207477.001]
  • [Cites] Cancer. 2006 Jan 1;106(1):79-86 [16323173.001]
  • [Cites] J Natl Cancer Inst. 2006 Feb 1;98(3):154-5 [16449669.001]
  • [Cites] Mol Cancer. 2006;5:28 [16848908.001]
  • [Cites] Trends Immunol. 2006 Sep;27(9):405-12 [16870508.001]
  • [Cites] Nat Genet. 2000 Feb;24(2):132-8 [10655057.001]
  • [Cites] Prostate. 2001 Sep 15;48(4):248-53 [11536304.001]
  • (PMID = 20053773.001).
  • [ISSN] 1538-8514
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK067015-01; United States / NIDDK NIH HHS / DK / R25 DK067015-01; United States / NIDDK NIH HHS / DK / R25 DK067015; United States / NCI NIH HHS / CA / CA15083-25S3; United States / NCI NIH HHS / CA / U56 CA101599; United States / NCI NIH HHS / CA / U56 CA101599-01; United States / NCI NIH HHS / CA / CA101599-01; United States / NIDDK NIH HHS / DK / R25DK067015-01; United States / NCI NIH HHS / CA / P30 CA015083; United States / NCI NIH HHS / CA / U54 CA143931; United States / NCI NIH HHS / CA / U54 CA143931-01; United States / NCI NIH HHS / CA / CA143931-01; United States / NCI NIH HHS / CA / N01 CA015083
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ABCB1 protein, human; 0 / Androgens; 0 / Neoplasm Proteins; 0 / P-Glycoprotein; 0 / P-Glycoproteins; 0 / RNA, Messenger; 0 / Taxoids; 15H5577CQD / docetaxel; M801H13NRU / Azacitidine
  • [Other-IDs] NLM/ NIHMS159165; NLM/ PMC2806502
  •  go-up   go-down


26. Morote J, Esquena S, Abascal JM, Trilla E, Cecchini L, Raventós CX, Orsola A, Planas J, Catalán R, Reventós J: Usefulness of prostate-specific antigen nadir as predictor of androgen-independent progression of metastatic prostate cancer. Int J Biol Markers; 2005 Oct-Dec;20(4):209-16
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Usefulness of prostate-specific antigen nadir as predictor of androgen-independent progression of metastatic prostate cancer.
  • The objective of this study was to analyze the value of the nadir level of prostate-specific antigen (PSA) to predict androgen-independent progression (AIP) in metastatic prostate cancer patients after androgen deprivation therapy.
  • In a group of 185 metastatic prostate cancer patients who received androgen deprivation therapy serum PSA was determined every three months until AIP occurred.
  • Multiple regression analysis was performed to define independent clinical and PSA-related predictors of AIP.
  • Independent predictors of the duration of AIP-free survival (less than 12 months versus more than 12 months) were the extent of bone involvement (six or fewer hot spots versus more than six) with an odds ratio (O.R.) of 3.95, Gleason score (7 or less versus more than 7) with an O.R. of 3.47, and PSA nadir (2 microg/L or less versus more than 2 microg/L) with an O.R. of 14.63.
  • We conclude that the PSA nadir seems to be a good predictor of AIP in patients with metastatic prostate cancer after androgen deprivation therapy.
  • Time to PSA nadir, extent of bone involvement and Gleason score are also independent predictors.
  • The combination of these prognostic factors allows to stratify metastatic prostate cancer patients for the prediction of AIP.
  • [MeSH-major] Biomarkers, Tumor / blood. Neoplasm Metastasis / pathology. Prostate-Specific Antigen / blood. Prostatic Neoplasms / blood. Prostatic Neoplasms / pathology


27. Shi XB, Xue L, Zou JX, Gandour-Edwards R, Chen H, deVere White RW: Prolonged androgen receptor loading onto chromatin and the efficient recruitment of p160 coactivators contribute to androgen-independent growth of prostate cancer cells. Prostate; 2008 Dec 1;68(16):1816-26
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prolonged androgen receptor loading onto chromatin and the efficient recruitment of p160 coactivators contribute to androgen-independent growth of prostate cancer cells.
  • BACKGROUND: Growth of most ablation-resistant prostate cancers (CaPs) is dependent on androgen receptor (AR) activity in chromatin, but cancer cells in these tumors have acquired altered AR activation.
  • The purpose of this study was to assess the AR chromatin loading in an androgen-depleted environment.
  • METHODS: The expression of PSA in androgen-resistant CaP cells was determined using RT-PCR and Western blot analysis.
  • In order to investigate the binding of the AR to the PSA gene regulatory regions, chromatin immunoprecipitation (ChIP) was performed in the androgen-independent cds2 cell line in the presence or absence of androgens.
  • Furthermore, androgen-resistant CaP cells highly expressed both AR and the p160 coactivators and the AR was able to recruit TIF2.
  • CONCLUSION: Prolonged AR localization to the regulatory regions of AR targeted genes and the recruitment of p160 coactivators are a potential mechanism leading to androgen-independent activation of the AR.
  • [MeSH-major] Adenocarcinoma / metabolism. Androgens / metabolism. Cell Proliferation. Chromatin / metabolism. Prostatic Neoplasms / metabolism. Receptors, Androgen / metabolism. rho-Associated Kinases / metabolism
  • [MeSH-minor] Anilides / pharmacology. Antineoplastic Agents / pharmacology. Cell Line, Tumor. DNA, Neoplasm / genetics. Histone Acetyltransferases / metabolism. Humans. Male. Nitriles / pharmacology. Nuclear Receptor Coactivator 1. Nuclear Receptor Coactivator 2 / genetics. Nuclear Receptor Coactivator 2 / metabolism. Oligonucleotide Array Sequence Analysis. Prostate-Specific Antigen / metabolism. Protein Binding. Tosyl Compounds / pharmacology. Transcription Factors / metabolism

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. BICALUTAMIDE .
  • 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 CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18780293.001).
  • [ISSN] 1097-0045
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA77662-NCI; United States / NCI NIH HHS / CA / P30 CA93373-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Anilides; 0 / Antineoplastic Agents; 0 / Chromatin; 0 / DNA, Neoplasm; 0 / NCOA2 protein, human; 0 / Nitriles; 0 / Nuclear Receptor Coactivator 2; 0 / ROCK1 protein, human; 0 / Receptors, Androgen; 0 / Tosyl Compounds; 0 / Transcription Factors; A0Z3NAU9DP / bicalutamide; EC 2.3.1.48 / Histone Acetyltransferases; EC 2.3.1.48 / NCOA1 protein, human; EC 2.3.1.48 / Nuclear Receptor Coactivator 1; EC 2.7.11.1 / rho-Associated Kinases; EC 3.4.21.77 / Prostate-Specific Antigen
  •  go-up   go-down


28. Sinha R, Pinto JT, Facompre N, Kilheffer J, Baatz JE, El-Bayoumy K: Effects of naturally occurring and synthetic organoselenium compounds on protein profiling in androgen responsive and androgen independent human prostate cancer cells. Nutr Cancer; 2008;60(2):267-75
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effects of naturally occurring and synthetic organoselenium compounds on protein profiling in androgen responsive and androgen independent human prostate cancer cells.
  • Prostate cancer represents a major clinical public health challenge.
  • Both epidemiological and clinical intervention studies support the protective role of selenium against development of prostate cancer.
  • Thus, in the present investigation using androgen responsive (AR) lymph node carcinoma of the prostate (LNCaP) and its androgen-independent clone (AI) LNCaP C4-2 human prostate cancer cells, we compared the effects of selenomethionine (SM) and 1,4-phenylenebis(methylene)selenocyanate (p-XSC) on cell growth, DNA synthesis, and on proteomic profiles. p-XSC (5-20 microM) significantly inhibited cell growth in both cell types in a dose-dependent manner; SM was also effective but at much higher doses (50-100 microM).
  • This is the first report showing that SM and p-XSC are capable of altering these proteins; their roles in prostate cancer prevention warrant further investigations.
  • [MeSH-major] Androgens / pharmacology. Gene Expression Profiling. Neoplasm Proteins / genetics. Neoplasms, Hormone-Dependent / pathology. Organoselenium Compounds / pharmacology. Prostatic Neoplasms / pathology
  • [MeSH-minor] Blotting, Western. Dose-Response Relationship, Drug. Electrophoresis, Gel, Two-Dimensional. Gene Expression Regulation, Neoplastic / drug effects. Humans. Male. Mass Spectrometry. Oligonucleotide Array Sequence Analysis. RNA, Messenger / metabolism. Receptors, Androgen / metabolism. Tritium. Tumor Cells, Cultured

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. TRITIUM, RADIOACTIVE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18444160.001).
  • [ISSN] 0163-5581
  • [Journal-full-title] Nutrition and cancer
  • [ISO-abbreviation] Nutr Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA111842; United States / NCI NIH HHS / CA / CA29502; United States / NCI NIH HHS / CA / CA89815
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Neoplasm Proteins; 0 / Organoselenium Compounds; 0 / RNA, Messenger; 0 / Receptors, Androgen; 10028-17-8 / Tritium
  •  go-up   go-down


29. Sinibaldi VJ, Elza-Brown K, Schmidt J, Eisenberger MA, Rosenbaum E, Denmeade SR, Pili R, Walczak J, Baker SD, Zahurak M, Carducci MA: Phase II evaluation of docetaxel plus exisulind in patients with androgen independent prostate carcinoma. Am J Clin Oncol; 2006 Aug;29(4):395-8
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase II evaluation of docetaxel plus exisulind in patients with androgen independent prostate carcinoma.
  • OBJECTIVES: In this phase II study, the combination of docetaxel and exisulind (a GMP phosphodiesterase inhibitor) was given to patients with metastatic androgen independent prostate cancer (AIPC) to establish efficacy, assess toxicity, and determine pharmacokinetics of docetaxel administered alone and in combination with exisulind.
  • Only 3 out of 14 patients (21.4%) had a 50% decline in prostate specific antigen (PSA) level that lasted > or =4 weeks; 1 out of 14 patients (7%) had a lymph node response.
  • [MeSH-minor] Aged. Humans. Male. Middle Aged. Neoplasm Metastasis. Sulindac / administration & dosage. Sulindac / analogs & derivatives. Sulindac / pharmacokinetics. Survival Analysis. Taxoids / administration & dosage. Taxoids / pharmacokinetics

  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. DOCETAXEL .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16891869.001).
  • [ISSN] 1537-453X
  • [Journal-full-title] American journal of clinical oncology
  • [ISO-abbreviation] Am. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Taxoids; 15H5577CQD / docetaxel; 184SNS8VUH / Sulindac; K619IIG2R9 / sulindac sulfone
  •  go-up   go-down


30. Xu XF, Zhou SW, Zhang X, Ye ZQ, Zhang JH, Ma X, Zheng T, Li HZ: Prostate androgen-regulated gene: a novel potential target for androgen-independent prostate cancer therapy. Asian J Androl; 2006 Jul;8(4):455-62
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prostate androgen-regulated gene: a novel potential target for androgen-independent prostate cancer therapy.
  • AIM: To investigate the involvement of the prostate androgen-regulated (PAR) gene in the androgen receptor (AR) signaling pathway and the malignant phenotype of androgen-independent prostate cancer (PCa) cells.
  • Androgen and anti-androgen effects on PAR expression were evaluated by RT-PCR in LNCaP, PC3 cells and PC3 cells stably transfected with vector containing wild-type AR.
  • To determine the importance of PAR in the malignant proliferation of androgen-independent PCa cells, we used small interfering RNA (siRNA) transfection to knock down the expression of the gene in PC3 cells.
  • The reintroduction of AR into PC3 cells by stable transfection restored the androgen effect on PAR upregulation.
  • CONCLUSION: Because of the possibility that PAR is downstream from the AR, and because of its contribution to malignant proliferation in androgen-independent PCa cells, the gene could be a potential therapeutic target for androgen-independent PCa with AR signaling pathway alteration.
  • [MeSH-major] Gene Expression Regulation / physiology. Membrane Proteins / genetics. Neoplasm Proteins / genetics. Prostatic Neoplasms / drug therapy

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16763722.001).
  • [ISSN] 1008-682X
  • [Journal-full-title] Asian journal of andrology
  • [ISO-abbreviation] Asian J. Androl.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / DNA Primers; 0 / JTB protein, human; 0 / Membrane Proteins; 0 / Neoplasm Proteins; 0 / RNA, Small Interfering
  •  go-up   go-down


31. Yuan X, Li T, Wang H, Zhang T, Barua M, Borgesi RA, Bubley GJ, Lu ML, Balk SP: Androgen receptor remains critical for cell-cycle progression in androgen-independent CWR22 prostate cancer cells. Am J Pathol; 2006 Aug;169(2):682-96
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Androgen receptor remains critical for cell-cycle progression in androgen-independent CWR22 prostate cancer cells.
  • The majority of prostate cancers (PCa) that relapse after androgen deprivation therapy (androgen-independent PCa) continue to express androgen receptor (AR).
  • To study the functional importance of AR in these tumors, we derived androgen-independent CWR22 PCa xenografts in castrated mice and generated a cell line from one of these xenografts (CWR22R3).
  • Similarly to androgen-independent PCa in patients, the relapsed xenografts and cell line expressed AR and were resistant to treatment with bicalutamide.
  • Transfections with androgen-regulated reporter genes further indicated that the cells lacked androgen-independent AR transcriptional activity and were not hypersensitive to low androgen concentrations despite constitutive activation of the Erk/MAP kinases.
  • Nonetheless, AR remained essential for androgen-independent growth because retroviral shRNA-mediated AR down-regulation resulted in marked long-term growth suppression.
  • These results reveal a potentially critical function of AR in androgen-independent PCa that is distinct from its previously described transcriptional or nontranscriptional functions.

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. BICALUTAMIDE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cancer Res. 1999 Jun 1;59(11):2511-5 [10363963.001]
  • [Cites] J Steroid Biochem Mol Biol. 2005 Aug;96(3-4):251-8 [15982869.001]
  • [Cites] Cancer Res. 1999 Sep 1;59(17):4291-6 [10485474.001]
  • [Cites] J Biol Chem. 1998 Nov 20;273(47):31528-33 [9813067.001]
  • [Cites] Cancer Res. 1998 Dec 15;58(24):5718-24 [9865729.001]
  • [Cites] Clin Cancer Res. 1997 Aug;3(8):1383-8 [9815822.001]
  • [Cites] J Urol. 1999 Dec;162(6):2192-9 [10569618.001]
  • [Cites] Oncogene. 1999 Nov 4;18(46):6322-9 [10597231.001]
  • [Cites] Cell. 2001 Mar 9;104(5):719-30 [11257226.001]
  • [Cites] Cancer Res. 2001 Apr 1;61(7):2892-8 [11306464.001]
  • [Cites] Mol Endocrinol. 2001 May;15(5):765-82 [11328857.001]
  • [Cites] Cancer Res. 2001 Jun 1;61(11):4315-9 [11389051.001]
  • [Cites] J Androl. 2001 Jul-Aug;22(4):537-48 [11451350.001]
  • [Cites] J Biol Chem. 2001 Dec 7;276(49):46647-54 [11585838.001]
  • [Cites] Cancer Res. 2002 Feb 15;62(4):1008-13 [11861374.001]
  • [Cites] Nat Rev Cancer. 2001 Oct;1(1):34-45 [11900250.001]
  • [Cites] J Clin Oncol. 2002 Jul 1;20(13):3001-15 [12089231.001]
  • [Cites] J Biol Chem. 2002 Jul 19;277(29):26321-6 [12015321.001]
  • [Cites] Urology. 2002 Sep;60(3 Suppl 1):132-8; discussion 138-9 [12231070.001]
  • [Cites] Cancer Res. 2003 Apr 15;63(8):1981-9 [12702592.001]
  • [Cites] J Cell Biol. 2003 May 12;161(3):547-56 [12743104.001]
  • [Cites] Nat Genet. 2003 Jul;34(3):263-4 [12796781.001]
  • [Cites] J Clin Oncol. 2003 Jul 15;21(14):2673-8 [12860943.001]
  • [Cites] Mol Endocrinol. 2003 Sep;17(9):1726-37 [12775765.001]
  • [Cites] J Biol Chem. 2003 Oct 31;278(44):42992-3000 [12933816.001]
  • [Cites] Nat Med. 2004 Jan;10(1):33-9 [14702632.001]
  • [Cites] J Biol Chem. 2004 Feb 20;279(8):7119-30 [14662770.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Feb 17;101(7):1892-7 [14769924.001]
  • [Cites] J Clin Oncol. 2004 Mar 15;22(6):1025-33 [15020604.001]
  • [Cites] Mol Endocrinol. 2004 Apr;18(4):769-75 [14630999.001]
  • [Cites] J Biol Chem. 2004 Apr 9;279(15):14579-86 [14668339.001]
  • [Cites] Steroids. 2004 Aug;69(8-9):517-22 [15288763.001]
  • [Cites] Mol Endocrinol. 1993 Dec;7(12):1541-50 [8145761.001]
  • [Cites] Cancer Res. 1994 Dec 1;54(23):6049-52 [7525052.001]
  • [Cites] N Engl J Med. 1995 May 25;332(21):1393-8 [7723794.001]
  • [Cites] Nat Genet. 1995 Apr;9(4):401-6 [7795646.001]
  • [Cites] Cancer Res. 1996 Jul 1;56(13):3042-6 [8674060.001]
  • [Cites] Cell Growth Differ. 1996 Nov;7(11):1571-8 [8930407.001]
  • [Cites] Mol Endocrinol. 1997 Apr;11(4):450-9 [9092797.001]
  • [Cites] J Clin Oncol. 1997 Aug;15(8):2928-38 [9256137.001]
  • [Cites] J Urol. 1998 Jan;159(1):149-53 [9400459.001]
  • [Cites] Oncogene. 1998 Apr 16;16(15):1913-20 [9591774.001]
  • [Cites] Mol Endocrinol. 1998 Jul;12(7):941-53 [9658399.001]
  • [Cites] Biochem Biophys Res Commun. 1998 Jul 20;248(2):361-7 [9675141.001]
  • [Cites] J Biol Chem. 1998 Aug 7;273(32):20213-22 [9685369.001]
  • [Cites] Cancer Res. 1999 Jan 15;59(2):279-84 [9927031.001]
  • [Cites] Cancer Res. 1999 May 15;59(10):2297-301 [10344732.001]
  • [Cites] Cancer Cell. 2004 Nov;6(5):517-27 [15542435.001]
  • [Cites] Mol Cancer Ther. 2005 Apr;4(4):505-15 [15827323.001]
  • [Cites] Prostate. 1999 Sep 15;41(1):7-11 [10440870.001]
  • (PMID = 16877366.001).
  • [ISSN] 0002-9440
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / K01 DK064739; United States / NIDDK NIH HHS / DK / K01-DK64739; United States / NCI NIH HHS / CA / R01-CA65647
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Anilides; 0 / Nitriles; 0 / RNA, Messenger; 0 / Receptors, Androgen; 0 / Tosyl Compounds; 0 / Transcription Factors; A0Z3NAU9DP / bicalutamide; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 3.4.21.77 / Prostate-Specific Antigen
  • [Other-IDs] NLM/ PMC1698802
  •  go-up   go-down


32. Johnson TR, Khandrika L, Kumar B, Venezia S, Koul S, Chandhoke R, Maroni P, Donohue R, Meacham RB, Koul HK: Focal adhesion kinase controls aggressive phenotype of androgen-independent prostate cancer. Mol Cancer Res; 2008 Oct;6(10):1639-48
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Focal adhesion kinase controls aggressive phenotype of androgen-independent prostate cancer.
  • In the present study, we investigated the interplay between FAK and ERK in androgen-independent prostate cancer cells (PC3 and DU145 cells).
  • Taken together, these data show, for the first time, a requirement for FAK in aggressive phenotype of prostate cancer cells; reveal interdependence of FAK and ERK1/2 for clonogenic and invasive activity of androgen-independent prostate cancer cells; suggest a role for ERK regulation of FAK in substrate-dependent survival; and show for the first time, in any cell type, the regulation of FAK expression by ERK signaling pathway.
  • [MeSH-minor] Androgens / metabolism. Anoikis. Cell Line, Tumor. Cell Proliferation. Cell Survival. Enzyme Activation. Humans. MAP Kinase Signaling System. Male. Matrix Metalloproteinase 9 / metabolism. Mitogen-Activated Protein Kinase 1 / antagonists & inhibitors. Mitogen-Activated Protein Kinase 1 / metabolism. Mitogen-Activated Protein Kinase 3 / antagonists & inhibitors. Mitogen-Activated Protein Kinase 3 / metabolism. Neoplasm Invasiveness. Phenotype. Phosphorylation. RNA, Small Interfering / metabolism. Tumor Stem Cell Assay

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • 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 .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18922979.001).
  • [ISSN] 1541-7786
  • [Journal-full-title] Molecular cancer research : MCR
  • [ISO-abbreviation] Mol. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P20 CA103680; United States / PHS HHS / / R01-54084
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / RNA, Small Interfering; EC 2.7.10.2 / Focal Adhesion Protein-Tyrosine Kinases; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 3.4.24.35 / Matrix Metalloproteinase 9
  •  go-up   go-down


33. Mehra R, Tomlins SA, Yu J, Cao X, Wang L, Menon A, Rubin MA, Pienta KJ, Shah RB, Chinnaiyan AM: Characterization of TMPRSS2-ETS gene aberrations in androgen-independent metastatic prostate cancer. Cancer Res; 2008 May 15;68(10):3584-90
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Characterization of TMPRSS2-ETS gene aberrations in androgen-independent metastatic prostate cancer.
  • Recurrent gene fusions between the androgen-regulated gene TMPRSS2 and the ETS transcription factor family members ERG, ETV1, and ETV4 have been identified as a critical event in prostate cancer development.
  • In this study, we characterized the prevalence and diversity of these rearrangements in hormone-refractory metastatic prostate cancer.
  • We used a fluorescence in situ hybridization (FISH) split probe strategy to comprehensively evaluate TMPRSS2-ETS aberrations across 97 nonosseous metastatic sites of prostate cancer from 30 rapid autopsies of men who died of androgen-independent disease.
  • The most common prostate cancer gene fusion, TMPRSS2-ERG, can be generated by the mechanism of interstitial deletion (Edel) about 39% to 60% of the time in clinically localized disease.
  • Interestingly, we observed that all of the androgen-independent metastatic prostate cancer sites harboring TMPRSS2-ERG were associated with Edel.
  • These findings suggest that TMPRSS2-ERG with Edel is an aggressive and, in this study, uniformly lethal molecular subtype of prostate cancer associated with androgen-independent disease.

  • Genetic Alliance. consumer health - Prostate cancer.
  • Genetic Alliance. consumer health - Metastatic cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Oncogene. 2008 Jan 10;27(3):253-63 [17637754.001]
  • [Cites] J Clin Pathol. 2007 Nov;60(11):1238-43 [17259299.001]
  • [Cites] Clin Cancer Res. 2000 Mar;6(3):1038-45 [10741732.001]
  • [Cites] Cancer. 2004 Jun 1;100(11):2362-6 [15160339.001]
  • [Cites] Cancer Res. 1996 Jul 1;56(13):3091-102 [8674067.001]
  • [Cites] Cancer Res. 2004 Dec 15;64(24):9209-16 [15604294.001]
  • [Cites] Science. 2005 Oct 28;310(5748):644-8 [16254181.001]
  • [Cites] Cancer Res. 2006 Apr 1;66(7):3396-400 [16585160.001]
  • [Cites] Genes Chromosomes Cancer. 2006 Jul;45(7):717-9 [16575875.001]
  • [Cites] Cancer Res. 2006 Sep 1;66(17):8337-41 [16951139.001]
  • [Cites] Cancer Res. 2006 Sep 1;66(17):8347-51 [16951141.001]
  • [Cites] Cancer Res. 2006 Nov 1;66(21):10242-6 [17079440.001]
  • [Cites] Cancer Res. 2006 Nov 15;66(22):10658-63 [17108102.001]
  • [Cites] Mod Pathol. 2007 Apr;20(4):467-73 [17334351.001]
  • [Cites] Mod Pathol. 2007 May;20(5):538-44 [17334343.001]
  • [Cites] Oncogene. 2007 Apr 19;26(18):2667-73 [17043636.001]
  • [Cites] Cancer Biol Ther. 2007 Jan;6(1):40-5 [17172822.001]
  • [Cites] Oncogene. 2007 Jul 5;26(31):4596-9 [17237811.001]
  • [Cites] Nature. 2007 Aug 2;448(7153):595-9 [17671502.001]
  • [Cites] J Clin Invest. 2007 Sep;117(9):2351-61 [17786228.001]
  • [Cites] Cancer Res. 2007 Sep 1;67(17):7991-5 [17804708.001]
  • [Cites] Oncogene. 2008 Mar 27;27(14):1993-2003 [17922029.001]
  • (PMID = 18483239.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA069568-110020; United States / NCI NIH HHS / CA / U01 CA111275-01; United States / NCI NIH HHS / CA / R01 CA102872; United States / NCI NIH HHS / CA / P50CA69568; United States / NCI NIH HHS / CA / CA069568-110020; United States / NCI NIH HHS / CA / UO1 CA111275-01; United States / NCI NIH HHS / CA / P50 CA069568; United States / NCI NIH HHS / CA / U01 CA111275
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / ERG protein, human; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins c-ets; 0 / Trans-Activators; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.- / TMPRSS2 protein, human
  • [Other-IDs] NLM/ NIHMS104651; NLM/ PMC2677168
  •  go-up   go-down


34. Lyons LS, Rao S, Balkan W, Faysal J, Maiorino CA, Burnstein KL: Ligand-independent activation of androgen receptors by Rho GTPase signaling in prostate cancer. Mol Endocrinol; 2008 Mar;22(3):597-608
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ligand-independent activation of androgen receptors by Rho GTPase signaling in prostate cancer.
  • Prostate cancer invariably recurs after androgen deprivation therapy.
  • Growth of this recurrent/androgen-independent form of prostate cancer may be due to increased androgen receptor (AR) transcriptional activity in the absence of androgen.
  • This ligand-independent AR activation is promoted by some growth factors but the mechanism is not well understood.
  • Vav3, a Rho guanosine triphosphatase guanine nucleotide exchange factor, which is activated by growth factors, is up-regulated in human prostate cancer.
  • We show here that Vav3 levels increase during in vivo progression of prostate cancer to androgen independence.
  • Vav3 strikingly enhanced growth factor activation of AR in the absence of androgen.
  • Because Vav3 may be chronically activated in prostate cancer by growth factor receptors, we examined the effects of a constitutively active (Ca) form of Vav3 on AR transcriptional activity.
  • Ca Vav3 caused nuclear localization and ligand-independent activation of AR via the Rho guanosine triphosphatase, Rac1.
  • Expression of active Rac1 conferred androgen-independent growth of prostate cancer cells in culture, soft agar, and mice.
  • These findings suggest that Vav3/Rac 1 signaling is an important modulator of ligand-independent AR transcriptional activity in prostate cancer progression.

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Growth Factors. 2004 Sep;22(3):179-84 [15518241.001]
  • [Cites] J Biol Chem. 2002 Nov 22;277(47):45377-92 [12228230.001]
  • [Cites] J Steroid Biochem Mol Biol. 2005 Aug;96(3-4):251-8 [15982869.001]
  • [Cites] J Biol Chem. 2006 Apr 7;281(14):9118-26 [16469733.001]
  • [Cites] Mol Endocrinol. 2006 May;20(5):1061-72 [16384856.001]
  • [Cites] J Biol Chem. 2006 Sep 22;281(38):27882-93 [16870607.001]
  • [Cites] Mol Endocrinol. 2006 Oct;20(10):2315-25 [16762975.001]
  • [Cites] Cancer Cell. 2006 Oct;10(4):309-19 [17045208.001]
  • [Cites] Cancer Res. 2006 Nov 1;66(21):10613-20 [17079486.001]
  • [Cites] Mol Pharmacol. 2007 Jul;72(1):73-85 [17430995.001]
  • [Cites] Cancer Res. 2007 Oct 1;67(19):9089-96 [17909013.001]
  • [Cites] Cancer Res. 2000 Apr 15;60(8):2132-5 [10786674.001]
  • [Cites] J Pathol. 2000 Jul;191(3):227-8 [10878541.001]
  • [Cites] Growth Horm IGF Res. 2000 Apr;10 Suppl A:S32-3 [10984284.001]
  • [Cites] Crit Rev Eukaryot Gene Expr. 2002;12(3):193-207 [12449343.001]
  • [Cites] Urology. 2003 Nov;62(5 Suppl 1):21-6 [14607214.001]
  • [Cites] J Biol Chem. 2003 Nov 21;278(47):46862-8 [12954644.001]
  • [Cites] Nat Med. 2004 Jan;10(1):33-9 [14702632.001]
  • [Cites] J Cell Biochem. 2004 Feb 15;91(3):483-90 [14755679.001]
  • [Cites] J Biol Chem. 2004 Feb 20;279(8):7119-30 [14662770.001]
  • [Cites] Prostate. 2004 Jun 1;59(4):401-8 [15065088.001]
  • [Cites] Endocr Rev. 2004 Apr;25(2):276-308 [15082523.001]
  • [Cites] Tumori. 2004 Mar-Apr;90(2):163-70 [15237576.001]
  • [Cites] Oncogene. 2004 Jul 15;23(32):5513-22 [15077174.001]
  • [Cites] Cancer Res. 1983 Apr;43(4):1809-18 [6831420.001]
  • [Cites] Prostate. 1993;22(2):109-18 [7681204.001]
  • [Cites] Cancer Res. 1994 Oct 15;54(20):5474-8 [7522959.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Oct 15;93(21):11802-7 [8876218.001]
  • [Cites] Steroids. 1996 Sep;61(9):531-9 [8883219.001]
  • [Cites] FEBS Lett. 1997 Jan 20;401(2-3):133-7 [9013873.001]
  • [Cites] Oncogene. 1998 May 14;16(19):2513-26 [9627117.001]
  • [Cites] J Mol Med (Berl). 1998 Jun;76(7):469-79 [9660165.001]
  • [Cites] Cancer Res. 1998 Oct 15;58(20):4640-5 [9788616.001]
  • [Cites] Nat Med. 1999 Mar;5(3):280-5 [10086382.001]
  • [Cites] Mol Cell Biol. 1999 Jul;19(7):5143-54 [10373563.001]
  • [Cites] Semin Oncol. 1999 Aug;26(4):407-21 [10482183.001]
  • [Cites] Mol Cell Biol. 1999 Nov;19(11):7870-85 [10523675.001]
  • [Cites] Mol Cell Endocrinol. 2000 Sep 25;167(1-2):43-53 [11000519.001]
  • [Cites] Urol Res. 2000 Aug;28(4):211-9 [11011957.001]
  • [Cites] EMBO J. 2000 Nov 15;19(22):6173-84 [11080163.001]
  • [Cites] Mol Cell Biol. 2000 Dec;20(24):9212-24 [11094073.001]
  • [Cites] J Natl Cancer Inst. 2000 Dec 6;92(23):1918-25 [11106683.001]
  • [Cites] J Biol Chem. 2001 Feb 2;276(5):3231-7 [11060289.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Jul 31;98(16):9014-9 [11470914.001]
  • [Cites] Cancer Res. 2001 Aug 15;61(16):6276-80 [11507082.001]
  • [Cites] J Natl Cancer Inst. 2001 Nov 21;93(22):1687-97 [11717329.001]
  • [Cites] Urology. 2001 Dec;58(6):1008-15 [11744478.001]
  • [Cites] J Exp Med. 2002 Jan 21;195(2):189-200 [11805146.001]
  • [Cites] EMBO J. 2002 Feb 15;21(4):736-48 [11847121.001]
  • [Cites] Cancer Res. 2002 Feb 15;62(4):1008-13 [11861374.001]
  • [Cites] J Biol Chem. 2002 Mar 1;277(9):7076-85 [11751884.001]
  • [Cites] Nat Rev Cancer. 2001 Oct;1(1):34-45 [11900250.001]
  • [Cites] Mol Cell Biol. 2002 Apr;22(8):2487-97 [11909943.001]
  • [Cites] J Clin Oncol. 2002 Jul 1;20(13):3001-15 [12089231.001]
  • [Cites] Urology. 2002 Sep;60(3 Suppl 1):132-8; discussion 138-9 [12231070.001]
  • [Cites] J Biol Chem. 2002 Oct 11;277(41):38087-94 [12163482.001]
  • [Cites] Clin Cancer Res. 2002 Nov;8(11):3438-44 [12429632.001]
  • [Cites] Cancer Biol Ther. 2005 Jan;4(1):4-5 [16052746.001]
  • (PMID = 18079321.001).
  • [ISSN] 0888-8809
  • [Journal-full-title] Molecular endocrinology (Baltimore, Md.)
  • [ISO-abbreviation] Mol. Endocrinol.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R21 DK065281; United States / NIDDK NIH HHS / DK / DK065281
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AR protein, human; 0 / Guanine Nucleotide Exchange Factors; 0 / Proto-Oncogene Proteins c-vav; 0 / RAC1 protein, human; 0 / RNA, Messenger; 0 / Receptors, Androgen; 0 / VAV3 protein, human; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; EC 3.6.5.2 / rac1 GTP-Binding Protein
  • [Other-IDs] NLM/ PMC2262175
  •  go-up   go-down


35. Ohlmann CH, Markert E, Gerharz M, Pfister D, Dienes HP, Engelmann U, Heidenreich A: [Feasibility of targeted therapy based on immunohistochemical expression analysis in androgen-independent prostate cancer]. Urologe A; 2008 Sep;47(9):1218-23
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Feasibility of targeted therapy based on immunohistochemical expression analysis in androgen-independent prostate cancer].
  • Targeted therapies present an interesting treatment option in prostate cancer.
  • The aim of our study was to analyze the expression profile of several molecular markers that are candidates for targeted therapy in patients with progressive androgen-independent prostate cancer (AIPC).
  • Based on the expression profile, the efficacy of a combination therapy with a signal transduction inhibitor (STI) and docetaxel was evaluated.Tumor tissue obtained from biopsy of the prostate or lymph node and visceral metastasis was analyzed for the immunohistochemical expression of epidermal growth factor receptor (EGFR), platelet-derived growth factor receptor beta (PDGFRbeta), Her-2/neu, c-KIT, and vascular endothelial growth factor (VEGF).
  • Four of the eight patients (50%) showed a decline in prostate-specific antigen of > or =50%, and median survival time was 13.5 months at a median follow-up of 23.6 (11-35) months.The results show that expression of molecular targets is found in about 90% of patients with AIPC.
  • [MeSH-major] Antibodies, Monoclonal / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Biomarkers, Tumor / genetics. Neoplasms, Hormone-Dependent / drug therapy. Neoplasms, Hormone-Dependent / genetics. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / genetics. Protein-Tyrosine Kinases / antagonists & inhibitors. Receptors, Androgen / genetics. Taxoids / administration & dosage
  • [MeSH-minor] Antibodies, Monoclonal, Humanized. Benzamides. Bevacizumab. Biopsy. Cetuximab. Disease Progression. Drug Resistance, Neoplasm. Gene Expression Profiling. Humans. Imatinib Mesylate. Lymph Nodes / pathology. Male. Piperazines / administration & dosage. Piperazines / adverse effects. Prospective Studies. Prostate / pathology. Prostate-Specific Antigen / blood. Pyrimidines / administration & dosage. Pyrimidines / adverse effects. Trastuzumab

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • Hazardous Substances Data Bank. DOCETAXEL .
  • Hazardous Substances Data Bank. Trastuzumab .
  • Hazardous Substances Data Bank. CETUXIMAB .
  • Hazardous Substances Data Bank. IMATINIB MESYLATE .
  • 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 .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18679646.001).
  • [ISSN] 0340-2592
  • [Journal-full-title] Der Urologe. Ausg. A
  • [ISO-abbreviation] Urologe A
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Benzamides; 0 / Biomarkers, Tumor; 0 / Piperazines; 0 / Pyrimidines; 0 / Receptors, Androgen; 0 / Taxoids; 15H5577CQD / docetaxel; 2S9ZZM9Q9V / Bevacizumab; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 3.4.21.77 / Prostate-Specific Antigen; P188ANX8CK / Trastuzumab; PQX0D8J21J / Cetuximab
  •  go-up   go-down


36. Dehm SM, Tindall DJ: Ligand-independent androgen receptor activity is activation function-2-independent and resistant to antiandrogens in androgen refractory prostate cancer cells. J Biol Chem; 2006 Sep 22;281(38):27882-93
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ligand-independent androgen receptor activity is activation function-2-independent and resistant to antiandrogens in androgen refractory prostate cancer cells.
  • Androgen ablation inhibits androgen receptor (AR) activity and is as an effective treatment for advanced prostate cancer (PCa).
  • Although this stage of the disease is androgen-refractory, or androgen depletion-independent (ADI), most tumors remain AR-dependent through aberrant mechanisms of AR activation.
  • We employed the LNCaP/C4-2 model of PCa progression to study AR activity in androgen-dependent and ADI PCa cells.
  • In this report, we show that the AR is transcriptionally inactive in androgen-dependent LNCaP cells in the absence of androgens.
  • However, in ADI C4-2 cells, the AR displays a high level of constitutive, androgen-independent transcriptional activity.
  • To study the mechanisms of ligand-dependent and ligand-independent AR activation in these AR-expressing cells, we generated a reporter system based on swapping the DNA binding domain of the AR with the DNA binding domain of the yeast Gal4 transcription factor.
  • In androgen-dependent PCa cells, the well characterized C-terminal AR activation function-2 (AF-2) domain was critical for strong, ligand-dependent activity.
  • Conversely, in ADI PCa cells, constitutive, ligand-independent AR activity was AF-2-independent but instead dependent on N-terminal AR domains.
  • Importantly, the ligand- and AF-2-independent mode of AR activation observed in ADI PCa cells was completely resistant to the antiandrogen, bicalutamide.
  • Our data thus demonstrate that the AR can inappropriately activate transcription in ADI PCa cells via mechanisms that are resistant to castration and AR antagonism, the two modes of androgen ablation used to treat advanced PCa.
  • [MeSH-major] Androgen Antagonists / pharmacology. Neoplasms, Hormone-Dependent / drug therapy. Nuclear Proteins / physiology. Prostatic Neoplasms / drug therapy. Receptors, Androgen / physiology
  • [MeSH-minor] Binding Sites. Cell Line, Tumor. Drug Resistance, Neoplasm. Humans. Ligands. Male. Promoter Regions, Genetic. Prostate-Specific Antigen / genetics. Protein Structure, Tertiary. Transcriptional Activation

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • 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 = 16870607.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA91956; United States / PHS HHS / / D65236; United States / NIDDK NIH HHS / DK / DK60920
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Ligands; 0 / Nuclear Proteins; 0 / Receptors, Androgen; EC 3.4.21.77 / Prostate-Specific Antigen
  •  go-up   go-down


37. Mellado B, Codony J, Ribal MJ, Visa L, Gascón P: Molecular biology of androgen-independent prostate cancer: the role of the androgen receptor pathway. Clin Transl Oncol; 2009 Jan;11(1):5-10
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular biology of androgen-independent prostate cancer: the role of the androgen receptor pathway.
  • Prostate cancer (PC) cells express the androgen receptor (AR) and need the presence of androgens to survive.
  • Androgen suppression is the gold standard first-line therapy for metastatic disease.
  • Several mechanisms that enhance AR signalling in an androgen-depleted environment have been elucidated:.
  • (1) AR mutations that allow activation by low androgen levels or by other endogenous steroids, (2) AR amplification and/or overexpression, (3) increased local intracrine synthesis of androgens, (4) changes in AR cofactors and (5) cross-talk with cytokines and growth factors.
  • [MeSH-major] Drug Resistance, Neoplasm / genetics. Prostatic Neoplasms / metabolism. Receptors, Androgen / genetics. Receptors, Androgen / metabolism. Signal Transduction / physiology
  • [MeSH-minor] Androgen Antagonists / therapeutic use. Humans. Male. Molecular Biology / trends

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • 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 = 19155198.001).
  • [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] Spain
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Receptors, Androgen
  • [Number-of-references] 42
  •  go-up   go-down


38. Bühler P, Wolf P, Katzenwadel A, Schultze-Seemann W, Wetterauer U, Freudenberg N, Elsässer-Beile U: Primary prostate cancer cultures are models for androgen-independent transit amplifying cells. Oncol Rep; 2010 Feb;23(2):465-70
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Primary prostate cancer cultures are models for androgen-independent transit amplifying cells.
  • Numerous efforts exist for developing primary prostate cancer cultures for studying the biology of this tumor entity and for evaluation of the effectiveness of novel therapies.
  • The aim of the present study was to characterize primary outgrowing prostate epithelial cells due to their basal or luminal characteristics and their potential for serving as androgen-responsible model.
  • From fresh prostate cancer radical prostatectomy specimens, pieces of approximately 2-4 mm diameter were placed on top of transwell culture chambers, which were coated with matrigel and cultured in prostate epithelial selection medium with 10% fetal calf serum.
  • From the monolayer of the outgrowing cells, RNA was isolated and the expression of androgen receptor (AR), prostate-specific antigen (PSA), Kallikrein 2 (KlK2), prostate-specific membrane antigen (PSMA), and prostate stem cell antigen (PSCA), cytokeratin (CK)5, and CK18 was determined by realtime quantitative PCR.
  • The outgrowing cells from the prostate cancer tissue pieces could be characterized as epithelial cells with basal and transit amplifying characteristics as shown by co-expression of CK5 and CK18.
  • Due to the co-expression of basal and luminal marker genes, primary prostate cancer cultures can be charaterized as models of transit amplifying cells of the prostatic epithelium.
  • They do not represent the differentiated secretory androgen-responsive cell phenotype.
  • [MeSH-minor] Androgen Antagonists / pharmacology. Antigens, Neoplasm. Biomarkers, Tumor / analysis. Biomarkers, Tumor / genetics. Cell Culture Techniques. Cell Differentiation / drug effects. Cell Differentiation / genetics. Epithelial Cells / pathology. GPI-Linked Proteins. Gene Expression Regulation, Neoplastic / drug effects. Humans. Male. Membrane Glycoproteins / genetics. Membrane Glycoproteins / metabolism. Models, Biological. Neoplasm Proteins / genetics. Neoplasm Proteins / metabolism. Phenotype. Receptors, Androgen / genetics. Receptors, Androgen / metabolism. Tumor Cells, Cultured


39. Floryk D, Huberman E: Mycophenolic acid-induced replication arrest, differentiation markers and cell death of androgen-independent prostate cancer cells DU145. Cancer Lett; 2006 Jan 8;231(1):20-9
Hazardous Substances Data Bank. MYCOPHENOLATE MOFETIL .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mycophenolic acid-induced replication arrest, differentiation markers and cell death of androgen-independent prostate cancer cells DU145.
  • Here, we report that MPA also induces such a differentiation in the androgen-independent prostate cancer derived cell line DU145.
  • The inhibitor also induced the expression of CD55, clusterin, granulophysin, glucose-regulated protein 78, vasoactive intestinal polypeptide and prostate-specific transglutaminase, which are differentiation markers associated with the phenotype of normal prostate cells.
  • We suggest that inosine 5'-monophosphate dehydrogenase inhibitors, which are already used for the treatment of other diseases, may be used as potential differentiation therapy drugs to control prostate cancer.
  • [MeSH-minor] Androgen Antagonists / pharmacology. Biomarkers / analysis. Cell Cycle / drug effects. Cell Proliferation / drug effects. Drug Resistance, Neoplasm. Humans. Male. Phenotype. Tumor Cells, Cultured

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16356827.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 80826
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Antibiotics, Antineoplastic; 0 / Biomarkers; HU9DX48N0T / Mycophenolic Acid
  •  go-up   go-down


40. Patel PH, Kockler DR: Sipuleucel-T: a vaccine for metastatic, asymptomatic, androgen-independent prostate cancer. Ann Pharmacother; 2008 Jan;42(1):91-8
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Sipuleucel-T: a vaccine for metastatic, asymptomatic, androgen-independent prostate cancer.
  • OBJECTIVE: To review the design, efficacy, safety, dosing, therapeutic, and pharmacoeconomic considerations of sipuleucel-T, an investigational, autologous, dendritic, cell-based prostate cancer vaccine.
  • DATA SOURCES: English-language literature searches of MEDLINE (1966-September 2007) and the Cochrane Database (2007, Issue 3) were performed using the terms sipuleucel-T, APC8015, and prostate cancer vaccine.
  • STUDY SELECTION AND DATA EXTRACTION: All published articles or abstracts on human studies of sipuleucel-T for androgen-independent prostate cancer (AIPC) were reviewed for inclusion.
  • [MeSH-minor] Controlled Clinical Trials as Topic. Dendritic Cells / immunology. Humans. Male. Neoplasm Metastasis. Prognosis. Survival Analysis

  • Genetic Alliance. consumer health - Prostate cancer.
  • Genetic Alliance. consumer health - Metastatic cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18094343.001).
  • [ISSN] 1542-6270
  • [Journal-full-title] The Annals of pharmacotherapy
  • [ISO-abbreviation] Ann Pharmacother
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cancer Vaccines; 0 / Tissue Extracts; 0 / sipuleucel-T
  • [Number-of-references] 31
  •  go-up   go-down


41. Jeet V, Ow K, Doherty E, Curley B, Russell PJ, Khatri A: Broadening of transgenic adenocarcinoma of the mouse prostate (TRAMP) model to represent late stage androgen depletion independent cancer. Prostate; 2008 Apr 1;68(5):548-62
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Broadening of transgenic adenocarcinoma of the mouse prostate (TRAMP) model to represent late stage androgen depletion independent cancer.
  • BACKGROUND: The transgenic adenocarcinoma of the mouse prostate (TRAMP) model closely mimics PC-progression as it occurs in humans.
  • The development and characterization of androgen depletion independent (ADI) TRAMP sublines are reported.
  • METHODS: Sublines were derived from androgen-sensitive TRAMP-C1 and TRAMP-C2 cell lines by androgen deprivation in vitro and in vivo.
  • Androgen receptor (AR) status was assessed through quantitative real time PCR, Western blotting, and immunohistochemistry.
  • Proliferation/survival of sublines in response to androgen was assessed by WST-1 assay.
  • Compared to the parental lines, these showed (1) significantly faster growth rates in vitro and in vivo independent of androgen depletion, (2) greater tumorigenic, and invasive potential in vitro.
  • [MeSH-minor] Animals. Antigens, CD82 / metabolism. Biomarkers, Tumor / metabolism. Cadherins / metabolism. Cell Line, Tumor. Cell Proliferation. Disease Models, Animal. Disease Progression. Male. Mice. Mice, Inbred C57BL. Mice, Transgenic. Neoplasm Invasiveness / genetics. Receptors, Androgen / metabolism

  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18247402.001).
  • [ISSN] 0270-4137
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Antigens, CD82; 0 / Biomarkers, Tumor; 0 / Cadherins; 0 / Cd82 antigen, mouse; 0 / Receptors, Androgen
  •  go-up   go-down


42. Svatek R, Karakiewicz PI, Shulman M, Karam J, Perrotte P, Benaim E: Pre-treatment nomogram for disease-specific survival of patients with chemotherapy-naive androgen independent prostate cancer. Eur Urol; 2006 Apr;49(4):666-74
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pre-treatment nomogram for disease-specific survival of patients with chemotherapy-naive androgen independent prostate cancer.
  • OBJECTIVE: Our objective was to develop a nomogram that predicts the probability of cancer-specific survival in men with untreated androgen-independent prostate cancer (AIPC).
  • Univariate and multivariate Cox regression models were used to test the association between prostate-specific antigen (PSA) level at initiation of androgen deprivation, PSA doubling time (PSADT), PSA nadir on androgen deprivation therapy (ADT), time from ADT to AIPC, and AIPC-specific mortality.
  • In multivariate models, PSADT and time from androgen deprivation to AIPC remained statistically significant (p < or = 0.004).
  • [MeSH-major] Androgen Antagonists / therapeutic use. Nomograms. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / mortality
  • [MeSH-minor] Aged. Area Under Curve. Humans. Male. Middle Aged. Neoplasm Staging. Predictive Value of Tests. Probability. Proportional Hazards Models. Prostate-Specific Antigen / blood. ROC Curve. Retrospective Studies. Survival Analysis

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16423446.001).
  • [ISSN] 0302-2838
  • [Journal-full-title] European urology
  • [ISO-abbreviation] Eur. Urol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Androgen Antagonists; EC 3.4.21.77 / Prostate-Specific Antigen
  •  go-up   go-down


43. Wu M, Bai X, Xu G, Wei J, Zhu T, Zhang Y, Li Q, Liu P, Song A, Zhao L, Gang C, Han Z, Wang S, Zhou J, Lu Y, Ma D: Proteome analysis of human androgen-independent prostate cancer cell lines: variable metastatic potentials correlated with vimentin expression. Proteomics; 2007 Jun;7(12):1973-83
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Proteome analysis of human androgen-independent prostate cancer cell lines: variable metastatic potentials correlated with vimentin expression.
  • To better understand the molecular mechanisms of prostate cancer (PCA) dissemination and to develop new anti-metastasis therapies, key regulatory molecules involved in PCA metastasis were identified in two human androgen-independent PCA cell lines, highly metastatic 1E8-H and lowly metastatic 2B4-L cells.
  • To our knowledge, this study is the first to demonstrate that up-regulation of VIM expression positively correlates with the invasion and metastasis of androgen-independent PCA.
  • [MeSH-minor] Amino Acid Sequence. Animals. Cell Line, Tumor. Humans. Lung Neoplasms / secondary. Lymph Nodes / pathology. Male. Mice. Mice, Inbred BALB C. Molecular Sequence Data. Neoplasm Metastasis. Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization


44. Albertelli MA, O'Mahony OA, Brogley M, Tosoian J, Steinkamp M, Daignault S, Wojno K, Robins DM: Glutamine tract length of human androgen receptors affects hormone-dependent and -independent prostate cancer in mice. Hum Mol Genet; 2008 Jan 1;17(1):98-110
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Glutamine tract length of human androgen receptors affects hormone-dependent and -independent prostate cancer in mice.
  • The androgen receptor (AR) is involved in the initiation and progression of prostate cancer and its transition to androgen independence.
  • To clarify the effect of Q tract polymorphism on prostate cancer, we created mice bearing humanized AR genes (h/mAr) varying in Q tract length.
  • ARs with short Q tracts (12Q), which are transcriptionally more active, induce earlier disease in the transgene-induced TRAMP prostate cancer model than alleles with median (21Q) or long (48Q) tracts.
  • Remarkably, following androgen ablation, Q tract length has effects that are also allele-dependent and in directions opposite to those in hormone intact mice.
  • Differences in AR activity conferred by Q tract length thus appear to direct distinct pathways of androgen-independent as well as androgen-dependent progression, and highlight substantial risk that may be associated with alterations in the androgen axis.
  • This AR allelic series in humanized mice provides an experimental paradigm to dissect the role of AR in prostate cancer initiation and progression, to model response to treatment and to test therapies targeted specifically to the human AR.

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17906287.001).
  • [ISSN] 0964-6906
  • [Journal-full-title] Human molecular genetics
  • [ISO-abbreviation] Hum. Mol. Genet.
  • [Language] ENG
  • [Grant] United States / NCRR NIH HHS / RR / T32-RR07008; United States / NCI NIH HHS / CA / 5 P30 CA46592; United States / NCI NIH HHS / CA / P50 CA69568; United States / NIDDK NIH HHS / DK / 5P60 DK20572; United States / NIDDK NIH HHS / DK / R01 DK056356; United States / PHS HHS / / R01-56356
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AR protein, human; 0 / DNA Primers; 0 / Peptides; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Receptors, Androgen; 26700-71-0 / polyglutamine
  •  go-up   go-down


45. Narita S, So A, Ettinger S, Hayashi N, Muramaki M, Fazli L, Kim Y, Gleave ME: GLI2 knockdown using an antisense oligonucleotide induces apoptosis and chemosensitizes cells to paclitaxel in androgen-independent prostate cancer. Clin Cancer Res; 2008 Sep 15;14(18):5769-77
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] GLI2 knockdown using an antisense oligonucleotide induces apoptosis and chemosensitizes cells to paclitaxel in androgen-independent prostate cancer.
  • PURPOSE: GLI transcription factors mediate hedgehog signaling and have been implicated in several human malignancies, including prostate cancer.
  • The objectives of this study were to characterize GLI2 expression levels in human prostate cancer cell lines and tissues to test the effect of antisense oligonucleotide (ASO) targeting GLI2 on androgen-independent (AI) prostate cancer cell lines.
  • EXPERIMENTAL DESIGN: A tissue microarray was used to characterize differences in GLI2 expression in benign prostate hyperplasia, prostate cancer treated by neoadjuvant hormonal therapy and AI prostate cancer.
  • RESULTS: The expression of GLI2 was significantly higher in prostate cancer than in benign prostate hyperplasia, decreased after androgen ablation in a time-dependent fashion, but became highly expressed again in AI prostate cancer.
  • CONCLUSIONS: These findings suggest that increased levels of GLI2 correlates with AI progression and that GLI2 may be a therapeutic target in castrate-resistant prostate cancer.
  • [MeSH-minor] Androgens / pharmacology. Animals. Antineoplastic Agents, Phytogenic / therapeutic use. Apoptosis. Base Sequence. Cell Line, Tumor. Disease Progression. Dose-Response Relationship, Drug. Humans. Male. Membrane Proteins / analysis. Mice. Mice, Nude. Neoplasm Transplantation. Neoplasms, Hormone-Dependent / genetics. Neoplasms, Hormone-Dependent / metabolism. Saccharomyces cerevisiae Proteins / analysis

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. TAXOL .
  • 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 = 18794086.001).
  • [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; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Antineoplastic Agents, Phytogenic; 0 / GLI2 protein, human; 0 / Kruppel-Like Transcription Factors; 0 / MRL1 protein, S cerevisiae; 0 / Membrane Proteins; 0 / Nuclear Proteins; 0 / Oligonucleotides, Antisense; 0 / Saccharomyces cerevisiae Proteins; P88XT4IS4D / Paclitaxel
  •  go-up   go-down


46. Saporita AJ, Ai J, Wang Z: The Hsp90 inhibitor, 17-AAG, prevents the ligand-independent nuclear localization of androgen receptor in refractory prostate cancer cells. Prostate; 2007 Apr 1;67(5):509-20
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The Hsp90 inhibitor, 17-AAG, prevents the ligand-independent nuclear localization of androgen receptor in refractory prostate cancer cells.
  • BACKGROUND: Androgen receptor (AR) is the key molecule in androgen-refractory prostate cancer.
  • Despite androgen ablative conditions, AR remains active and is necessary for the growth of androgen-refractory prostate cancer cells.
  • We examined AR localization in androgen-dependent and androgen-refractory prostate cancer cells.
  • METHODS AND RESULTS: We demonstrate increased nuclear localization of a GFP-tagged AR in the absence of hormone in androgen-refractory C4-2 cells compared to parental androgen-sensitive human prostate cancer LNCaP cells.
  • Analysis of AR mutants impaired in ligand-binding indicates that the nuclear localization of AR in C4-2 cells is truly androgen-independent.
  • The hsp90 inhibitor, 17-allylamino-17-demethoxygeldanamycin (17-AAG), inhibits basal PSA expression and disrupts the ligand-independent nuclear localization of AR at doses much lower than required to inhibit androgen-induced nuclear import.
  • CONCLUSIONS: Hsp90 is a key regulator of ligand-independent nuclear localization and activation of AR in androgen-refractory prostate cancer cells.

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Steroid Biochem Mol Biol. 1997 Jul;62(4):233-42 [9408077.001]
  • [Cites] J Urol. 1998 Jul;160(1):220-9 [9628654.001]
  • [Cites] J Steroid Biochem Mol Biol. 1998 Apr;65(1-6):51-8 [9699857.001]
  • [Cites] Mol Endocrinol. 1998 Dec;12(12):1903-13 [9849964.001]
  • [Cites] Cancer Res. 1998 Dec 15;58(24):5718-24 [9865729.001]
  • [Cites] Cancer Res. 1999 Apr 15;59(8):1896-902 [10213498.001]
  • [Cites] Cancer Res. 2005 Sep 1;65(17):7959-67 [16140968.001]
  • [Cites] Prostate. 2000 Jul 1;44(2):91-103 Jul 1;44(2) [10881018.001]
  • [Cites] Mol Endocrinol. 2000 Aug;14(8):1162-74 [10935541.001]
  • [Cites] J Biol Chem. 2000 Dec 29;275(52):40846-55 [11006269.001]
  • [Cites] Cancer Res. 2001 Apr 1;61(7):2892-8 [11306464.001]
  • [Cites] Cancer Res. 1991 Jul 15;51(14):3748-52 [1712248.001]
  • [Cites] J Biol Chem. 2002 Feb 15;277(7):4597-600 [11751894.001]
  • [Cites] Cancer Res. 2002 Feb 15;62(4):1008-13 [11861374.001]
  • [Cites] Prostate. 2002 Mar 1;50(4):222-35 [11870800.001]
  • [Cites] Nat Rev Cancer. 2001 Oct;1(1):34-45 [11900250.001]
  • [Cites] Mol Endocrinol. 2002 May;16(5):924-37 [11981028.001]
  • [Cites] Clin Cancer Res. 2002 May;8(5):986-93 [12006510.001]
  • [Cites] Biochemistry. 2002 Oct 1;41(39):11824-31 [12269826.001]
  • [Cites] Mol Endocrinol. 2002 Dec;16(12):2692-705 [12456791.001]
  • [Cites] Endocrinology. 2003 Apr;144(4):1257-65 [12639908.001]
  • [Cites] J Clin Endocrinol Metab. 2003 Jul;88(7):2972-82 [12843129.001]
  • [Cites] Cancer Res. 2003 Aug 1;63(15):4552-60 [12907631.001]
  • [Cites] Cancer Res. 2003 Aug 1;63(15):4698-704 [12907652.001]
  • [Cites] J Biol Chem. 2003 Oct 24;278(43):41998-2005 [12923188.001]
  • [Cites] Clin Cancer Res. 2003 Oct 15;9(13):4961-71 [14581371.001]
  • [Cites] Nat Med. 2004 Jan;10(1):33-9 [14702632.001]
  • [Cites] Brain Res Mol Brain Res. 2004 Apr 7;123(1-2):27-36 [15046863.001]
  • [Cites] Mol Cell Endocrinol. 2004 Jan 15;213(2):121-9 [15062559.001]
  • [Cites] Prostate. 2004 Jul 1;60(2):98-108 [15162376.001]
  • [Cites] J Biol Chem. 1993 Oct 15;268(29):21455-8 [8407992.001]
  • [Cites] Mol Cell Endocrinol. 1992 Oct;88(1-3):165-74 [1459337.001]
  • [Cites] Biochemistry. 1992 Aug 18;31(32):7422-30 [1510931.001]
  • [Cites] Prostate. 1992;21(1):63-73 [1379363.001]
  • [Cites] Biochemistry. 1992 Mar 3;31(8):2393-9 [1540595.001]
  • [Cites] Cancer Res. 1983 Apr;43(4):1809-18 [6831420.001]
  • [Cites] EMBO J. 1987 Nov;6(11):3333-40 [3123217.001]
  • [Cites] J Biol Chem. 1997 Jul 25;272(30):18694-701 [9228040.001]
  • [Cites] Endocr Rev. 1997 Jun;18(3):306-60 [9183567.001]
  • [Cites] Mol Cell Endocrinol. 1997 Apr 25;129(1):17-26 [9175625.001]
  • [Cites] Mol Endocrinol. 1995 Feb;9(2):208-18 [7776971.001]
  • [Cites] J Biol Chem. 1994 May 6;269(18):13115-23 [8175737.001]
  • [Cites] Int J Cancer. 1994 May 1;57(3):406-12 [8169003.001]
  • [Cites] Mol Endocrinol. 1993 Nov;7(11):1418-29 [7906860.001]
  • [Cites] Clin Cancer Res. 2001 Jul;7(7):2076-84 [11448926.001]
  • (PMID = 17221841.001).
  • [ISSN] 0270-4137
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK051193-06S1; United States / NIDDK NIH HHS / DK / R01 DK051193; United States / NCI NIH HHS / CA / T32 CA80621; United States / NIDDK NIH HHS / DK / DK051193-06S1; United States / NCI NIH HHS / CA / CA090386-06A25083; United States / NCI NIH HHS / CA / P50 CA090386; United States / NCI NIH HHS / CA / T32 CA080621; United States / NCI NIH HHS / CA / R01 CA108675; United States / NCI NIH HHS / CA / R01 CA108675-06; United States / NCI NIH HHS / CA / P50 CA090386-06A25083; United States / NCI NIH HHS / CA / 1 P50 CA90386; United States / NCI NIH HHS / CA / CA080621-07; United States / NCI NIH HHS / CA / T32 CA080621-07; United States / NIDDK NIH HHS / DK / 5 R01 DK51993
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AR protein, human; 0 / Benzoquinones; 0 / HSP90 Heat-Shock Proteins; 0 / Lactams, Macrocyclic; 0 / Ligands; 0 / RNA, Neoplasm; 0 / Receptors, Androgen; 4GY0AVT3L4 / tanespimycin; EC 3.4.21.77 / Prostate-Specific Antigen
  • [Other-IDs] NLM/ NIHMS168558; NLM/ PMC2810394
  •  go-up   go-down


47. Iwasa Y, Mizokami A, Miwa S, Koshida K, Namiki M: Establishment and characterization of androgen-independent human prostate cancer cell lines, LN-REC4 and LNCaP-SF, from LNCaP. Int J Urol; 2007 Mar;14(3):233-9
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Establishment and characterization of androgen-independent human prostate cancer cell lines, LN-REC4 and LNCaP-SF, from LNCaP.
  • AIM: To investigate the mechanisms of androgen-independent growth in prostate cancer (PCa), we established two PCa cell lines, LN-REC4 and LNCaP-SF, from the androgen-dependent PCa cell line, LNCaP.
  • To show the character of LN-REC4 and LNCaP-SF cells, androgen sensitivity was investigated through examination of growth rate, and prostate-specific antigen (PSA), androgen receptor (AR), p21, p27, and cyclin D1 expression were examined by reverse transcription-polymerase chain reaction (RT-PCR).
  • RESULTS AND CONCLUSIONS: LN-REC4 cells proliferated better than LNCaP cells in castrated mice and did well irrespective of castration, although responsiveness for androgen of LN-REC4 cells attenuated less than that of LNCaP cells in vitro.
  • The PSA expression in LNCaP-SF cells was still induced by androgen.
  • These cell lines might be a useful tool for researching androgen-independent growth and treatments of recurred PCa.
  • [MeSH-minor] Androgens / pharmacology. Animals. Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. Cell Line, Tumor. Cell Proliferation. Culture Media, Conditioned. Cyclin D1 / genetics. Cyclin D1 / metabolism. Cyclin-Dependent Kinase Inhibitor p21 / genetics. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. Disease Models, Animal. Enzyme-Linked Immunosorbent Assay. Gene Expression Regulation, Neoplastic. Humans. Male. Mice. Mice, SCID. Neoplasm Transplantation. Proliferating Cell Nuclear Antigen / genetics. Proliferating Cell Nuclear Antigen / metabolism. Prostate-Specific Antigen / genetics. Prostate-Specific Antigen / metabolism. RNA, Neoplasm / genetics. Receptors, Androgen / genetics. Receptors, Androgen / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Vascular Endothelial Growth Factor A / genetics. Vascular Endothelial Growth Factor A / metabolism

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • 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
  • (PMID = 17430262.001).
  • [ISSN] 0919-8172
  • [Journal-full-title] International journal of urology : official journal of the Japanese Urological Association
  • [ISO-abbreviation] Int. J. Urol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Androgens; 0 / Biomarkers, Tumor; 0 / CDKN1A protein, human; 0 / Culture Media, Conditioned; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Proliferating Cell Nuclear Antigen; 0 / RNA, Neoplasm; 0 / Receptors, Androgen; 0 / Vascular Endothelial Growth Factor A; 0 / p27 antigen; 136601-57-5 / Cyclin D1; EC 3.4.21.77 / Prostate-Specific Antigen
  •  go-up   go-down


48. Asim M, Siddiqui IA, Hafeez BB, Baniahmad A, Mukhtar H: Src kinase potentiates androgen receptor transactivation function and invasion of androgen-independent prostate cancer C4-2 cells. Oncogene; 2008 Jun 5;27(25):3596-604
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Src kinase potentiates androgen receptor transactivation function and invasion of androgen-independent prostate cancer C4-2 cells.
  • Prostate cancer is one of the most prominent malignancies of elderly men in many Western countries including Europe and the United States with increasing trend worldwide.
  • The growth of normal prostate as well as of prostate carcinoma cells depends on functional androgen receptor (AR) signaling.
  • Here we show that Src, a nonreceptor tyrosine kinase, is overexpressed in androgen-independent prostate carcinoma C4-2 cells.
  • Interestingly, the expression of Src was found to progressively increase (up to threefold) in transgenic adenocarcinoma of mouse prostate mice as a function of age and cancer progression.
  • Blocking Src kinase function by a specific inhibitor, PP2, resulted in decreased AR transactivation function on two different reporters, mouse mammary tumor virus (MMTV) and prostate-specific antigen (PSA).
  • We suggest that targeting Src kinase could be an effective strategy to inhibit prostate cancer growth and metastasis.
  • [MeSH-major] Gene Expression Regulation, Enzymologic. Gene Expression Regulation, Neoplastic. Prostatic Neoplasms / pathology. Receptors, Androgen / metabolism
  • [MeSH-minor] Androgens / metabolism. Animals. Cell Line, Tumor. Humans. Male. Mice. Mice, Transgenic. Models, Biological. Neoplasm Invasiveness. Transcription, Genetic. Transgenes

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate 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 .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18223692.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / P50DK065303-01; United States / NCI NIH HHS / CA / R01CA101039; United States / NCI NIH HHS / CA / R01CA120451; United States / NCI NIH HHS / CA / R01CA78809
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Androgens; 0 / Receptors, Androgen
  •  go-up   go-down


49. Chua CW, Lee DT, Ling MT, Zhou C, Man K, Ho J, Chan FL, Wang X, Wong YC: FTY720, a fungus metabolite, inhibits in vivo growth of androgen-independent prostate cancer. Int J Cancer; 2005 Dec 20;117(6):1039-48
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] FTY720, a fungus metabolite, inhibits in vivo growth of androgen-independent prostate cancer.
  • Our study evaluates the therapeutic potential of FTY720 in the treatment of androgen-independent prostate cancer using a human prostate cancer xenograft in nude mice.
  • CWR22R, an androgen-independent human prostate tumor xenograft was inoculated into castrated nude mice and the animals were administrated with either normal saline or FTY720 (10 mg/kg) through intraperitoneal (i.p.) injection for 20 days.
  • Body weight and tumor volume were recorded every 2 days, and serum prostate specific antigen (PSA) levels were also measured before and after the treatment.
  • In addition, the potential inhibitory effect of FTY720 on prostate cancer angiogenesis and metastasis was investigated by immunostaining of CD31, VEGF, E-cadherin and beta-catenin.
  • Our results suggest a potential novel agent in the suppression of androgen-independent prostate cancer.
  • [MeSH-minor] Animals. Antigens, CD31 / analysis. Apoptosis / drug effects. Body Weight. Cadherins / analysis. Caspase 3. Caspases / analysis. Cell Division / drug effects. Fingolimod Hydrochloride. Humans. Immunohistochemistry. In Situ Nick-End Labeling. Male. Mice. Mice, Nude. Neoplasm Metastasis / prevention & control. Neoplasm Transplantation. Neovascularization, Pathologic / prevention & control. Orchiectomy. Prostate-Specific Antigen / blood. Proto-Oncogene Proteins c-bcl-2 / analysis. Sphingosine / analogs & derivatives. Vascular Endothelial Growth Factor A / analysis. beta Catenin / analysis

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate 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 .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2005 Wiley-Liss, Inc
  • (PMID = 15986440.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Antigens, CD31; 0 / Cadherins; 0 / Propylene Glycols; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Vascular Endothelial Growth Factor A; 0 / beta Catenin; EC 3.4.21.77 / Prostate-Specific Antigen; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Casp3 protein, mouse; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases; G926EC510T / Fingolimod Hydrochloride; NGZ37HRE42 / Sphingosine
  •  go-up   go-down


50. D'Antonio JM, Ma C, Monzon FA, Pflug BR: Longitudinal analysis of androgen deprivation of prostate cancer cells identifies pathways to androgen independence. Prostate; 2008 May 15;68(7):698-714
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Longitudinal analysis of androgen deprivation of prostate cancer cells identifies pathways to androgen independence.
  • BACKGROUND: Following androgen ablation therapy, the majority of prostate cancer patients develop treatment resistance with a median time of 18-24 months to disease progression.
  • METHODS: To identify molecular targets that promote prostate cancer cell survival and contribute to androgen independence, we evaluated changes in LNCaP cell gene expression during 12 months of androgen deprivation.
  • At time points reflecting critical growth and phenotypic changes, we performed Affymetrix expression array analysis to examine the effects of androgen deprivation during the acute response, during the period of apparent quiescence, and following the emergence of a highly proliferative, androgen-independent prostate cancer cell phenotype (LNCaP-AI).
  • RESULTS: We discovered alterations in gene expression for molecules associated with promoting prostate cancer cell growth and survival, and regulating cell cycle progression and apoptosis.
  • Additionally, expression of AR co-regulators, adrenal androgen metabolizing enzymes, and markers of neuroendocrine disease were significantly altered.
  • CONCLUSIONS: These findings contribute greatly to our understanding of androgen-independent prostate cancer.
  • The value of this longitudinal approach lies in the ability to examine gene expression changes throughout the adaptive response to androgen deprivation; it provides a more dynamic illustration of genes which contribute to disease progression in addition to specific genes which constitute an androgen-independent phenotype.
  • [MeSH-major] Androgen Antagonists / pharmacology. Androgens / physiology. Antineoplastic Agents, Hormonal / pharmacology. Gene Expression Regulation, Neoplastic / physiology. Prostatic Neoplasms / genetics
  • [MeSH-minor] Apoptosis / drug effects. Apoptosis / genetics. Cell Cycle / drug effects. Cell Cycle / genetics. Cell Line, Tumor. Cell Survival / drug effects. Drug Resistance, Neoplasm / drug effects. Endothelin-1 / genetics. Endothelin-1 / metabolism. Gene Expression Profiling. Humans. Male. Receptor, Endothelin A / genetics. Receptor, Endothelin A / metabolism. Receptors, Androgen / genetics. Receptors, Androgen / metabolism

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • SciCrunch. ArrayExpress: Data: Microarray .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • (PMID = 18302219.001).
  • [ISSN] 0270-4137
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 5P30CA047904-18; United States / NCI NIH HHS / CA / R01CA095239
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Androgens; 0 / Antineoplastic Agents, Hormonal; 0 / Endothelin-1; 0 / Receptor, Endothelin A; 0 / Receptors, Androgen
  •  go-up   go-down


51. Rocchi P, Beraldi E, Ettinger S, Fazli L, Vessella RL, Nelson C, Gleave M: Increased Hsp27 after androgen ablation facilitates androgen-independent progression in prostate cancer via signal transducers and activators of transcription 3-mediated suppression of apoptosis. Cancer Res; 2005 Dec 1;65(23):11083-93
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Increased Hsp27 after androgen ablation facilitates androgen-independent progression in prostate cancer via signal transducers and activators of transcription 3-mediated suppression of apoptosis.
  • One strategy to improve therapies in prostate cancer involves targeting cytoprotective genes activated by androgen withdrawal to delay the emergence of the androgen-independent (AI) phenotype.
  • The objectives of this study were to define changes in Hsp27 levels after androgen ablation and to evaluate the functional relevance of these changes in AI progression.
  • Using a tissue microarray of 232 specimens of hormone-naïve and post-hormone ablation-treated prostate cancer, we found that Hsp27 levels increase after androgen ablation to become highly expressed (>4-fold, P < or = 0.01) in AI tumors.
  • Hsp27 overexpression rendered LNCaP cells highly resistant to androgen withdrawal both in vitro and in vivo.
  • Tumor volume and serum prostate-specific antigen levels increased 4.3- and 10-fold faster after castration when Hsp27 was overexpressed.
  • Hsp27 ASO treatment in athymic mice bearing LNCaP tumors significantly delayed LNCaP tumor growth after castration, decreasing mean tumor volume and serum prostate-specific antigen levels by 57% and 69%, respectively.
  • These findings identify Hsp27 as a modulator of Stat3-regulated apoptosis after androgen ablation and as a potential therapeutic target in advanced prostate cancer.
  • [MeSH-major] Heat-Shock Proteins / biosynthesis. Neoplasm Proteins / biosynthesis. Prostatic Neoplasms / metabolism. STAT3 Transcription Factor / metabolism

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16322258.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / HSP27 Heat-Shock Proteins; 0 / HSPB1 protein, human; 0 / Heat-Shock Proteins; 0 / Neoplasm Proteins; 0 / Oligonucleotides, Antisense; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / STAT3 Transcription Factor; 0 / STAT3 protein, human; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Casp3 protein, mouse; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases
  •  go-up   go-down


52. Lo Nigro C, Maffi M, Fischel JL, Formento P, Milano G, Merlano M: The combination of docetaxel and the somatostatin analogue lanreotide on androgen-independent docetaxel-resistant prostate cancer: experimental data. BJU Int; 2008 Aug 5;102(5):622-7
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The combination of docetaxel and the somatostatin analogue lanreotide on androgen-independent docetaxel-resistant prostate cancer: experimental data.
  • OBJECTIVE: To evaluate the effects of the association between docetaxel and the somatostatin analogue lanreotide on the androgen-independent prostate cancer cell line PC3, either sensitive or made resistant to docetaxel (PC3R), as new drugs and new combinations have promising clinical activity in hormone-refractory prostate cancer.
  • CONCLUSION: The present results provide a promising therapeutic approach for using somatostatin analogues in hormone-refractory prostate cancer, in which lanreotide could interact with docetaxel in PC3R cells, with possible explanatory mechanisms which involve P glycoprotein-mediated docetaxel resistance.
  • [MeSH-minor] Blotting, Western. Cell Line, Tumor. Drug Evaluation. Drug Resistance, Neoplasm. Humans. Male. Mitogen-Activated Protein Kinase Kinases / drug effects. Peptides, Cyclic / administration & dosage. Signal Transduction / drug effects. Somatostatin / administration & dosage. Somatostatin / analogs & derivatives. Taxoids / administration & dosage

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • Hazardous Substances Data Bank. DOCETAXEL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18494832.001).
  • [ISSN] 1464-410X
  • [Journal-full-title] BJU international
  • [ISO-abbreviation] BJU Int.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Peptides, Cyclic; 0 / Taxoids; 118992-92-0 / lanreotide; 15H5577CQD / docetaxel; 51110-01-1 / Somatostatin; EC 2.7.12.2 / Mitogen-Activated Protein Kinase Kinases
  •  go-up   go-down


53. Dehm SM, Tindall DJ: Regulation of androgen receptor signaling in prostate cancer. Expert Rev Anticancer Ther; 2005 Feb;5(1):63-74
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Regulation of androgen receptor signaling in prostate cancer.
  • Prostate cancer is a significant cause of morbidity and mortality worldwide.
  • Normal prostate tissue is regulated by androgens, which activate the androgen receptor, a nuclear receptor transcription factor.
  • Most prostate tumors retain androgen dependence, therefore, current therapies for advanced prostate cancer either reduce androgen levels or prevent binding to the androgen receptor.
  • Despite this regimen, prostate cancer invariably progresses to a fatal, androgen-refractory state.
  • Although these relapsed tumors are androgen independent, they are still dependent on the androgen receptor for their growth and survival.
  • The focus of this review will be to highlight our current understanding of the mechanisms of androgen receptor activation in androgen-refractory prostate cancer.
  • How these mechanisms of androgen receptor activation could be targeted in this advanced stage of the disease is also discussed.
  • [MeSH-major] Androgens / physiology. Prostatic Neoplasms / physiopathology. Receptors, Androgen / physiology. Signal Transduction
  • [MeSH-minor] Antineoplastic Agents, Hormonal / pharmacology. Antineoplastic Agents, Hormonal / therapeutic use. Drug Resistance, Neoplasm. Humans. Male

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15757439.001).
  • [ISSN] 1744-8328
  • [Journal-full-title] Expert review of anticancer therapy
  • [ISO-abbreviation] Expert Rev Anticancer Ther
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Androgens; 0 / Antineoplastic Agents, Hormonal; 0 / Receptors, Androgen
  • [Number-of-references] 96
  •  go-up   go-down


54. Joshua AM, Nordman I, Venkataswaran R, Clarke S, Stockler MR, Boyer MJ: Weekly docetaxel as second line treatment after mitozantrone for androgen-independent prostate cancer. Intern Med J; 2005 Aug;35(8):468-72
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Weekly docetaxel as second line treatment after mitozantrone for androgen-independent prostate cancer.
  • BACKGROUND: Two recent phase III trials have shown an improvement in survival with the use of docetaxel in metastatic androgen-independent prostate cancer (AIPC) compared to mitozantrone.
  • End-points included prostate specific antigen response, common toxicity criteria, time to progression and overall survival.
  • CONCLUSIONS: Weekly docetaxel is a safe and active second-line treatment after mitozantrone for androgen-resistant prostate cancer, with similar levels of activity to the first-line setting.
  • [MeSH-minor] Aged. Dose-Response Relationship, Drug. Drug Administration Schedule. Humans. Infusions, Intravenous. Male. Maximum Tolerated Dose. Middle Aged. Mitoxantrone / adverse effects. Mitoxantrone / therapeutic use. Neoplasm Staging. Neoplasms, Hormone-Dependent. Prognosis. Prospective Studies. Prostate-Specific Antigen / blood. Risk Assessment. Survival Rate. Taxoids / adverse effects. Taxoids / therapeutic use. Treatment Outcome

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • Hazardous Substances Data Bank. DOCETAXEL .
  • Hazardous Substances Data Bank. NOVANTRONE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16176469.001).
  • [ISSN] 1444-0903
  • [Journal-full-title] Internal medicine journal
  • [ISO-abbreviation] Intern Med J
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Taxoids; 15H5577CQD / docetaxel; BZ114NVM5P / Mitoxantrone; EC 3.4.21.77 / Prostate-Specific Antigen
  •  go-up   go-down


55. Katsogiannou M, El Boustany C, Gackiere F, Delcourt P, Athias A, Mariot P, Dewailly E, Jouy N, Lamaze C, Bidaux G, Mauroy B, Prevarskaya N, Slomianny C: Caveolae contribute to the apoptosis resistance induced by the alpha(1A)-adrenoceptor in androgen-independent prostate cancer cells. PLoS One; 2009;4(9):e7068
Hazardous Substances Data Bank. CHOLESTEROL .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Caveolae contribute to the apoptosis resistance induced by the alpha(1A)-adrenoceptor in androgen-independent prostate cancer cells.
  • BACKGROUND: During androgen ablation prostate cancer cells' growth and survival become independent of normal regulatory mechanisms.
  • These androgen-independent cells acquire the remarkable ability to adapt to the surrounding microenvironment whose factors, such as neurotransmitters, influence their survival.
  • Although findings are becoming evident about the expression of alpha(1A)-adrenoceptors in prostate cancer epithelial cells, their exact functional role in androgen-independent cells has yet to be established.
  • Previous work has demonstrated that membrane lipid rafts associated with key signalling proteins mediate growth and survival signalling pathways in prostate cancer cells.
  • METHODOLOGY/PRINCIPAL FINDINGS: In order to analyze the membrane topology of the alpha(1A)-adrenoceptor we explored its presence by a biochemical approach in purified detergent resistant membrane fractions of the androgen-independent prostate cancer cell line DU145.
  • Further, immunohistofluorescence revealed the relation between high levels of alpha(1A)-adrenoceptor and caveolin-1 expression with advanced stage prostate cancer.
  • CONCLUSIONS/SIGNIFICANCE: In conclusion, we propose that alpha(1A)-adrenoceptor stimulation in androgen-independent prostate cancer cells via caveolae constitutes one of the mechanisms contributing to their protection from TG-induced apoptosis.
  • [MeSH-major] Apoptosis. Caveolae / metabolism. Drug Resistance, Neoplasm. Prostatic Neoplasms / pathology

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Semin Oncol. 1988 Aug;15(4):371-89 [3043671.001]
  • [Cites] Prostate Suppl. 1989;2:5-16 [2619992.001]
  • [Cites] Prostate Suppl. 1992;4:129-38 [1574453.001]
  • [Cites] Nature. 1994 Sep 22;371(6495):346-7 [8090205.001]
  • [Cites] J Biol Chem. 1994 Dec 30;269(52):32848-57 [7806510.001]
  • [Cites] Br J Urol. 1994 Nov;74(5):585-9 [7530122.001]
  • [Cites] Cell. 1995 Jan 27;80(2):249-57 [7834744.001]
  • [Cites] Cell. 1995 Jun 2;81(5):801-9 [7774019.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Sep 12;92(19):8655-9 [7567992.001]
  • [Cites] FEBS Lett. 2000 Jan 21;466(1):6-10 [10648802.001]
  • [Cites] J Biol Chem. 2000 Apr 14;275(15):11470-7 [10753965.001]
  • [Cites] Cancer Res. 2000 Aug 15;60(16):4550-5 [10969806.001]
  • [Cites] Clin Biochem. 2000 Oct;33(7):541-7 [11124339.001]
  • [Cites] J Urol. 2001 Mar;165(3):1033-6 [11176535.001]
  • [Cites] Cancer Res. 2001 May 15;61(10):3882-5 [11358800.001]
  • [Cites] Cancer Res. 2001 Jun 1;61(11):4386-92 [11389065.001]
  • [Cites] Nat Rev Mol Cell Biol. 2000 Oct;1(1):31-9 [11413487.001]
  • [Cites] Mol Cell. 2001 Mar;7(3):661-71 [11463390.001]
  • [Cites] J Urol. 1995 Dec;154(6):2096-9 [7500467.001]
  • [Cites] Br J Pharmacol. 1995 Jul;115(5):781-6 [8548177.001]
  • [Cites] Br J Pharmacol. 1996 Nov;119(5):797-803 [8922723.001]
  • [Cites] Prostate. 1997 Feb 15;30(3):202-15 [9122046.001]
  • [Cites] Nature. 1997 Jun 5;387(6633):569-72 [9177342.001]
  • [Cites] Naunyn Schmiedebergs Arch Pharmacol. 1998 Feb;357(2):100-10 [9521482.001]
  • [Cites] Clin Cancer Res. 1998 Aug;4(8):1873-80 [9717814.001]
  • [Cites] Nat Med. 1998 Sep;4(9):1062-4 [9734401.001]
  • [Cites] J Biol Chem. 1998 Dec 11;273(50):33533-9 [9837934.001]
  • [Cites] Annu Rev Cell Dev Biol. 1998;14:111-36 [9891780.001]
  • [Cites] Cancer Res. 1999 Jan 15;59(2):279-84 [9927031.001]
  • [Cites] Eur Urol. 1999;36 Suppl 1:31-4; discussion 65 [10393470.001]
  • [Cites] J Urol. 1999 Oct;162(4):1537-42 [10492251.001]
  • [Cites] Mol Cell Biol. 1999 Nov;19(11):7289-304 [10523618.001]
  • [Cites] J Biol Chem. 1957 May;226(1):497-509 [13428781.001]
  • [Cites] CA Cancer J Clin. 2005 Mar-Apr;55(2):74-108 [15761078.001]
  • [Cites] Ann Med. 2004;36(8):584-95 [15768830.001]
  • [Cites] Mol Biol Cell. 2005 May;16(5):2234-47 [15728718.001]
  • [Cites] Prostate. 2005 Sep 1;64(4):408-18 [15789364.001]
  • [Cites] J Cell Biochem. 2006 Jan 1;97(1):18-32 [16216007.001]
  • [Cites] Biochim Biophys Acta. 2005 Dec 30;1746(3):234-51 [16368465.001]
  • [Cites] Cancer Res. 2006 Feb 15;66(4):2038-47 [16489003.001]
  • [Cites] Cell Calcium. 2006 Apr;39(4):357-66 [16442617.001]
  • [Cites] Endocr Relat Cancer. 2006 Mar;13(1):181-95 [16601287.001]
  • [Cites] Prostate. 2006 May 15;66(7):761-7 [16425183.001]
  • [Cites] J Mol Cell Cardiol. 2006 Jul;41(1):17-25 [16730745.001]
  • [Cites] Br J Pharmacol. 2007 Feb;150(3):261-70 [17179950.001]
  • [Cites] Circulation. 2007 Feb 13;115(6):763-72 [17283256.001]
  • [Cites] Cytometry A. 2007 Mar;71(3):125-31 [17252584.001]
  • [Cites] Nat Rev Mol Cell Biol. 2007 Mar;8(3):185-94 [17318224.001]
  • [Cites] Prostate. 2007 May 1;67(6):614-22 [17299799.001]
  • [Cites] Apoptosis. 2007 May;12(5):887-96 [17453158.001]
  • [Cites] Neuropathol Appl Neurobiol. 2007 Jun;33(3):317-27 [17493012.001]
  • [Cites] Biochim Biophys Acta. 2007 Aug;1773(8):1213-26 [17112607.001]
  • [Cites] Nat Rev Mol Cell Biol. 2008 Jan;9(1):47-59 [18097445.001]
  • [Cites] Eur J Pharmacol. 2008 Jan 14;578(2-3):349-58 [17936747.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Jan 8;105(1):124-8 [18172219.001]
  • [Cites] J Biol Chem. 2008 Feb 1;283(5):2973-85 [18048357.001]
  • [Cites] J Biol Chem. 2008 Apr 11;283(15):10162-73 [18230611.001]
  • [Cites] Cancer Metastasis Rev. 2008 Dec;27(4):715-35 [18506396.001]
  • [Cites] J Mol Biol. 2005 Mar 4;346(4):1109-20 [15701521.001]
  • [Cites] Cardiovasc Res. 2001 Sep;51(4):709-16 [11530104.001]
  • [Cites] Science. 2001 Sep 28;293(5539):2449-52 [11498544.001]
  • [Cites] J Urol. 2002 Mar;167(3):1458-63 [11832770.001]
  • [Cites] Endocr Relat Cancer. 2002 Mar;9(1):61-73 [11914183.001]
  • [Cites] Biophys J. 2002 May;82(5):2526-35 [11964241.001]
  • [Cites] Curr Urol Rep. 2000 Aug;1(2):89-96 [12084321.001]
  • [Cites] Arterioscler Thromb Vasc Biol. 2002 Aug 1;22(8):1267-72 [12171786.001]
  • [Cites] J Urol. 2002 Oct;168(4 Pt 1):1589-96 [12352463.001]
  • [Cites] Prostate Cancer Prostatic Dis. 2002;5(2):88-95 [12496995.001]
  • [Cites] Cancer Res. 2003 May 1;63(9):2037-41 [12727816.001]
  • [Cites] J Clin Invest. 2003 Jun;111(11):1691-701 [12782672.001]
  • [Cites] Sci STKE. 2004 Jan 20;2004(216):re2 [14734786.001]
  • [Cites] J Mol Endocrinol. 2004 Apr;32(2):325-38 [15072542.001]
  • [Cites] J Cell Biol. 1973 May;57(2):551-65 [4121290.001]
  • (PMID = 19763272.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ADRA1A protein, human; 0 / Neurotransmitter Agents; 0 / Receptors, Adrenergic, alpha-1; 0 / Sphingomyelins; 67526-95-8 / Thapsigargin; 97C5T2UQ7J / Cholesterol
  • [Other-IDs] NLM/ PMC2742726
  •  go-up   go-down


56. Montironi R, Mazzucchelli R, Barbisan F, Stramazzotti D, Santinelli A, Scarpelli M, Lòpez Beltran A: HER2 expression and gene amplification in pT2a Gleason score 6 prostate cancer incidentally detected in cystoprostatectomies: comparison with clinically detected androgen-dependent and androgen-independent cancer. Hum Pathol; 2006 Sep;37(9):1137-44
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] HER2 expression and gene amplification in pT2a Gleason score 6 prostate cancer incidentally detected in cystoprostatectomies: comparison with clinically detected androgen-dependent and androgen-independent cancer.
  • Previous studies have demonstrated HER2 protein overexpression and/or gene amplification in a subset of patients with clinically significant prostate cancer (PCa), especially in the androgen-independent phase of the disease.
  • Comparison was made with clinically detected PCa, both untreated and hormonally treated, and with androgen-independent PCa.
  • It also included 9 specimens of transurethral resection of the prostate with hormone-independent cancer and 8 cases of normal prostate tissue from CyP specimens without PCa and prostatic intraepithelial neoplasia.
  • Prostate cancer showed HER2 overexpression in 16% of cases in the CyP group and in 36% and 47.5% in the untreated and treated groups, respectively.
  • HER2 overexpression was present in 78% of androgen-independent cancers.
  • In PCa, the proportion of nuclei with gene amplification was 0.7% (in 3 cases) in the CyP group, 2.6% (in 10 cases) and 2.5% (in 12 cases) in the untreated and treated groups, respectively, and 9% (in 6 cases) in the androgen-independent PCa.
  • Ki-67 expression in HGPIN and PCa in CyP specimens was lower than in the radical prostatectomies and cases of transurethral resection of the prostate.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cystectomy. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Incidental Findings. Ki-67 Antigen / metabolism. Male. Middle Aged. Neoplasm Staging. Prostate / metabolism. Prostate / pathology. Prostate / surgery. Prostatectomy. Receptors, Androgen / metabolism

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16938518.001).
  • [ISSN] 0046-8177
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ki-67 Antigen; 0 / Receptors, Androgen; EC 2.7.10.1 / Receptor, ErbB-2
  •  go-up   go-down


57. Trump DL, Potter DM, Muindi J, Brufsky A, Johnson CS: Phase II trial of high-dose, intermittent calcitriol (1,25 dihydroxyvitamin D3) and dexamethasone in androgen-independent prostate cancer. Cancer; 2006 May 15;106(10):2136-42
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase II trial of high-dose, intermittent calcitriol (1,25 dihydroxyvitamin D3) and dexamethasone in androgen-independent prostate cancer.
  • BACKGROUND: Data suggest that vitamin D plays a role in the treatment and prevention of prostate cancer.
  • RESULTS: Forty-three men with androgen-independent prostate cancer were entered; 37 received at least 1 month of calcitriol given at a dose of 12 microg every day x 3 per week.
  • The majority of patients had bone metastases and rising prostate-specific antigen (PSA) levels.
  • [MeSH-minor] Aged. Dose-Response Relationship, Drug. Drug Administration Schedule. Drug Therapy, Combination. Follow-Up Studies. Humans. Male. Maximum Tolerated Dose. Middle Aged. Neoplasm Staging. Neoplasms, Hormone-Dependent / drug therapy. Neoplasms, Hormone-Dependent / pathology. Neoplasms, Hormone-Dependent / surgery. Patient Selection. Prostatectomy. Risk Assessment. Survival Analysis. Treatment Outcome

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. 1,25-DIHYDROXYCHOLECALCIFEROL .
  • Hazardous Substances Data Bank. DEXAMETHASONE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2006 American Cancer Society
  • (PMID = 16598750.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA67267; United States / NCI NIH HHS / CA / CA85142; United States / NCI NIH HHS / CA / CA95045
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 7S5I7G3JQL / Dexamethasone; FXC9231JVH / Calcitriol
  •  go-up   go-down


58. Kozlowski P, Wong J, Goldenberg SL: Serial tumour blood-flow measurements in androgen-dependent and -independent Shionogi tumour models. BJU Int; 2005 Mar;95(4):644-9
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Serial tumour blood-flow measurements in androgen-dependent and -independent Shionogi tumour models.
  • OBJECTIVE: To investigate the relationship between blood supply and hormonal status of hormone-dependent and -independent tumours in mice.
  • Serial measurements were taken throughout the initial tumour growth period, and during regression and subsequent androgen-independent (AI) relapse of the tumours in male mice, and throughout the growth of AI tumours in female mice.
  • The Tukey-Kramer test was used to identify differences between androgen-dependent (AD), male AI and female AI tumours.
  • [MeSH-minor] Animals. Blood Flow Velocity. Contrast Media. Female. Magnetic Resonance Imaging. Male. Mice. Neoplasm Transplantation

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15705096.001).
  • [ISSN] 1464-4096
  • [Journal-full-title] BJU international
  • [ISO-abbreviation] BJU Int.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Contrast Media
  •  go-up   go-down


59. Attia S, Eickhoff J, Wilding G, McNeel D, Blank J, Ahuja H, Jumonville A, Eastman M, Shevrin D, Glode M, Alberti D, Staab MJ, Horvath D, Straus J, Marnocha R, Liu G: Randomized, double-blinded phase II evaluation of docetaxel with or without doxercalciferol in patients with metastatic, androgen-independent prostate cancer. Clin Cancer Res; 2008 Apr 15;14(8):2437-43
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Randomized, double-blinded phase II evaluation of docetaxel with or without doxercalciferol in patients with metastatic, androgen-independent prostate cancer.
  • PURPOSE: Docetaxel is standard of care for androgen-independent prostate cancer (AIPC).
  • The primary end point was prostate-specific antigen (PSA) response.
  • [MeSH-minor] Aged. Aged, 80 and over. Androgens / physiology. Calcium / blood. Calcium / urine. Double-Blind Method. Humans. Male. Middle Aged. Neoplasm Metastasis

  • Genetic Alliance. consumer health - Prostate cancer.
  • Genetic Alliance. consumer health - Metastatic cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. DOCETAXEL .
  • Hazardous Substances Data Bank. CALCIUM, ELEMENTAL .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18413835.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / T32 CA009614
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Ergocalciferols; 0 / Taxoids; 15H5577CQD / docetaxel; 3DIZ9LF5Y9 / 1 alpha-hydroxyergocalciferol; SY7Q814VUP / Calcium
  •  go-up   go-down


60. Diallo JS, Péant B, Lessard L, Delvoye N, Le Page C, Mes-Masson AM, Saad F: An androgen-independent androgen receptor function protects from inositol hexakisphosphate toxicity in the PC3/PC3(AR) prostate cancer cell lines. Prostate; 2006 Sep 1;66(12):1245-56
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] An androgen-independent androgen receptor function protects from inositol hexakisphosphate toxicity in the PC3/PC3(AR) prostate cancer cell lines.
  • Because few prostate cancer (PCa) cell lines have been used to study IP6, we assessed its efficacy in a panel of PCa cell lines.
  • METHODS AND RESULTS: Using WST-1 assays we observed that, although androgens did not modulate its efficacy, IP6 was more active in androgen receptor (AR) negative cells than in AR-positive cells.
  • CONCLUSION: We conclude that resistance to IP6 can be linked to a ligand-independent AR function.
  • [MeSH-major] Androgens / physiology. Phytic Acid / adverse effects. Prostatic Neoplasms / pathology. Prostatic Neoplasms / physiopathology. Receptors, Androgen / physiology
  • [MeSH-minor] Apoptosis / drug effects. Apoptosis / physiology. Caspase 3. Caspases / metabolism. Cell Line, Tumor. DNA Fragmentation. DNA, Neoplasm / genetics. Drug Resistance, Neoplasm. E2F Transcription Factors / genetics. E2F Transcription Factors / metabolism. Gene Expression Regulation, Neoplastic / drug effects. Humans. Male. NF-kappa B / genetics. NF-kappa B / metabolism. Prostate / chemistry. Prostate / drug effects. Prostate / metabolism. Prostate / pathology. RNA, Small Interfering / genetics. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Protein p53 / metabolism

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2006 Wiley-Liss, Inc.
  • (PMID = 16705740.001).
  • [ISSN] 0270-4137
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / DNA, Neoplasm; 0 / E2F Transcription Factors; 0 / NF-kappa B; 0 / RNA, Small Interfering; 0 / Receptors, Androgen; 0 / Tumor Suppressor Protein p53; 7IGF0S7R8I / Phytic Acid; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases
  •  go-up   go-down


61. Bander NH, Milowsky MI, Nanus DM, Kostakoglu L, Vallabhajosula S, Goldsmith SJ: Phase I trial of 177lutetium-labeled J591, a monoclonal antibody to prostate-specific membrane antigen, in patients with androgen-independent prostate cancer. J Clin Oncol; 2005 Jul 20;23(21):4591-601
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase I trial of 177lutetium-labeled J591, a monoclonal antibody to prostate-specific membrane antigen, in patients with androgen-independent prostate cancer.
  • PURPOSE: To determine the maximum tolerated dose (MTD), toxicity, human anti-J591 response, pharmacokinetics (PK), organ dosimetry, targeting, and biologic activity of (177)Lutetium-labeled anti-prostate-specific membrane antigen (PSMA) monoclonal antibody J591 ((177)Lu-J591) in patients with androgen-independent prostate cancer (PC).
  • PATIENTS AND METHODS: Thirty-five patients with progressing androgen-independent PC received (177)Lu-J591.
  • Biologic activity was seen with four patients experiencing >or= 50% declines in prostate-specific antigen (PSA) levels lasting from 3+ to 8 months.
  • Acceptable toxicity, excellent targeting of known sites of PC metastases, and biologic activity in patients with androgen-independent PC warrant further investigation.
  • [MeSH-major] Antibodies, Monoclonal / immunology. Lutetium / therapeutic use. Prostate-Specific Antigen / immunology. Prostatic Neoplasms / radiotherapy. Radioisotopes / therapeutic use
  • [MeSH-minor] Aged. Aged, 80 and over. Bone Marrow / drug effects. Cell Membrane / immunology. Humans. Male. Middle Aged. Neoplasm Metastasis / radionuclide imaging

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer Screening.
  • COS Scholar Universe. author profiles.
  • 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 .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] J Clin Oncol. 2005 Jul 20;23(21):4567-9 [15837975.001]
  • (PMID = 15837970.001).
  • [ISSN] 0732-183X
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / M01RR00047
  • [Publication-type] Clinical Trial; Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / J591 monoclonal antibody; 0 / Radioisotopes; 5H0DOZ21UJ / Lutetium; EC 3.4.21.77 / Prostate-Specific Antigen
  •  go-up   go-down


62. Sissung TM, Baum CE, Deeken J, Price DK, Aragon-Ching J, Steinberg SM, Dahut W, Sparreboom A, Figg WD: ABCB1 genetic variation influences the toxicity and clinical outcome of patients with androgen-independent prostate cancer treated with docetaxel. Clin Cancer Res; 2008 Jul 15;14(14):4543-9
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] ABCB1 genetic variation influences the toxicity and clinical outcome of patients with androgen-independent prostate cancer treated with docetaxel.
  • PURPOSE: Polymorphisms that are associated with ABCB1 expression and function may be linked to treatment efficacy and the development of neutropenia and neurotoxicity in patients with androgen-independent prostate cancer receiving docetaxel.
  • EXPERIMENTAL DESIGN: Patients with androgen-independent prostate cancer treated with docetaxel alone (n = 23) or docetaxel and thalidomide (n = 50) were genotyped for the ABCB1 1236C>T, 2677 G>T/A, and 3435 C>T alleles by direct sequencing, and diplotypes were constructed using an EM algorithm.
  • [MeSH-minor] Androgens / metabolism. Drug Resistance, Neoplasm / genetics. Gene Frequency. Genotype. Humans. Kaplan-Meier Estimate. Male. P-Glycoproteins. Polymerase Chain Reaction. Thalidomide / therapeutic use

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. DOCETAXEL .
  • Hazardous Substances Data Bank. THALIDOMIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Jpn J Cancer Res. 1999 Dec;90(12):1380-6 [10665657.001]
  • [Cites] Cancer Chemother Rep. 1966 Mar;50(3):163-70 [5910392.001]
  • [Cites] Muscle Nerve. 2001 Aug;24(8):1050-7 [11439380.001]
  • [Cites] Acta Otolaryngol. 2001 Sep;121(6):735-42 [11678173.001]
  • [Cites] Eur J Cancer. 2002 Mar;38(4):497-504 [11872341.001]
  • [Cites] Nat Rev Cancer. 2002 Jan;2(1):48-58 [11902585.001]
  • [Cites] Proc Natl Acad Sci U S A. 1987 Nov;84(21):7735-8 [2444983.001]
  • [Cites] Proc Natl Acad Sci U S A. 1989 Jan;86(2):695-8 [2563168.001]
  • [Cites] Cell. 1991 Jul 12;66(1):85-94 [1712673.001]
  • [Cites] Blood. 1992 Dec 1;80(11):2729-34 [1360266.001]
  • [Cites] Cancer Treat Rev. 1993 Oct;19(4):351-86 [8106152.001]
  • [Cites] Cell. 1994 May 20;77(4):491-502 [7910522.001]
  • [Cites] J Chromatogr B Biomed Sci Appl. 1997 Jun 6;693(2):437-41 [9210450.001]
  • [Cites] Neurosci Lett. 1997 Aug 22;232(1):41-4 [9292887.001]
  • [Cites] Recent Results Cancer Res. 1998;144:93-115 [9304712.001]
  • [Cites] Clin Cancer Res. 2006 Feb 1;12(3 Pt 1):854-9 [16467099.001]
  • [Cites] Cancer Chemother Pharmacol. 2006 May;57(5):599-606 [16136308.001]
  • [Cites] J Clin Pharmacol. 2006 Mar;46(3):373-9 [16490813.001]
  • [Cites] Clin Pharmacol Ther. 2006 Jun;79(6):570-80 [16765145.001]
  • [Cites] Clin Cancer Res. 2006 Jul 1;12(13):4127; author reply 4127-9 [16818714.001]
  • [Cites] Clin Cancer Res. 2006 Oct 1;12(19):5786-93 [17020985.001]
  • [Cites] Clin Cancer Res. 2006 Oct 15;12(20 Pt 1):6204 [17062699.001]
  • [Cites] Eur J Cancer. 2006 Nov;42(17):2893-6 [16950614.001]
  • [Cites] Pharmacogenet Genomics. 2006 Dec;16(12):855-61 [17108809.001]
  • [Cites] Science. 2007 Jan 26;315(5811):525-8 [17185560.001]
  • [Cites] Expert Opin Pharmacother. 2007 Feb;8(2):119-27 [17257083.001]
  • [Cites] Clin Cancer Res. 2008 Jun 1;14(11):3312-8 [18519758.001]
  • [Cites] BJU Int. 2008 Aug 5;102(5):617-21 [18537956.001]
  • [Cites] Prostate. 2004 Apr 1;59(1):77-90 [14991868.001]
  • [Cites] Clin Pharmacokinet. 2004;43(9):553-76 [15217301.001]
  • [Cites] J Clin Oncol. 2004 Jul 1;22(13):2532-9 [15226321.001]
  • [Cites] N Engl J Med. 2004 Oct 7;351(15):1502-12 [15470213.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Mar 28;97(7):3473-8 [10716719.001]
  • (PMID = 18628469.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z01 BC010453-06
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ABCB1 protein, human; 0 / Androgens; 0 / Antineoplastic Agents; 0 / P-Glycoprotein; 0 / P-Glycoproteins; 0 / Taxoids; 15H5577CQD / docetaxel; 4Z8R6ORS6L / Thalidomide
  • [Other-IDs] NLM/ NIHMS105257; NLM/ PMC2723795
  •  go-up   go-down


63. Klotz L: Maximal androgen blockade for advanced prostate cancer. Best Pract Res Clin Endocrinol Metab; 2008 Apr;22(2):331-40
Hazardous Substances Data Bank. BICALUTAMIDE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Maximal androgen blockade for advanced prostate cancer.
  • Maximal androgen blockade (MAB) refers to the combination of medical (gonadotrophin-releasing hormone agonist) or surgical castration with an anti-androgen for the treatment of advanced prostate cancer.
  • A substantial body of basic research has improved our understanding of the interactions between the anti-androgens, the androgen receptor, and androgen response elements in the genome.
  • Anti-androgens act by two primary mechanisms: inhibition of ligand (androgen) binding to the androgen receptor, and inhibition of androgen-independent activation of the receptor.
  • The latter mechanism occurs via several pathways, including inhibiting nuclear co-activators, activating co-suppressors, and inhibiting transcription of a variety of androgen-regulated genes.
  • It is more accurate to refer to these compounds as androgen-receptor antagonists, since they inhibit activation whether this is androgen-mediated or not.
  • Within the class of non-steroidal anti-androgens, there is variation in the degree to which ligand-independent activation is inhibited.
  • In prostate cancer patients at high risk for mortality (based on extent of disease or prostate-specific antigen kinetics), combination therapy with bicalutamide should be considered in preference to monotherapy.
  • [MeSH-major] Androgen Antagonists / administration & dosage. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Anilides / administration & dosage. Anilides / adverse effects. Antineoplastic Agents, Hormonal / administration & dosage. Antineoplastic Agents, Hormonal / adverse effects. Antineoplastic Agents, Hormonal / economics. Antineoplastic Combined Chemotherapy Protocols / economics. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Combined Modality Therapy / adverse effects. Disease Progression. Dose-Response Relationship, Drug. Humans. Male. Meta-Analysis as Topic. Neoplasm Staging. Neoplasms, Hormone-Dependent / drug therapy. Nitriles / administration & dosage. Nitriles / adverse effects. Orchiectomy / adverse effects. Orchiectomy / methods. Randomized Controlled Trials as Topic. Survival Analysis. Tosyl Compounds / administration & dosage. Tosyl Compounds / adverse effects. Withholding Treatment

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18471790.001).
  • [ISSN] 1521-690X
  • [Journal-full-title] Best practice & research. Clinical endocrinology & metabolism
  • [ISO-abbreviation] Best Pract. Res. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Anilides; 0 / Antineoplastic Agents, Hormonal; 0 / Nitriles; 0 / Tosyl Compounds; A0Z3NAU9DP / bicalutamide
  • [Number-of-references] 37
  •  go-up   go-down


64. Culig Z, Bartsch G: Androgen axis in prostate cancer. J Cell Biochem; 2006 Oct 1;99(2):373-81
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Androgen axis in prostate cancer.
  • Endocrine therapy for advanced prostate cancer is based on androgen ablation or blockade of the androgen receptor (AR).
  • AR action in prostate cancer has been investigated in a number of cell lines, their derivatives, and transgenic animals.
  • AR expression is heterogenous in prostate cancer in vivo; it could be detected in most primary tumors and their metastases.
  • AR expression increases after chronic androgen ablation in vitro.
  • In contrast, the AR pathway may be by-passed during chronic treatment with a nonsteroidal anti-androgen.
  • AR sensitivity in prostate cancer increases as a result of activation of the Ras/mitogen-activated protein kinase pathway.
  • One of the major difficulties in endocrine therapy for prostate cancer is acquisition of agonistic properties of AR antagonists observed in the presence of mutated AR.
  • Cofactors SRC-1, RAC3, p300/CBP, TIF-2, and Tip60 are upregulated in advanced prostate cancer.
  • Most studies on ligand-independent activation of the AR are focused on Her-2/neu and interleukin-6 (IL-6).
  • On the basis of studies that showed overexpression and activation of the AR in advanced prostate cancer, it was suggested that novel therapies that reduce AR expression will provide a benefit to patients.
  • There is experimental evidence showing that prostate tumor growth in vitro and in vivo is inhibited following administration of chemopreventive drugs or antisense oligonucleotides that downregulate AR mRNA and protein expression.
  • [MeSH-minor] Androgen Antagonists / therapeutic use. Animals. Cell Line, Tumor. Drug Resistance, Neoplasm. Gene Expression. Humans. Male. Models, Biological. Mutation. Neoplasms, Hormone-Dependent / drug therapy. Neoplasms, Hormone-Dependent / genetics. Neoplasms, Hormone-Dependent / metabolism. Receptors, Androgen / genetics. Receptors, Androgen / metabolism


65. Bigler D, Gioeli D, Conaway MR, Weber MJ, Theodorescu D: Rap2 regulates androgen sensitivity in human prostate cancer cells. Prostate; 2007 Oct 1;67(14):1590-9
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Rap2 regulates androgen sensitivity in human prostate cancer cells.
  • BACKGROUND: Progression of prostate cancer to a fatal androgen-independent disease is associated with activation of MAP kinase, consistent with chronic stimulation of the Ras-signaling pathway.
  • We have previously shown that Ras activation is sufficient to induce androgen-independent growth of prostate cancer cells.
  • Here we ask if Rap proteins play a role in determining androgen sensitivity of human prostate cancer cells either alone or in the context of an activated Ras.
  • METHODS: To evaluate the role of Rap proteins in androgen responsiveness we use Rap over-expression with or without mutated Ras co-transfection and Rap siRNA knockdown to evaluate androgen-dependent prostate-specific antigen (PSA) promoter reporter expression and cell growth in androgen-dependent LNCaP and independent C4-2 human prostate cancer cells.
  • Rap2a affects androgen-dependent PSA reporter expression in a dose-dependent manner in LNCaP and C4-2 cells.
  • We show that Rap2a antagonizes the enhanced PSA reporter expression conferred by an active RasV12 gene in prostate cancer cells. siRNA knockdown data indicate that Rap2 has a greater effect on androgen-stimulated growth in LNCaP than in C4-2 cells.
  • CONCLUSIONS: We show that Rap2 is involved in androgen-mediated transcriptional and growth responses of human prostate cancer cells.
  • [MeSH-minor] Animals. Cell Line, Tumor. GTP Phosphohydrolases / metabolism. Humans. Male. Mice. Prostate-Specific Antigen. RNA, Neoplasm / analysis. RNA, Small Interfering / pharmacology. Signal Transduction. Telomere-Binding Proteins / genetics. Telomere-Binding Proteins / metabolism

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17918750.001).
  • [ISSN] 0270-4137
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA104106; United States / NCI NIH HHS / CA / CA105402
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / RNA, Neoplasm; 0 / RNA, Small Interfering; 0 / TERF2IP protein, human; 0 / Telomere-Binding Proteins; EC 3.4.21.77 / Prostate-Specific Antigen; EC 3.6.1.- / GTP Phosphohydrolases; EC 3.6.1.- / RAP2A protein, human; EC 3.6.5.2 / rap GTP-Binding Proteins
  •  go-up   go-down


66. Zhou C, Ling MT, Kin-Wah Lee T, Man K, Wang X, Wong YC: FTY720, a fungus metabolite, inhibits invasion ability of androgen-independent prostate cancer cells through inactivation of RhoA-GTPase. Cancer Lett; 2006 Feb 20;233(1):36-47
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] FTY720, a fungus metabolite, inhibits invasion ability of androgen-independent prostate cancer cells through inactivation of RhoA-GTPase.
  • The failure of controlling androgen-independent and metastatic prostate cancer growth is the main cause of death in prostate cancer patients.
  • In this study, we have demonstrated evidence on the inhibitory effects of a fungus metabolite, FTY720, on the clonogenesity as well as invasion ability of androgen-independent prostate cancer cells.
  • First, using colony forming assay, we found that FTY720 treatment led to decreased colony forming ability of androgen-independent prostate cancer cell lines DU145 and PC3, indicating its negative role on cancer cell survival.
  • In addition, treatment with relatively low dose of FTY720 (i.e. inhibitory concentration of 50% cell survival) resulted in suppression of prostate cancer cell migration and invasion abilities demonstrated by Wound closure, 3D collagen gel invasion assays and stress fiber staining.
  • Furthermore, we found that the inhibitory effect of FTY720 on prostate cancer invasion was associated with down-regulation of GTP-bound active form of RhoA.
  • Since activation of RhoA-GTPase is associated with metastasis in many types of malignancies, our results not only suggest a new agent for the treatment of advanced prostate cancer, but also implicate a possible novel anticancer drug especially against metastatic cancers.
  • [MeSH-minor] Cell Line, Tumor. Cell Movement / drug effects. Cytoskeleton / drug effects. Fingolimod Hydrochloride. Humans. Male. Neoplasm Invasiveness

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16473668.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Propylene Glycols; EC 3.6.5.2 / rhoA GTP-Binding Protein; G926EC510T / Fingolimod Hydrochloride; NGZ37HRE42 / Sphingosine
  •  go-up   go-down


67. Montagnani Marelli M, Moretti RM, Mai S, Procacci P, Limonta P: Gonadotropin-releasing hormone agonists reduce the migratory and the invasive behavior of androgen-independent prostate cancer cells by interfering with the activity of IGF-I. Int J Oncol; 2007 Jan;30(1):261-71
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gonadotropin-releasing hormone agonists reduce the migratory and the invasive behavior of androgen-independent prostate cancer cells by interfering with the activity of IGF-I.
  • Androgen-independent prostate carcinoma is characterized by a high proliferation rate and by a strong metastatic behavior.
  • We have previously shown that GnRH agonists exert a direct and specific inhibitory action on the proliferation of androgen-independent prostate cancer cells (DU 145).
  • The present experiments were performed to clarify whether GnRH agonists might also affect the migratory and the invasive behavior of androgen-independent prostate cancer cells and to define their mechanism of action.
  • We found that, in androgen-independent prostate cancer cells, Leuprolide: a) interferes with the IGF-I system (receptor protein expression and tyrosine-phosphorylation);.
  • b) abrogates the IGF-I-induced phosphorylation of Akt (a kinase previously shown by us to mediate the pro-metastatic activity of IGF-I in prostate cancer cells);.
  • These data indicate that GnRH agonists, in addition to their well known antiproliferative effect, can also exert a significant inhibitory activity on the migratory and invasive behavior of androgen-independent prostate cancer cells, expressing the GnRH receptor.
  • [MeSH-minor] Antineoplastic Agents, Hormonal / pharmacology. Cell Line, Tumor. Humans. Male. Microscopy, Electron, Scanning. Neoplasm Invasiveness / prevention & control

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • Hazardous Substances Data Bank. LEUPROLIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17143537.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Androgens; 0 / Antineoplastic Agents, Hormonal; 33515-09-2 / Gonadotropin-Releasing Hormone; 67763-96-6 / Insulin-Like Growth Factor I; EFY6W0M8TG / Leuprolide
  •  go-up   go-down


68. Fujimoto N, Miyamoto H, Mizokami A, Harada S, Nomura M, Ueta Y, Sasaguri T, Matsumoto T: Prostate cancer cells increase androgen sensitivity by increase in nuclear androgen receptor and androgen receptor coactivators; a possible mechanism of hormone-resistance of prostate cancer cells. Cancer Invest; 2007 Feb;25(1):32-7
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prostate cancer cells increase androgen sensitivity by increase in nuclear androgen receptor and androgen receptor coactivators; a possible mechanism of hormone-resistance of prostate cancer cells.
  • Although androgen-hypersensitivity is one of the possible pathways of hormone-resistance in prostate cancer, the mechanisms of androgen-hypersensitivity are still largely unknown.
  • Using androgen-hypersensitive prostate cancer cells LN-TR2, established from androgen-sensitive LNCaP cells by the long term treatment with tumor necrosis factor alpha, we explored the mechanisms of androgen-hypersensitivity in prostate cancer cells which may thus play a role in hormone-resistance.
  • We examined the androgen receptor (AR) DNA sequence and the expression levels of AR and 8 AR cofactors in LNCaP and LN-TR2 cells.
  • We observed higher expressions of nuclear AR upon androgen-treatment and 2 AR coactivators, ARA55 and TIF2, in LN-TR2 compared to LNCaP cells.
  • An overexpression of ARA55 or TIF2 enhanced androgen-induced AR transcriptional activity in LNCaP cell.
  • In the presence of those AR coactivators, AR activity was observed even at low concentrations of androgen.
  • Taken together, our results suggest that prostate cancer cells change androgen-sensitivity by an overexpression of nuclear AR and AR coactivators, thus, resulting in transition from androgen-dependent to androgen-independent prostate cancer cells.
  • An increase in nuclear AR and AR coactivators may cause androgen-hypersensitivity of prostate cancer cells and thus play a role in hormone-resistance, at least in some patients with prostate cancer.
  • [MeSH-major] Drug Resistance, Neoplasm / physiology. Neoplasms, Hormone-Dependent / metabolism. Prostatic Neoplasms / metabolism. Receptors, Androgen / metabolism
  • [MeSH-minor] Androgen Antagonists / pharmacology. Antineoplastic Agents, Hormonal / pharmacology. Blotting, Western. Cell Line, Tumor. Cell Nucleus / metabolism. Humans. Immunohistochemistry. Intracellular Signaling Peptides and Proteins / metabolism. LIM Domain Proteins. Male. Nuclear Receptor Coactivator 2 / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Transfection. Tumor Necrosis Factor-alpha / metabolism

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17364555.001).
  • [ISSN] 0735-7907
  • [Journal-full-title] Cancer investigation
  • [ISO-abbreviation] Cancer Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Antineoplastic Agents, Hormonal; 0 / Intracellular Signaling Peptides and Proteins; 0 / LIM Domain Proteins; 0 / NCOA2 protein, human; 0 / Nuclear Receptor Coactivator 2; 0 / Receptors, Androgen; 0 / TGFB1I1 protein, human; 0 / Tumor Necrosis Factor-alpha
  •  go-up   go-down


69. You Z, Shi XB, DuRaine G, Haudenschild D, Tepper CG, Lo SH, Gandour-Edwards R, de Vere White RW, Reddi AH: Interleukin-17 receptor-like gene is a novel antiapoptotic gene highly expressed in androgen-independent prostate cancer. Cancer Res; 2006 Jan 1;66(1):175-83
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Interleukin-17 receptor-like gene is a novel antiapoptotic gene highly expressed in androgen-independent prostate cancer.
  • We have recently identified a new gene, interleukin-17 receptor-like (IL-17RL), which is expressed in normal prostate and prostate cancer.
  • This investigation is focused on the role of IL-17RL in prostate cancer.
  • We found that IL-17RL was expressed at significantly higher levels in several androgen-independent prostate cancer cell lines (PC3, DU145, cds1, cds2, and cds3) and tumors compared with the androgen-dependent cell lines (LNCaP and MLC-SV40) and tumors.
  • In an in vivo model of human prostate tumor growth in nude mice (CWR22 xenograft model), IL-17RL expression in tumors was induced by androgen deprivation.
  • The relapsed androgen-independent tumors expressed higher levels of IL-17RL compared with the androgen-dependent tumors.
  • Reciprocally, knocking down IL-17RL expression by small interfering RNA induced apoptosis in all the prostate cancer cell lines studied.
  • Taken together, these results show that IL-17RL is a novel antiapoptotic gene, which may confer partially the property of androgen-independent growth of prostate cancer by promoting cell survival.
  • Thus, IL-17RL is a potential therapeutic target in the treatment of prostate cancer.
  • [MeSH-minor] Animals. Caspase Inhibitors. Caspases / metabolism. Cell Adhesion / genetics. Cell Line, Tumor. Drug Resistance, Neoplasm. Enzyme Activation. Extracellular Matrix / genetics. Extracellular Matrix / metabolism. Humans. Isoenzymes. Male. Mice. Mice, Nude. Neoplasms, Hormone-Dependent / genetics. Neoplasms, Hormone-Dependent / metabolism. Neoplasms, Hormone-Dependent / pathology. RNA, Small Interfering / genetics. Tumor Necrosis Factor-alpha / pharmacology

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16397230.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NIAMS NIH HHS / AR / 5R01AR047345-03
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Caspase Inhibitors; 0 / IL17RC protein, human; 0 / Isoenzymes; 0 / RNA, Small Interfering; 0 / Receptors, Interleukin; 0 / Tumor Necrosis Factor-alpha; EC 3.4.22.- / Caspases
  •  go-up   go-down


70. Paule B, Terry S, Kheuang L, Soyeux P, Vacherot F, de la Taille A: The NF-kappaB/IL-6 pathway in metastatic androgen-independent prostate cancer: new therapeutic approaches? World J Urol; 2007 Oct;25(5):477-89
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The NF-kappaB/IL-6 pathway in metastatic androgen-independent prostate cancer: new therapeutic approaches?
  • The IL-6 acts as an autocrine and paracrine growth factor of androgen-independent prostate cancer.
  • An aberrant expression of the IL-6 gene and an increase in IL-6 expression are detected in bone metastatic and hormone-refractory prostate cancer.
  • These data provide a rational framework for targeting NF-kappaB and IL-6 activity in novel biologically based therapies for aggressive and androgen independent prostate cancers.
  • [MeSH-minor] Cell Communication / drug effects. Cell Communication / physiology. Gene Expression Regulation, Neoplastic / drug effects. Humans. Male. Neoplasm Metastasis / drug therapy. Neoplasm Metastasis / physiopathology. Osteoblasts / drug effects. Osteoblasts / pathology


71. Hokaiwado N, Takeshita F, Naiki-Ito A, Asamoto M, Ochiya T, Shirai T: Glutathione S-transferase Pi mediates proliferation of androgen-independent prostate cancer cells. Carcinogenesis; 2008 Jun;29(6):1134-8
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Glutathione S-transferase Pi mediates proliferation of androgen-independent prostate cancer cells.
  • Prostate cancers generally acquire an androgen-independent growth capacity with progression, resulting in resistance to antiandrogen therapy.
  • Therefore, identification of the genes regulated through this process may be important for understanding the mechanisms of prostate carcinogenesis.
  • We here utilized androgen-dependent/independent transplantable tumors, newly established with the 'transgenic rat adenocarcinoma in prostate' (TRAP) model, to analyze their gene expression using microarrays.
  • Among the overexpressed genes in androgen-independent prostate cancers compared with the androgen-dependent tumors, glutathione S-transferase pi (GST-pi) was included.
  • In line with this, human prostate cancer cell lines PC3 and DU145 (androgen independent) had higher expression of GST-pi compared with LNCaP (androgen dependent) as determined by semiquantitative reverse transcription-polymerase chain reaction analysis.
  • To investigate the roles of GST-pi expression in androgen-independent human prostate cancers, GST-pi was knocked down by a small interfering RNA (siRNA), resulting in significant decrease of the proliferation rate in the androgen-independent PC3 cell line.
  • These findings suggest that GST-pi might play important roles in proliferation of androgen-independent human prostate cancer cells.
  • [MeSH-minor] Androgens. Animals. Animals, Genetically Modified. Apoptosis. Blotting, Western. Cell Line, Tumor. Humans. In Situ Nick-End Labeling. Male. Neoplasm Transplantation. Oligonucleotide Array Sequence Analysis. RNA, Small Interfering. Rats. Reverse Transcriptase Polymerase Chain Reaction

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Mol Cell Probes. 2000 Aug;14(4):211-7 [10970725.001]
  • [Cites] Cancer Res. 2007 Oct 1;67(19):9248-57 [17909032.001]
  • [Cites] Cancer Res. 2001 Jun 15;61(12):4693-700 [11406539.001]
  • [Cites] Cancer Res. 2001 Jun 15;61(12):4820-6 [11406558.001]
  • [Cites] Clin Cancer Res. 2001 Sep;7(9):2727-30 [11555585.001]
  • [Cites] Am J Pathol. 2001 Nov;159(5):1815-26 [11696442.001]
  • [Cites] Cancer Res. 2001 Dec 15;61(24):8611-6 [11751372.001]
  • [Cites] Carcinogenesis. 2002 Mar;23(3):463-7 [11895861.001]
  • [Cites] Nat Rev Cancer. 2001 Oct;1(1):34-45 [11900250.001]
  • [Cites] Jpn J Cancer Res. 2002 Jul;93(7):767-73 [12149142.001]
  • [Cites] Nat Biotechnol. 2002 Oct;20(10):1006-10 [12244328.001]
  • [Cites] Cancer Detect Prev. 2002;26(5):376-80 [12518868.001]
  • [Cites] Prostate. 2003 May 15;55(3):199-205 [12692786.001]
  • [Cites] Clin Cancer Res. 2003 Jul;9(7):2673-7 [12855646.001]
  • [Cites] Cancer Res. 2003 Jul 15;63(14):3919-22 [12873985.001]
  • [Cites] Anticancer Res. 2003 May-Jun;23(3C):2897-902 [12926131.001]
  • [Cites] J Surg Res. 2003 Jul;113(1):102-8 [12943817.001]
  • [Cites] J Natl Cancer Inst. 2003 Nov 5;95(21):1634-7 [14600096.001]
  • [Cites] Biochem Biophys Res Commun. 2003 Nov 21;311(3):786-92 [14623342.001]
  • [Cites] J Urol. 2004 Jun;171(6 Pt 1):2195-8 [15126784.001]
  • [Cites] Oncogene. 2004 May 13;23(22):3945-52 [15007384.001]
  • [Cites] Prostate Cancer Prostatic Dis. 2002;5(1):22-7 [15195126.001]
  • [Cites] Urology. 2004 Oct;64(4):821-5 [15491741.001]
  • [Cites] Prostate. 2004 Dec 1;61(4):332-53 [15389811.001]
  • [Cites] Jpn J Cancer Res. 1988 May;79(5):573-5 [3136108.001]
  • [Cites] Cancer Lett. 1990 Nov 19;55(1):25-9 [2245407.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Nov 22;91(24):11733-7 [7972132.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 1997 Jun;6(6):443-50 [9184779.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Apr 28;95(9):5275-80 [9560266.001]
  • [Cites] Oncogene. 1999 Feb 11;18(6):1313-24 [10022813.001]
  • [Cites] Nat Med. 1999 Jun;5(6):707-10 [10371512.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2005 Jan;14(1):176-81 [15668493.001]
  • [Cites] Prostate. 2005 Jun 1;63(4):347-57 [15602745.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Aug 23;102(34):12177-82 [16091473.001]
  • [Cites] Cancer Res. 2005 Oct 15;65(20):9485-94 [16230413.001]
  • [Cites] Cancer Sci. 2006 Aug;97(8):689-96 [16863503.001]
  • [Cites] Urology. 2007 Jan;69(1):11-6 [17270599.001]
  • [Cites] Cancer Detect Prev. 2007;31(1):59-63 [17291695.001]
  • [Cites] Hum Pathol. 2007 Sep;38(9):1394-401 [17555796.001]
  • [Cites] Int J Cancer. 2001 May 20;95(3):152-5 [11307147.001]
  • (PMID = 18413363.001).
  • [ISSN] 1460-2180
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Androgens; 0 / RNA, Small Interfering; EC 2.5.1.18 / Glutathione S-Transferase pi
  • [Other-IDs] NLM/ PMC2443274
  •  go-up   go-down


72. Bonaccorsi L, Muratori M, Marchiani S, Forti G, Baldi E: The androgen receptor and prostate cancer invasion. Mol Cell Endocrinol; 2006 Feb 26;246(1-2):157-62
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The androgen receptor and prostate cancer invasion.
  • Recent evidence indicates that androgen-sensitive prostate cancer cells are characterized by a less pronounced malignant phenotype.
  • We demonstrate that transfection with an androgen receptor (AR) expression vector of the androgen-independent (AI) prostate cancer cell line PC3 decreases invasion and adhesion of these cells through modulation of alpha6beta4 integrin expression.
  • Treatment of PC3-AR cells with the synthetic androgen R1881 further reduced invasion without modifying alpha6beta4 expression on the cell surface, suggesting interference with the invasion process in response to EGF by an alternative mechanism.
  • Interestingly, immunoconfocal and immunoprecipitation experiments demonstrated also the occurrence of co-localization and interaction of AR with EGFR in PC3-AR cells and in another androgen-dependent PC cell line, LNCaP.
  • [MeSH-major] Neoplasm Invasiveness / physiopathology. Prostatic Neoplasms / physiopathology. Receptors, Androgen / metabolism. Signal Transduction

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16376012.001).
  • [ISSN] 0303-7207
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Integrins; 0 / Receptors, Androgen; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
  •  go-up   go-down


73. Miyoshi Y, Uemura H, Nakamura M, Hasumi H, Sugiura S, Makiyama K, Nakaigawa N, Kishida T, Ogawa T, Yao M, Kubota Y: Treatment of androgen-independent, hormone-refractory prostate cancer with docetaxel in Japanese patients. Int J Clin Oncol; 2005 Jun;10(3):182-6
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Treatment of androgen-independent, hormone-refractory prostate cancer with docetaxel in Japanese patients.
  • BACKGROUND: Although patients with prostate cancer with metastatic lesions initially respond to androgen ablation therapy, most patients ultimately develop a hormone-refractory state.
  • Effective treatment for men with hormone-refractory prostate cancer (HRPC) has not been established.
  • Change in serum prostate-specific antigen (PSA) was determined as the primary endpoint.
  • [MeSH-minor] Aged. Androgens / pharmacology. Antineoplastic Agents, Hormonal / pharmacology. Drug Resistance, Neoplasm. Humans. Male. Middle Aged. Prostate-Specific Antigen. Survival Analysis

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • Hazardous Substances Data Bank. DOCETAXEL .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15990966.001).
  • [ISSN] 1341-9625
  • [Journal-full-title] International journal of clinical oncology
  • [ISO-abbreviation] Int. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Androgens; 0 / Antineoplastic Agents, Hormonal; 0 / Antineoplastic Agents, Phytogenic; 0 / Taxoids; 15H5577CQD / docetaxel; EC 3.4.21.77 / Prostate-Specific Antigen
  •  go-up   go-down


74. Kobayashi T, Inoue T, Shimizu Y, Terada N, Maeno A, Kajita Y, Yamasaki T, Kamba T, Toda Y, Mikami Y, Yamada T, Kamoto T, Ogawa O, Nakamura E: Activation of Rac1 is closely related to androgen-independent cell proliferation of prostate cancer cells both in vitro and in vivo. Mol Endocrinol; 2010 Apr;24(4):722-34
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Activation of Rac1 is closely related to androgen-independent cell proliferation of prostate cancer cells both in vitro and in vivo.
  • We and others previously showed that signaling through cSrc or atypical protein kinase C (aPKC) pathway regulates the proliferation of prostate cancer cells and is associated with their progression to castrate-resistance in vivo.
  • In the present study, we show that androgen-induced activation of cSrc regulates the activity of aPKC through the small molecular weight G protein Rac1 in androgen-dependent LNCaP cells.
  • In fact, forced expression of a constitutively active Rac1 mutant in LNCaP cells promoted cell proliferation under androgen-depleted conditions both in vitro and in vivo.
  • Moreover, LNCaP C4-2 and AILNCaP cells, the syngeneic androgen-independent sublines from LNCaP cells, harbored abundant Rac1-GTP.
  • Importantly, the inhibition of Rac1 suppressed cell proliferation and induced apoptotic cell death in all prostate cancer cell lines tested irrespective of their androgen-dependence.
  • In immunohistochemical evaluation of tumor specimens from prostate cancer patients, Rac1 pathway appeared to be activated in the majority of castrate-resistant diseases.
  • Collectively, our present results both in vitro and in vivo highly implicate that Rac1 can be a potential therapeutic target for patients with advanced prostate cancer, especially those with castrate-resistant status.
  • [MeSH-minor] Animals. Apoptosis / drug effects. Apoptosis / genetics. Blotting, Western. Castration. Cell Line. Cell Line, Tumor. Cell Proliferation. Flow Cytometry. Humans. Immunoblotting. Immunohistochemistry. In Vitro Techniques. Male. Metribolone / pharmacology. Mice. Mice, Inbred BALB C. Mice, Nude. Neoplasm Transplantation. Phosphorylation / drug effects. Protein Kinase C / metabolism. Proto-Oncogene Proteins pp60(c-src) / genetics. Proto-Oncogene Proteins pp60(c-src) / metabolism. Signal Transduction / drug effects. Signal Transduction / genetics

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cell. 2009 Jul 23;138(2):245-56 [19632176.001]
  • [Cites] Mol Cancer Res. 2006 Feb;4(2):79-92 [16513839.001]
  • [Cites] Cancer Res. 2006 Nov 1;66(21):10449-59 [17079466.001]
  • [Cites] Nature. 2002 Dec 12;420(6916):629-35 [12478284.001]
  • [Cites] Blood. 2006 Feb 1;107(3):870-9 [16204315.001]
  • [Cites] Cell. 1992 Aug 7;70(3):401-10 [1643658.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 May 18;101(20):7618-23 [15128949.001]
  • [Cites] J Oral Maxillofac Surg. 2004 Jun;62(6):702-7 [15170282.001]
  • [Cites] EMBO J. 2000 Oct 16;19(20):5406-17 [11032808.001]
  • [Cites] Urology. 2005 Aug;66(2):332-7 [16098362.001]
  • [Cites] Genes Dev. 1997 Sep 15;11(18):2295-322 [9308960.001]
  • [Cites] Nat Rev Cancer. 2004 Jun;4(6):470-80 [15170449.001]
  • [Cites] Cancer Res. 2005 Nov 1;65(21):9906-13 [16267015.001]
  • [Cites] Curr Biol. 2001 Nov 27;11(23):1836-46 [11728306.001]
  • [Cites] J Urol. 2005 Feb;173(2):342-59 [15643172.001]
  • [Cites] Science. 2005 Aug 5;309(5736):933-5 [16081735.001]
  • [Cites] Cell. 1996 May 17;85(4):573-83 [8653792.001]
  • [Cites] Cancer Res. 2005 Apr 1;65(7):2547-53 [15805247.001]
  • [Cites] Cancer Cell. 2002 Apr;1(3):237-46 [12086860.001]
  • [Cites] Endocr Rev. 2004 Apr;25(2):276-308 [15082523.001]
  • [Cites] Development. 2000 Jun;127(12):2629-42 [10821761.001]
  • [Cites] Genes Cells. 2001 Feb;6(2):107-19 [11260256.001]
  • [Cites] Mol Biol Cell. 1998 Mar;9(3):561-73 [9487126.001]
  • [Cites] CA Cancer J Clin. 2006 Mar-Apr;56(2):106-30 [16514137.001]
  • [Cites] Mol Biol Cell. 2005 May;16(5):2207-17 [15728722.001]
  • [Cites] Nat Rev Cancer. 2006 Jun;6(6):459-71 [16723992.001]
  • [Cites] Nat Rev Cancer. 2005 Jul;5(7):505-15 [16069815.001]
  • [Cites] J Urol. 2002 Jul;168(1):9-12 [12050481.001]
  • [Cites] Cancer Cell. 2006 Oct;10(4):309-19 [17045208.001]
  • [Cites] Endocr Relat Cancer. 2007 Jun;14(2):245-56 [17639041.001]
  • [Cites] J Biol Chem. 2001 Jul 13;276(28):25876-82 [11337492.001]
  • [Cites] Nat Rev Cancer. 2002 Feb;2(2):133-42 [12635176.001]
  • [Cites] Oncogene. 2004 Jul 15;23(32):5513-22 [15077174.001]
  • [Cites] Cancer Res. 1999 Apr 1;59(7):1391-9 [10197600.001]
  • [Cites] Cancer Res. 2009 Jan 1;69(1):151-60 [19117998.001]
  • [Cites] Cell. 1982 Dec;31(2 Pt 1):465-74 [6297767.001]
  • [Cites] Oncogene. 2008 Oct 23;27(49):6365-75 [18679417.001]
  • [Cites] J Pathol. 1996 Apr;178(4):437-41 [8691323.001]
  • [Cites] J Cell Biol. 2001 Jul 9;154(1):177-86 [11448999.001]
  • [Cites] J Biol Chem. 2003 Sep 5;278(36):34339-46 [12810717.001]
  • [Cites] Oncogene. 2006 May 11;25(20):2931-6 [16331248.001]
  • [Cites] Cell. 2000 Oct 13;103(2):227-38 [11057896.001]
  • [Cites] Mol Endocrinol. 2006 Dec;20(12):3053-69 [16931574.001]
  • [Cites] Cancer Res. 2004 Oct 1;64(19):7156-68 [15466214.001]
  • [Cites] Adv Cancer Res. 2002;84:57-80 [11883532.001]
  • [Cites] Cancer Res. 2005 Oct 15;65(20):9185-9 [16230377.001]
  • [Cites] J Biol Chem. 2002 Feb 15;277(7):4770-7 [11713255.001]
  • [Cites] J Biochem. 2003 Jan;133(1):9-16 [12761193.001]
  • [Cites] Gene. 2002 Mar 20;286(2):155-74 [11943472.001]
  • [Cites] Neoplasia. 2007 Feb;9(2):90-100 [17357254.001]
  • [Cites] Steroids. 2004 Aug;69(8-9):517-22 [15288763.001]
  • [Cites] Cancer Res. 2005 Nov 1;65(21):9611-6 [16266977.001]
  • [Cites] Am J Physiol Heart Circ Physiol. 2005 Dec;289(6):H2325-33 [16155095.001]
  • [Cites] Curr Biol. 1998 Mar 26;8(7):377-85 [9545195.001]
  • [Cites] Br J Cancer. 2006 Oct 23;95(8):1081-6 [17003780.001]
  • [Cites] Mol Cell Biol. 2002 Apr;22(8):2862-70 [11909978.001]
  • (PMID = 20203103.001).
  • [ISSN] 1944-9917
  • [Journal-full-title] Molecular endocrinology (Baltimore, Md.)
  • [ISO-abbreviation] Mol. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 2C323EGI97 / Metribolone; EC 2.7.10.2 / Proto-Oncogene Proteins pp60(c-src); EC 2.7.11.13 / PKC-3 protein; EC 2.7.11.13 / Protein Kinase C; EC 3.6.5.2 / rac1 GTP-Binding Protein
  •  go-up   go-down


75. Loberg RD, McGregor N, Ying C, Sargent E, Pienta KJ: In vivo evaluation of AT-101 (R-(-)-gossypol acetic acid) in androgen-independent growth of VCaP prostate cancer cells in combination with surgical castration. Neoplasia; 2007 Dec;9(12):1030-7
Hazardous Substances Data Bank. Gossypol .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] In vivo evaluation of AT-101 (R-(-)-gossypol acetic acid) in androgen-independent growth of VCaP prostate cancer cells in combination with surgical castration.
  • PURPOSE: Upregulation of Bcl-2 family members is a well-established mechanism in the development of androgen-independent prostate cancer.
  • Inhibition of the antiapoptotic proteins Bcl-2 and Mcl-1 may delay the transition to androgen-independent growth.
  • EXPERIMENTAL DESIGN: We have established a prostate cancer model with VCaP prostate cancer cells in vivo to study the transition to androgen independence.
  • Here, we investigated the efficacy of AT-101 (R-(-)-gossypol acetic acid; a pan small molecule inhibitor of Bcl-2, Bcl-x(L), and Mcl-1) in combination with surgical castration to delay the onset of androgen-independent growth in vivo.
  • ) 5 days/week) in combination with surgical castration delayed the onset of androgen-independent prostate cancer growth in vivo.
  • CONCLUSIONS: We conclude that AT-101 in combination with surgical castration delays the onset of androgen-independent prostate cancer in vivo by disrupting the antiapoptotic activity of Bcl-2 upregulation during the transition to androgen independence.

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Anticancer Res. 2004 Jan-Feb;24(1):91-100 [15015581.001]
  • [Cites] Nat Med. 2004 Jan;10(1):33-9 [14702632.001]
  • [Cites] Proc Natl Acad Sci U S A. 1984 Nov;81(22):7166-70 [6334305.001]
  • [Cites] Genes Dev. 1999 Aug 1;13(15):1899-911 [10444588.001]
  • [Cites] Clin Cancer Res. 2004 Nov 15;10(22):7757-63 [15570010.001]
  • [Cites] Cancer Res. 2004 Dec 15;64(24):9209-16 [15604294.001]
  • [Cites] Mol Cancer Ther. 2005 Jan;4(1):13-21 [15657349.001]
  • [Cites] Pancreas. 2005 Nov;31(4):317-24 [16258364.001]
  • [Cites] BJU Int. 2006 Jan;97(1):170-8 [16336351.001]
  • [Cites] Urol Oncol. 2006 Mar-Apr;24(2):161-8 [16520280.001]
  • [Cites] Neoplasia. 2006 Mar;8(3):163-72 [16611409.001]
  • [Cites] Breast Cancer Res Treat. 2001 Apr;66(3):239-48 [11510695.001]
  • [Cites] J Natl Cancer Inst. 2001 Nov 21;93(22):1687-97 [11717329.001]
  • [Cites] Nat Rev Cancer. 2001 Oct;1(1):34-45 [11900250.001]
  • [Cites] J Steroid Biochem Mol Biol. 2002 Jul;81(3):191-201 [12163131.001]
  • [Cites] Expert Opin Biol Ther. 2003 Apr;3(2):293-304 [12662143.001]
  • [Cites] N Engl J Med. 2003 Jul 24;349(4):366-81 [12878745.001]
  • [Cites] Semin Oncol. 2003 Oct;30(5 Suppl 16):133-42 [14613034.001]
  • [Cites] N Engl J Med. 2004 Oct 7;351(15):1488-90 [15470210.001]
  • (PMID = 18084610.001).
  • [ISSN] 1476-5586
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA069568; United States / PHS HHS / / P01 A093900; United States / NCI NIH HHS / CA / P50 CA69568
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Mcl1 protein, mouse; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Neoplasm Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Messenger; 0 / RNA, Neoplasm; EC 3.4.22.- / Caspases; KAV15B369O / Gossypol; S7RL72610R / gossypol acetic acid
  • [Other-IDs] NLM/ PMC2134900
  • [Keywords] NOTNLM ; Apoptosis / BH3 domain / Bcl-2 / hormone refractory / orchiectomy
  •  go-up   go-down


76. Beer TM, Higano CS, Saleh M, Dreicer R, Hudes G, Picus J, Rarick M, Fehrenbacher L, Hannah AL: Phase II study of KOS-862 in patients with metastatic androgen independent prostate cancer previously treated with docetaxel. Invest New Drugs; 2007 Dec;25(6):565-70
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase II study of KOS-862 in patients with metastatic androgen independent prostate cancer previously treated with docetaxel.
  • Based on the pre-clinical spectrum of activity in taxane-resistant cell lines, we evaluated KOS-862 (epothilone D; 12,13-desoxyepothilone B) as second-line chemotherapy in androgen-independent prostate cancer.Thirty-eight men with metastatic androgen-independent prostate cancer and evidence of progression following docetaxel-based chemotherapy were treated with KOS-862, 100 mg/m(2) (maximum of 240 mg) i.v. weekly for 3 weeks, repeated every 4 weeks.
  • [MeSH-minor] Aged. Aged, 80 and over. Disease Progression. Dose-Response Relationship, Drug. Humans. Infusions, Intravenous. Male. Middle Aged. Neoplasm Metastasis. Prostate-Specific Antigen / blood. Survival Rate. Treatment Outcome


77. Howard EW, Ling MT, Chua CW, Cheung HW, Wang X, Wong YC: Garlic-derived S-allylmercaptocysteine is a novel in vivo antimetastatic agent for androgen-independent prostate cancer. Clin Cancer Res; 2007 Mar 15;13(6):1847-56
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Garlic-derived S-allylmercaptocysteine is a novel in vivo antimetastatic agent for androgen-independent prostate cancer.
  • PURPOSE: There is epidemiologic evidence that high garlic consumption decreases the incidence of prostate cancer, and compounds isolated from garlic have been shown to have cancer-preventive and tumor-suppressive effects.
  • Recent in vitro studies in our laboratory have shown that garlic-derived organosulfur compound S-allylmercaptocysteine suppresses invasion and cell motility of androgen-independent prostate cancer cells via the up-regulation of cell-adhesion molecule E-cadherin.
  • EXPERIMENTAL DESIGN: We used a newly established fluorescent orthotopic androgen-independent prostate cancer mouse model to assess the ability of S-allylmercaptocysteine to inhibit tumor growth and dissemination.
  • CONCLUSIONS: Our results provide in vivo evidence supporting the potential use of S-allylmercaptocysteine as an E-cadherin up-regulating antimetastatic agent for the treatment of androgen-independent prostate cancer.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Cysteine / analogs & derivatives. Drug Resistance, Neoplasm. Garlic / chemistry. Neoplasm Metastasis / prevention & control. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / pathology

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • Hazardous Substances Data Bank. CYSTEINE .
  • 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 = 17363541.001).
  • [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] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Antineoplastic Agents; 0 / Antineoplastic Agents, Hormonal; 0 / S-allylmercaptocysteine; 147336-22-9 / Green Fluorescent Proteins; K848JZ4886 / Cysteine
  •  go-up   go-down


78. Posadas EM, Gulley J, Arlen PM, Trout A, Parnes HL, Wright J, Lee MJ, Chung EJ, Trepel JB, Sparreboom A, Chen C, Jones E, Steinberg SM, Daniels A, Figg WD, Dahut WL: A phase II study of perifosine in androgen independent prostate cancer. Cancer Biol Ther; 2005 Oct;4(10):1133-7
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A phase II study of perifosine in androgen independent prostate cancer.
  • The primary objective of this study was to determine the clinical efficacy of this agent in the treatment of androgen-independent prostate cancer (AIPC) using PSA and clinical criteria.
  • No significant clinical activity against prostate cancer was observed.
  • [MeSH-minor] Aged. Aged, 80 and over. Disease Progression. Drug Administration Schedule. Humans. Leukapheresis. Male. Middle Aged. Neoplasm Metastasis. Prostate-Specific Antigen / blood. Time Factors. Treatment Outcome


79. Beer TM, Goldman B, Synold TW, Ryan CW, Vasist LS, Van Veldhuizen PJ Jr, Dakhil SR, Lara PN Jr, Drelichman A, Hussain MH, Crawford ED: Southwest Oncology Group phase II study of ispinesib in androgen-independent prostate cancer previously treated with taxanes. Clin Genitourin Cancer; 2008 Sep;6(2):103-9
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Southwest Oncology Group phase II study of ispinesib in androgen-independent prostate cancer previously treated with taxanes.
  • In this study, we sought to assess the efficacy of ispinesib, a mitotic kinesin spindle protein (KSP) inhibitor in androgen-independent prostate cancer progressing after docetaxel.
  • PATIENTS AND METHODS: Patients were treated with ispinesib 18 mg/m2 every 21 days and assessed for prostate-specific antigen (PSA) and measurable disease response at regular intervals.
  • Immunohistochemical analysis of archival tumor specimens did not demonstrate significant KSP expression in most of the prostate cancer cases studied.
  • CONCLUSION: Ispinesib was inactive in this study of patients with androgen-independent, and largely docetaxelresistant, prostate cancer.
  • The lack of efficacy might be explained by the low expression of the drug target seen in prostate cancer, whereas not detecting monopolar spindles in circulating lymphocytes with drug treatment likely reflects the lack of dividing cells in peripheral blood.
  • [MeSH-minor] Aged. Aged, 80 and over. Disease-Free Survival. Drug Evaluation. Drug Resistance, Neoplasm. Humans. Male. Middle Aged. Prostate-Specific Antigen / analysis. Prostatic Neoplasms / drug therapy. Taxoids / therapeutic use

  • Genetic Alliance. consumer health - Prostate cancer.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18824433.001).
  • [ISSN] 1558-7673
  • [Journal-full-title] Clinical genitourinary cancer
  • [ISO-abbreviation] Clin Genitourin Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA20319; United States / NCI NIH HHS / CA / CA32102; United States / NCI NIH HHS / CA / CA35431; United States / NCI NIH HHS / CA / CA38926; United States / NCI NIH HHS / CA / CA42777; United States / NCI NIH HHS / CA / CA45377; United States / NCI NIH HHS / CA / CA45807; United States / NCI NIH HHS / CA / CA46441
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / KIF11 protein, human; 0 / Quinazolines; 0 / Taxoids; BKT5F9C2NI / ispinesib; EC 3.4.21.77 / Prostate-Specific Antigen; EC 3.6.1.- / Kinesin
  •  go-up   go-down


80. Marra M, Santini D, Meo G, Vincenzi B, Zappavigna S, Baldi A, Rosolowski M, Tonini G, Loeffler M, Lupu R, Addeo SR, Abbruzzese A, Budillon A, Caraglia M: Cyr61 downmodulation potentiates the anticancer effects of zoledronic acid in androgen-independent prostate cancer cells. Int J Cancer; 2009 Nov 1;125(9):2004-13
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cyr61 downmodulation potentiates the anticancer effects of zoledronic acid in androgen-independent prostate cancer cells.
  • We have analyzed the gene modulation induced by zoledronic acid (ZOL) in androgen-resistant prostate cancer PC3 cells with cDNA microarray platform to identify new molecular targets of ZOL in prostate cancer.
  • [MeSH-minor] Cell Cycle / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Humans. Male. Neoplasm Invasiveness. Oligonucleotide Array Sequence Analysis. Promoter Regions, Genetic. Protein Prenylation. Signal Transduction / drug effects

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2009 UICC.
  • (PMID = 19530242.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / CYR61 protein, human; 0 / Cysteine-Rich Protein 61; 0 / Diphosphonates; 0 / Imidazoles; 6XC1PAD3KF / zoledronic acid
  •  go-up   go-down


81. Takayanagi A, Masumori N, Hashimoto J, Kyoda Y, Yanase M, Tsukamoto T: Effect of delayed maximal androgen blockade therapy for patients with advanced prostate cancer who fail to respond to initial androgen deprivation monotherapy. Jpn J Clin Oncol; 2010 Dec;40(12):1154-8
MedlinePlus Health Information. consumer health - Prostate Cancer Screening.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of delayed maximal androgen blockade therapy for patients with advanced prostate cancer who fail to respond to initial androgen deprivation monotherapy.
  • OBJECTIVES: We analyzed the efficacy of additional antiandrogens as second- and third-line treatments after the failure of initial androgen deprivation monotherapy.
  • METHODS: This retrospective study included 53 patients with advanced prostate cancer initially treated with androgen deprivation monotherapy alone.
  • An antiandrogen was added to androgen deprivation monotherapy as the second-line treatment after the failure of the initial androgen deprivation monotherapy.
  • RESULTS: The initial androgen deprivation monotherapy was effective in all 53 patients for a median of 9.6 months.
  • Thirty-three (62.3%) patients showed a prostate-specific antigen response to the second-line treatment for a median of 10.7 months.
  • Of the 46 patients who received the third-line treatment, 16 (34.8%) showed a prostate-specific antigen response for a median of 6.0 months.
  • In multivariate analysis, a nadir prostate-specific antigen of 4.0 ng/ml or greater during androgen deprivation monotherapy and prostate-specific antigen doubling time of less than 10 months after androgen deprivation monotherapy failure were independent risk factors for prostate cancer death after androgen deprivation monotherapy failure, with hazards ratios of 5.59 and 8.00, respectively.
  • CONCLUSIONS: In this study, the second- and third-line treatments were effective for patients with advanced prostate cancer.
  • Nadir prostate-specific antigen during androgen deprivation monotherapy and prostate-specific antigen doubling time just after the failure of androgen deprivation monotherapy are factors that can predict the prognosis.
  • [MeSH-major] Androgen Antagonists / therapeutic use. Antineoplastic Agents, Hormonal / therapeutic use. Biomarkers, Tumor / blood. Neoplasms, Hormone-Dependent / drug therapy. Prostate-Specific Antigen / blood. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Aged. Aged, 80 and over. Analysis of Variance. Drug Administration Schedule. Humans. Kaplan-Meier Estimate. Male. Middle Aged. Neoplasm Staging. Proportional Hazards Models. Retrospective Studies. Time Factors. Treatment Failure. Treatment Outcome

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20647233.001).
  • [ISSN] 1465-3621
  • [Journal-full-title] Japanese journal of clinical oncology
  • [ISO-abbreviation] Jpn. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Antineoplastic Agents, Hormonal; 0 / Biomarkers, Tumor; EC 3.4.21.77 / Prostate-Specific Antigen
  •  go-up   go-down


82. Feigenberg SJ, Hanlon AL, Horwitz EM, Uzzo RG, Eisenberg DF, Pollack A: What pretreatment prostate-specific antigen level warrants long-term androgen deprivation? Int J Radiat Oncol Biol Phys; 2005 Mar 15;61(4):1003-10
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] What pretreatment prostate-specific antigen level warrants long-term androgen deprivation?
  • PURPOSE: Several large randomized prospective studies have demonstrated a survival benefit with the addition of long-term androgen deprivation to definitive radiotherapy for patients with Gleason score 8-10 or T3-T4 prostate cancer.
  • However, these studies were performed before the routine use of prostate-specific antigen (PSA) measurement.
  • The purpose of this study was to determine what pretreatment (initial) PSA (iPSA) level, if any, warrants the addition of long-term androgen deprivation in the PSA era.
  • METHODS AND MATERIALS: The data set evaluated consisted of 1003 prostate cancer patients treated definitively with three-dimensional conformal radiotherapy between May 1, 1989 and November 30, 1999 (median follow-up, 61 months).
  • Specifically excluded were patients with T3-T4 disease or Gleason score greater than 7 or those who had undergone androgen deprivation as a part of their initial therapy.
  • Cox multivariate regression analysis was used to confirm independent predictors of outcome among the clinical and treatment-related factors: iPSA (grouped as defined by the recursive partitioning analysis), Gleason score (2-6 vs. 7), T stage (T1c-T2a vs. T2b-T2c), and total radiation dose (continuous).
  • On multivariate regression analysis, with the iPSA grouped as above, the Gleason score and radiation dose were independent predictors of outcome in this patient group (all p < 0.001).
  • Patients with a PSA level >30 ng/mL in the absence of Gleason score >7 or T3 disease do poorly when treated with radiotherapy alone and should be considered for long-term androgen deprivation or other aggressive systemic therapy.
  • [MeSH-major] Androgen Antagonists. Prostate-Specific Antigen / blood. Prostatic Neoplasms / blood. Prostatic Neoplasms / radiotherapy
  • [MeSH-minor] Aged. Aged, 80 and over. Humans. Male. Middle Aged. Neoplasm Staging. Patient Selection. Prognosis. Radiotherapy, Conformal. Reference Values. Regression Analysis. Risk Assessment. Statistics, Nonparametric

  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer Screening.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15752879.001).
  • [ISSN] 0360-3016
  • [Journal-full-title] International journal of radiation oncology, biology, physics
  • [ISO-abbreviation] Int. J. Radiat. Oncol. Biol. Phys.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Randomized Controlled Trial
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgen Antagonists; EC 3.4.21.77 / Prostate-Specific Antigen
  •  go-up   go-down


83. Stangelberger A, Schally AV, Varga JL, Zarandi M, Cai RZ, Baker B, Hammann BD, Armatis P, Kanashiro CA: Inhibition of human androgen-independent PC-3 and DU-145 prostate cancers by antagonists of bombesin and growth hormone releasing hormone is linked to PKC, MAPK and c-jun intracellular signalling. Eur J Cancer; 2005 Nov;41(17):2735-44
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inhibition of human androgen-independent PC-3 and DU-145 prostate cancers by antagonists of bombesin and growth hormone releasing hormone is linked to PKC, MAPK and c-jun intracellular signalling.
  • Bombesin/gastrin-releasing peptide (BN/GRP) antagonists RC-3940-II and RC-3940-Et, and growth hormone-releasing hormone (GHRH) antagonists MZ-J-7-118 and RC-J-29-18 inhibit the growth of human androgen-independent PC-3 and DU-145 prostate cancers in nude mice.
  • These findings suggest that antagonists of BN/GRP and GHRH inhibit the growth of androgen-independent prostate cancer by affecting intracellular signalling mechanisms of PKC, MAPK and c-jun.
  • [MeSH-major] Bombesin / antagonists & inhibitors. Genes, jun / physiology. Growth Hormone-Releasing Hormone / antagonists & inhibitors. Neoplasm Proteins / antagonists & inhibitors. Prostatic Neoplasms / metabolism

  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16291086.001).
  • [ISSN] 0959-8049
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 9034-39-3 / Growth Hormone-Releasing Hormone; EC 2.7.11.13 / Protein Kinase C; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; PX9AZU7QPK / Bombesin
  •  go-up   go-down


84. Yamanaka K, Rocchi P, Miyake H, Fazli L, Vessella B, Zangemeister-Wittke U, Gleave ME: A novel antisense oligonucleotide inhibiting several antiapoptotic Bcl-2 family members induces apoptosis and enhances chemosensitivity in androgen-independent human prostate cancer PC3 cells. Mol Cancer Ther; 2005 Nov;4(11):1689-98
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A novel antisense oligonucleotide inhibiting several antiapoptotic Bcl-2 family members induces apoptosis and enhances chemosensitivity in androgen-independent human prostate cancer PC3 cells.
  • Bcl-2 and Bcl-xL are associated with treatment resistance and progression in many cancers, including prostate cancer.
  • The objective of this study was to determine whether a novel bispecific antisense oligonucleotide targeting both Bcl-2 and Bcl-xL induces apoptosis and enhances chemosensitivity in androgen-independent PC3 prostate cancer cells.
  • These findings illustrate that combined suppression of antiapoptotic Bcl-2 family members using this antisense oligonucleotide could be an attractive strategy for inhibiting cancer progression through alteration of the apoptotic rheostat in androgen-independent prostate cancer.
  • [MeSH-minor] Blotting, Western. Cell Line, Tumor. Cell Proliferation. Cell Survival. Dose-Response Relationship, Drug. Down-Regulation. Humans. Inhibitor of Apoptosis Proteins / metabolism. Inhibitory Concentration 50. Male. Myeloid Cell Leukemia Sequence 1 Protein. Neoplasm Metastasis. Neoplasm Proteins / metabolism. Oligonucleotide Array Sequence Analysis. Oligonucleotides / chemistry. Paclitaxel / chemistry. Paclitaxel / pharmacology. Prostate / metabolism. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. bcl-2 Homologous Antagonist-Killer Protein / metabolism. bcl-2-Associated X Protein / metabolism. bcl-Associated Death Protein / metabolism. bcl-X Protein / metabolism

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. TAXOL .
  • 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 = 16275990.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Antineoplastic Agents; 0 / Inhibitor of Apoptosis Proteins; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Neoplasm Proteins; 0 / Oligonucleotides; 0 / Oligonucleotides, Antisense; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Messenger; 0 / bcl-2 Homologous Antagonist-Killer Protein; 0 / bcl-2-Associated X Protein; 0 / bcl-Associated Death Protein; 0 / bcl-X Protein; P88XT4IS4D / Paclitaxel
  •  go-up   go-down


85. Morgenbesser SD, McLaren RP, Richards B, Zhang M, Akmaev VR, Winter SF, Mineva ND, Kaplan-Lefko PJ, Foster BA, Cook BP, Dufault MR, Cao X, Wang CJ, Teicher BA, Klinger KW, Greenberg NM, Madden SL: Identification of genes potentially involved in the acquisition of androgen-independent and metastatic tumor growth in an autochthonous genetically engineered mouse prostate cancer model. Prostate; 2007 Jan 1;67(1):83-106
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification of genes potentially involved in the acquisition of androgen-independent and metastatic tumor growth in an autochthonous genetically engineered mouse prostate cancer model.
  • BACKGROUND: A major focus of prostate cancer research has been to identify genes that are deregulated during tumor progression, potentially providing diagnostic markers and therapeutic targets.
  • METHODS: We have employed serial analysis of gene expression (SAGE) and microarray hybridization to identify alterations that occur during malignant transformation in the Transgenic Adenocarcinoma of the Mouse Prostate (TRAMP) model.
  • Cluster analysis of microarray profiles with samples from various stages of the disease demonstrated that androgen-independent (AI) primary tumors are similar to metastases; 180 transcripts have expression patterns suggesting an involvement in the genesis of late-stage tumors, and our data support a role for phospholipase A2 group IIA in the acquisition of their highly aggressive characteristics.
  • CONCLUSIONS: Our analyses identified well-characterized genes that were previously known to be involved in prostate cancer, validating our study, and also uncovered transcripts that had not previously been implicated in prostate cancer progression.
  • [MeSH-major] Adenocarcinoma / genetics. Androgens / genetics. Disease Models, Animal. Gene Expression Profiling. Genes, Neoplasm / physiology. Genetic Engineering / methods. Oligonucleotide Array Sequence Analysis. Prostatic Neoplasms / genetics

  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2006 Wiley-Liss, Inc.
  • (PMID = 17013881.001).
  • [ISSN] 1097-0045
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA73747; United States / NCI NIH HHS / CA / CA84296
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Validation Studies
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens
  •  go-up   go-down


86. Lee SC, Chan WK, Lee TW, Lam WH, Wang X, Chan TH, Wong YC: Effect of a prodrug of the green tea polyphenol (-)-epigallocatechin-3-gallate on the growth of androgen-independent prostate cancer in vivo. Nutr Cancer; 2008;60(4):483-91
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of a prodrug of the green tea polyphenol (-)-epigallocatechin-3-gallate on the growth of androgen-independent prostate cancer in vivo.
  • In this study, in addition to the EGCG compound, a synthetic derivative, the peracetate of EGCG (EGCG-P), was used to investigate the inhibitory effects on growth of androgen-independent prostate cancer in vivo.
  • The aim of our study was to compare the differences between EGCG and EGCG-P on their inhibitory effect on androgen-independent prostate cancer, CWR22R, xenograft model in nude mice.
  • Serum prostate-specific antigen (PSA) levels were also measured before and after the treatment.
  • Moreover, the potential suppression of angiogenesis by EGCG and EGCG-P on prostate cancer was examined by IHC against CD31.
  • The suppression of growth of the tumor was correlated with the decrease of serum PSA level together with the reduction in tumor angiogenesis and an increase in apoptosis on prostate cancer cells.
  • The results showed that treatment of EGCG and EGCG-P inhibited tumor growth and angiogenesis while promoting apoptosis of the prostate cancer cells in vivo.
  • Our results suggest that EGCG-P may be a more stable and useful compound for increasing the therapeutic anticancer effects in androgen-independent prostate cancer.
  • [MeSH-minor] Acetates / pharmacology. Animals. Apoptosis / drug effects. Biological Availability. Humans. Immunohistochemistry. Ki-67 Antigen / analysis. Male. Mice. Mice, Nude. Neoplasm Transplantation. Neovascularization, Pathologic / drug therapy. Proliferating Cell Nuclear Antigen / analysis. Prostate-Specific Antigen. Transplantation, Heterologous

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • Hazardous Substances Data Bank. Green tea .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18584482.001).
  • [ISSN] 1532-7914
  • [Journal-full-title] Nutrition and cancer
  • [ISO-abbreviation] Nutr Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Acetates; 0 / Androgens; 0 / Ki-67 Antigen; 0 / Prodrugs; 0 / Proliferating Cell Nuclear Antigen; 0 / Tea; 8R1V1STN48 / Catechin; BQM438CTEL / epigallocatechin gallate; EC 3.4.21.77 / Prostate-Specific Antigen
  •  go-up   go-down


87. Halin S, Hammarsten P, Wikström P, Bergh A: Androgen-insensitive prostate cancer cells transiently respond to castration treatment when growing in an androgen-dependent prostate environment. Prostate; 2007 Mar 1;67(4):370-7
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] Androgen-insensitive prostate cancer cells transiently respond to castration treatment when growing in an androgen-dependent prostate environment.
  • BACKGROUND: Castration-induced involution of the normal prostate is caused by primary effects in the prostate stroma and vasculature, but if this is the case also in tumors is unknown.
  • METHODS: Androgen-independent AT-1 prostate tumor cells were therefore injected into the ventral prostate (VP) in Copenhagen rats.
  • CONCLUSIONS: Androgen-independent tumor cell respond to castration when growing in an androgen-dependent environment.
  • The microenvironment determines how prostate epithelial cells respond to castration.
  • [MeSH-minor] Animals. Anoxia / metabolism. Anoxia / pathology. Cell Division. Epithelial Cells / cytology. Epithelial Cells / metabolism. Male. Neoplasm Transplantation. Organ Size. Prostate / blood supply. Prostate / cytology. Prostate / metabolism. Rats. Rats, Inbred Strains. Receptors, Androgen / metabolism

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17192959.001).
  • [ISSN] 0270-4137
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Receptors, Androgen
  •  go-up   go-down


88. Li W, Liu Y, Zhang JW, Ai CZ, Xiang N, Liu HX, Yang L: Anti-androgen-independent prostate cancer effects of ginsenoside metabolites in vitro: mechanism and possible structure-activity relationship investigation. Arch Pharm Res; 2009 Jan;32(1):49-57
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Anti-androgen-independent prostate cancer effects of ginsenoside metabolites in vitro: mechanism and possible structure-activity relationship investigation.
  • Treatment of androgen-independent prostate cancer (AIPC) remains unsatisfactory.
  • [MeSH-minor] Androgen Antagonists / pharmacology. Apoptosis / drug effects. Bacteria / metabolism. Biotransformation. Cell Cycle / drug effects. Cell Line, Tumor. Cell Survival / drug effects. Cyclin A / metabolism. Cyclin D1 / metabolism. Dose-Response Relationship, Drug. Drug Resistance, Neoplasm. Glycosylation. Humans. Hydrophobic and Hydrophilic Interactions. Intestines / microbiology. Male. Mitochondria / drug effects. Mitochondria / pathology. Molecular Structure. Structure-Activity Relationship

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • 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 = 19183876.001).
  • [ISSN] 0253-6269
  • [Journal-full-title] Archives of pharmacal research
  • [ISO-abbreviation] Arch. Pharm. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Antineoplastic Agents; 0 / CCND1 protein, human; 0 / Cyclin A; 0 / Ginsenosides; 136601-57-5 / Cyclin D1
  •  go-up   go-down


89. Kageyama Y, Hyochi N, Kihara K, Sugiyama H: The androgen receptor as putative therapeutic target in hormone-refractory prostate cancer. Recent Pat Anticancer Drug Discov; 2007 Nov;2(3):203-11
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The androgen receptor as putative therapeutic target in hormone-refractory prostate cancer.
  • The androgen receptor (AR) plays a central role in the initiation and growth of prostate cancer.
  • Androgen deprivation therapy (ADT) has been a gold standard for advanced prostate cancer for decades.
  • Unfortunately, suppressive effects of ADT do not last long and hormone-refractory prostate cancer develops within several years.
  • In spite of extensive research on mechanisms of hormone-independent growth of prostate cancer, there are few effective treatment options for recurrent tumors and most patients die from the disease in a short period of time.
  • Accumulating evidence suggests that the AR signaling system remains intact and activated despite low levels of androgens in hormone-resistant prostate cancer.
  • Currently, modifications to the AR via mutations, amplification and phosphorylation have been proposed as underlying mechanisms of hormone-resistance of prostate cancer cells.
  • In addition, changes in AR cofactors are implicated in ligand-independent activation of AR signaling.
  • Thus, the development of novel and more effective treatment modalities targeting the AR and AR-related molecules may provide better management of androgen-independent prostate cancer.
  • Although recent patents on the AR related to prostate cancer are focused on antiandrogens, future trend will be shifted to agents or methods suppressing molecules or pathways that activate AR signaling in low androgen environments.
  • [MeSH-major] Antineoplastic Agents, Hormonal / therapeutic use. Prostatic Neoplasms / drug therapy. Receptors, Androgen / physiology
  • [MeSH-minor] Androgen Antagonists / pharmacology. Androgen Antagonists / therapeutic use. Animals. Drug Resistance, Neoplasm. Humans. Male. Patents as Topic

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18221063.001).
  • [ISSN] 1574-8928
  • [Journal-full-title] Recent patents on anti-cancer drug discovery
  • [ISO-abbreviation] Recent Pat Anticancer Drug Discov
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United Arab Emirates
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Antineoplastic Agents, Hormonal; 0 / Receptors, Androgen
  • [Number-of-references] 117
  •  go-up   go-down


90. Syrovets T, Gschwend JE, Büchele B, Laumonnier Y, Zugmaier W, Genze F, Simmet T: Inhibition of IkappaB kinase activity by acetyl-boswellic acids promotes apoptosis in androgen-independent PC-3 prostate cancer cells in vitro and in vivo. J Biol Chem; 2005 Feb 18;280(7):6170-80
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inhibition of IkappaB kinase activity by acetyl-boswellic acids promotes apoptosis in androgen-independent PC-3 prostate cancer cells in vitro and in vivo.
  • Here we show that the natural compounds acetyl-beta-boswellic acid and acetyl-11-keto-beta-boswellic acid (AKbetaBA) inhibit proliferation and elicit cell death in chemoresistant androgen-independent PC-3 prostate cancer cells in vitro and in vivo.
  • Thus, AKbetaBA and related compounds acting on IKK might provide a novel approach for the treatment of chemoresistant human tumors such as androgen-independent human prostate cancers.
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Proliferation / drug effects. Chick Embryo. Chorioallantoic Membrane. Cyclodextrins / pharmacology. Fibroblasts. I-kappa B Kinase. Male. Mice. Mice, Nude. NF-kappa B / metabolism. Neoplasm Invasiveness. Signal Transduction / drug effects. Xenograft Model Antitumor Assays

  • MedlinePlus Health Information. consumer health - Prostate 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 = 15576374.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 3-O-acetyl-beta-boswellic acid; 0 / Androgens; 0 / Cyclodextrins; 0 / NF-kappa B; 0 / Triterpenes; EC 2.7.1.- / Chuk protein, mouse; EC 2.7.1.- / Ikbke protein, mouse; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.10 / I-kappa B Kinase; EC 2.7.11.10 / Ikbkb protein, mouse
  •  go-up   go-down


91. He QJ, Yang B, Lou YJ, Fang RY: Contragestazol (DL111-IT) inhibits proliferation of human androgen-independent prostate cancer cell line PC3 in vitro and in vivo. Asian J Androl; 2005 Dec;7(4):389-93
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Contragestazol (DL111-IT) inhibits proliferation of human androgen-independent prostate cancer cell line PC3 in vitro and in vivo.
  • AIM: To evaluate the antiproliferative activity of contragestazol (DL111-IT) on the human prostate cancer cell line PC3 in vitro and in vivo and to elucidate its potential molecular mechanisms.
  • RESULTS: DL111-IT exhibited high efficiency on cell growth inhibition of the human androgen-independent prostate cancer cell line PC3.
  • CONCLUSION: DL111-IT inhibits the proliferation of human androgen-independent prostate cancer cell line PC3 in vitro and in vivo by a cell cycle regulation pathway.
  • [MeSH-minor] Animals. Cell Division / drug effects. Cell Line, Tumor. Cyclin D1 / metabolism. Cyclin-Dependent Kinase 4 / metabolism. Dose-Response Relationship, Drug. Female. G0 Phase / drug effects. G1 Phase / drug effects. Humans. In Vitro Techniques. Male. Mice. Mice, Inbred BALB C. Mice, Nude. Neoplasm Transplantation. Retinoblastoma Protein / metabolism. Transplantation, Heterologous

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate 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 = 16281086.001).
  • [ISSN] 1008-682X
  • [Journal-full-title] Asian journal of andrology
  • [ISO-abbreviation] Asian J. Androl.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Androgens; 0 / Immunosuppressive Agents; 0 / Retinoblastoma Protein; 0 / Triazoles; 136601-57-5 / Cyclin D1; 69095-83-6 / 3-(2-ethylphenyl)-5-(3-methoxyphenyl)-1H-1,2,4-triazole; EC 2.7.11.22 / Cyclin-Dependent Kinase 4
  •  go-up   go-down


92. Rodney A, Dieringer P, Mathew P, Jonasch E, Tannir N, Pagliaro LC: Phase II study of capecitabine combined with gemcitabine in the treatment of androgen-independent prostate cancer previously treated with taxanes. Cancer; 2006 May 15;106(10):2143-7
Hazardous Substances Data Bank. FLUOROURACIL .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase II study of capecitabine combined with gemcitabine in the treatment of androgen-independent prostate cancer previously treated with taxanes.
  • BACKGROUND: The primary objective of the current study was to evaluate the effectiveness of capecitabine and gemcitabine in the treatment of patients with androgen-independent prostate cancer (AIPCa) who experienced disease progression after taxane therapy.
  • Response to therapy was determined by measuring prostate-specific antigen concentration.
  • There were no responses as defined by a 50% decline in prostate-specific antigen.
  • [MeSH-minor] Administration, Oral. Aged. Capecitabine. Dose-Response Relationship, Drug. Drug Administration Schedule. Drug Therapy, Combination. Fluorouracil / analogs & derivatives. Humans. Infusions, Intravenous. Male. Middle Aged. Neoplasm Staging. Neoplasms, Hormone-Dependent / drug therapy. Neoplasms, Hormone-Dependent / mortality. Neoplasms, Hormone-Dependent / pathology. Probability. Prognosis. Survival Analysis. Taxoids / administration & dosage. Treatment Outcome

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. CAPECITABINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2006 American Cancer Society
  • (PMID = 16598751.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA16672
  • [Publication-type] Clinical Trial, Phase II; Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Taxoids; 0W860991D6 / Deoxycytidine; 6804DJ8Z9U / Capecitabine; B76N6SBZ8R / gemcitabine; U3P01618RT / Fluorouracil
  •  go-up   go-down


93. Pruthi RS, Hubbard JS, Kouba E, Wallen E: Androgen-independent prostate cancer treated with resection of the solitary metastatic site. Urol Int; 2007;79(4):371-3
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Androgen-independent prostate cancer treated with resection of the solitary metastatic site.
  • The concept of resection of a solitary metastatic lesion is quite foreign in prostate cancer, as metastases to regional lymph nodes or to other distant sites are most likely suggestive of disseminated disease.
  • The current report demonstrates a very unique case, in whom excision of a solitary pulmonary metastasis has resulted in continued undetectable prostate-specific antigen values over 3 years after resection.
  • [MeSH-major] Adenocarcinoma / secondary. Lung Neoplasms / secondary. Lung Neoplasms / surgery. Prostate-Specific Antigen / blood. Prostatic Neoplasms / surgery
  • [MeSH-minor] Aged. Follow-Up Studies. Humans. Male. Neoplasm Staging. Prostatectomy / methods. Risk Assessment. Sentinel Lymph Node Biopsy / methods. Thoracic Surgery, Video-Assisted. Tomography, X-Ray Computed. Treatment Outcome


94. Uchida K, Masumori N, Takahashi A, Itoh N, Kato K, Matusik RJ, Tsukamoto T: Murine androgen-independent neuroendocrine carcinoma promotes metastasis of human prostate cancer cell line LNCaP. Prostate; 2006 Apr 1;66(5):536-45
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Murine androgen-independent neuroendocrine carcinoma promotes metastasis of human prostate cancer cell line LNCaP.
  • BACKGROUND: Although neuroendocrine (NE) cells in prostate cancer have been speculated to accelerate the growth and progression of surrounding cancer cells, the evidence is as yet inconclusive.
  • We investigated the effect of an NE allograft (NE-10) and its cell line, NE-CS, which were established from the prostate of the LPB-Tag 12T-10 transgenic mouse, on human prostate cancer cell line LNCaP.
  • [MeSH-minor] Adenocarcinoma / pathology. Animals. Carcinoma, Neuroendocrine / pathology. Cell Division. Cell Line, Tumor. Humans. Male. Mice. Mice, Nude. Neoplasm Metastasis. Neoplasm Transplantation. Transplantation, Heterologous. Transplantation, Homologous

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2005 Wiley-Liss, Inc.
  • (PMID = 16372327.001).
  • [ISSN] 0270-4137
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-76142
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens
  •  go-up   go-down


95. Li H, Price DK, Figg WD: ADH1, an N-cadherin inhibitor, evaluated in preclinical models of angiogenesis and androgen-independent prostate cancer. Anticancer Drugs; 2007 Jun;18(5):563-8
SciCrunch. DrugBank: Data: Chemical .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] ADH1, an N-cadherin inhibitor, evaluated in preclinical models of angiogenesis and androgen-independent prostate cancer.
  • The conversion from E-cadherin to N-cadherin has been observed in several human cancer types, including prostate cancer, with more homogenous expression of N-cadherin detected in high-grade prostate tumors.
  • [MeSH-minor] Animals. Aorta, Thoracic / drug effects. Blotting, Western. Endothelial Cells / drug effects. In Vitro Techniques. Male. Neoplasm Transplantation. Rats. Regional Blood Flow / drug effects. alpha Catenin / metabolism

  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • 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 = 17414625.001).
  • [ISSN] 0959-4973
  • [Journal-full-title] Anti-cancer drugs
  • [ISO-abbreviation] Anticancer Drugs
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / ADH-1 pepide; 0 / Androgens; 0 / Angiogenesis Inhibitors; 0 / Antineoplastic Agents; 0 / Cadherins; 0 / Oligopeptides; 0 / Peptides, Cyclic; 0 / alpha Catenin
  •  go-up   go-down


96. Efstathiou E, Bozas G, Kostakopoulos A, Kastritis E, Deliveliotis C, Antoniou N, Skarlos D, Papadimitriou C, Dimopoulos MA, Bamias A: Combination of docetaxel, estramustine phosphate, and zoledronic acid in androgen-independent metastatic prostate cancer: efficacy, safety, and clinical benefit assessment. Urology; 2005 Jan;65(1):126-30
Hazardous Substances Data Bank. DOCETAXEL .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Combination of docetaxel, estramustine phosphate, and zoledronic acid in androgen-independent metastatic prostate cancer: efficacy, safety, and clinical benefit assessment.
  • OBJECTIVES: Docetaxel is an effective agent for the treatment of androgen-independent prostate cancer (AIPC).
  • RESULTS: Of the 49 assessable patients, 22 (45%, 95% confidence interval [CI] 31% to 60%) had a prostate-specific antigen response.
  • [MeSH-minor] Aged. Aged, 80 and over. Alopecia / chemically induced. Androgen Antagonists / therapeutic use. Antineoplastic Agents, Hormonal / therapeutic use. Biomarkers, Tumor / blood. Combined Modality Therapy. Diphosphonates / administration & dosage. Disease Progression. Disease-Free Survival. Drug Resistance, Neoplasm. Estramustine / administration & dosage. Estramustine / adverse effects. Humans. Imidazoles / administration & dosage. Life Tables. Liver Neoplasms / drug therapy. Liver Neoplasms / secondary. Lung Neoplasms / drug therapy. Lung Neoplasms / secondary. Lymphatic Metastasis. Male. Middle Aged. Neoplasm Proteins / blood. Neutropenia / chemically induced. Orchiectomy. Pain / drug therapy. Palliative Care. Prostate-Specific Antigen / blood. Radiotherapy, High-Energy. Remission Induction. Survival Analysis. Taxoids / administration & dosage. Taxoids / adverse effects. Treatment Outcome

  • Genetic Alliance. consumer health - Prostate cancer.
  • Genetic Alliance. consumer health - Metastatic cancer.
  • MedlinePlus Health Information. consumer health - Bone Cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15667877.001).
  • [ISSN] 1527-9995
  • [Journal-full-title] Urology
  • [ISO-abbreviation] Urology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Antineoplastic Agents, Hormonal; 0 / Biomarkers, Tumor; 0 / Diphosphonates; 0 / Imidazoles; 0 / Neoplasm Proteins; 0 / Taxoids; 15H5577CQD / docetaxel; 35LT29625A / Estramustine; 6XC1PAD3KF / zoledronic acid; EC 3.4.21.77 / Prostate-Specific Antigen
  •  go-up   go-down


97. Narizhneva NV, Tararova ND, Ryabokon P, Shyshynova I, Prokvolit A, Komarov PG, Purmal AA, Gudkov AV, Gurova KV: Small molecule screening reveals a transcription-independent pro-survival function of androgen receptor in castration-resistant prostate cancer. Cell Cycle; 2009 Dec 15;8(24):4155-67
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Small molecule screening reveals a transcription-independent pro-survival function of androgen receptor in castration-resistant prostate cancer.
  • In prostate cancer (PCa) patients, initial responsiveness to androgen deprivation therapy is frequently followed by relapse due to development of treatment-resistant androgen-independent PCa.
  • This is typically associated with acquisition of mutations in AR that allow activity as a transcription factor in the absence of ligand, indicating that androgen-independent PCa remains dependent on AR function.
  • Our strategy to effectively target AR in androgen-independent PCa involved using a cell-based readout to isolate small molecules that inhibit AR transactivation function through mechanisms other than modulation of ligand binding.
  • A number of the identified inhibitors were toxic to AR-expressing PCa cells regardless of their androgen dependence.
  • These observations reveal a transcription-independent function of AR that is essential for PCa cell viability and, therefore, is an ideal target for anti-PCa treatment.

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Urology. 2002 Sep;60(3 Suppl 1):132-8; discussion 138-9 [12231070.001]
  • [Cites] Clin Cancer Res. 1996 Feb;2(2):277-85 [9816170.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Apr 26;102(17):6201-6 [15833816.001]
  • [Cites] Mol Cell Endocrinol. 2005 May 31;236(1-2):1-7 [15876478.001]
  • [Cites] J Steroid Biochem Mol Biol. 2005 Aug;96(3-4):251-8 [15982869.001]
  • [Cites] Int J Cancer. 2005 Nov 1;117(2):221-9 [15900601.001]
  • [Cites] J Biol Chem. 2005 Nov 11;280(45):37747-54 [16129672.001]
  • [Cites] Prostate. 2007 Dec 1;67(16):1801-15 [17935158.001]
  • [Cites] Best Pract Res Clin Endocrinol Metab. 2008 Apr;22(2):303-15 [18471788.001]
  • [Cites] Br J Pharmacol. 2008 May;154(2):440-50 [18414397.001]
  • [Cites] Rev Assoc Med Bras. 2008 Mar-Apr;54(2):178-82 [18506331.001]
  • [Cites] Cell Cycle. 2008 Jun 15;7(12):1745-62 [18594202.001]
  • [Cites] Curr Opin Pharmacol. 2008 Aug;8(4):440-8 [18674639.001]
  • [Cites] Cancer Res. 2008 Dec 1;68(23):9703-11 [19047148.001]
  • [Cites] Urol Oncol. 2009 Mar-Apr;27(2):165-9 [18367115.001]
  • [Cites] Proc Natl Acad Sci U S A. 2009 Apr 28;106(17):7233-8 [19363158.001]
  • [Cites] Science. 2009 May 8;324(5928):787-90 [19359544.001]
  • [Cites] J Med Chem. 2009 Jun 25;52(12):3597-617 [19432422.001]
  • [Cites] ACS Chem Biol. 2009 Jun 19;4(6):435-40 [19441848.001]
  • [Cites] Bioorg Med Chem Lett. 2005 Jan 17;15(2):271-6 [15603938.001]
  • [Cites] Cancer Res. 2001 Apr 1;61(7):2892-8 [11306464.001]
  • [Cites] Mol Cell Endocrinol. 2001 Oct 25;183(1-2):19-28 [11604220.001]
  • [Cites] Cancer Res. 2002 Feb 15;62(4):1008-13 [11861374.001]
  • [Cites] Cancer Res. 2002 Nov 15;62(22):6606-14 [12438256.001]
  • [Cites] Mol Cell Biol. 2003 Jan;23(1):104-18 [12482965.001]
  • [Cites] Cancer Res. 2003 Jan 1;63(1):149-53 [12517791.001]
  • [Cites] Nat Med. 2004 Jan;10(1):33-9 [14702632.001]
  • [Cites] Cancer Res. 2004 Mar 15;64(6):1951-8 [15026329.001]
  • [Cites] Ann N Y Acad Sci. 2004 Jun;1024:54-71 [15265773.001]
  • [Cites] Prostate. 1989;15(3):233-50 [2555799.001]
  • [Cites] Int J Cancer. 1994 May 1;57(3):406-12 [8169003.001]
  • [Cites] J Biol Chem. 1997 Jul 25;272(30):18694-701 [9228040.001]
  • [Cites] Am J Pathol. 1998 Jan;152(1):1-9 [9422516.001]
  • [Cites] Int J Biochem Cell Biol. 1997 Dec;29(12):1325-41 [9570131.001]
  • [CommentIn] Cell Cycle. 2010 Feb 1;9(3):440-1 [20130446.001]
  • (PMID = 19946220.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA110400-01; United States / NCI NIH HHS / CA / R41 CA110400; United States / NCI NIH HHS / CA / R41 CA110400-01; United States / NCI NIH HHS / CA / R42 CA 110400-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Antineoplastic Agents; 0 / Growth Inhibitors; 0 / RNA, Small Interfering; 0 / Receptors, Androgen; 0 / Small Molecule Libraries
  • [Other-IDs] NLM/ NIHMS188583; NLM/ PMC2896895
  •  go-up   go-down


98. Butterworth KT, McCarthy HO, Devlin A, Ming L, Robson T, McKeown SR, Worthington J: Hypoxia selects for androgen independent LNCaP cells with a more malignant geno- and phenotype. Int J Cancer; 2008 Aug 15;123(4):760-8
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hypoxia selects for androgen independent LNCaP cells with a more malignant geno- and phenotype.
  • To further assess the role of hypoxia in malignant progression in prostate cancer we exposed human androgen dependent prostate cancer cells (LNCaP) to cycles of chronic hypoxia and isolated a subline, LNCaP-H1.
  • The LNCaP-H1 subline showed altered growth characteristics and exhibited androgen independent growth both in vitro and in vivo.
  • This study shows that hypoxia can select for androgen independent prostate cancer cells which have a survival advantage and are more likely to invade and metastasize.
  • [MeSH-minor] Androgens / metabolism. Animals. Apoptosis / physiology. Cell Growth Processes / physiology. Cell Hypoxia / genetics. Cell Hypoxia / physiology. Cell Line, Tumor. Core Binding Factor Alpha 1 Subunit / biosynthesis. Core Binding Factor Alpha 1 Subunit / genetics. Gene Expression. Genotype. Humans. Male. Mice. Mice, Inbred BALB C. Mice, SCID. Mitochondria / physiology. Neoplasm Transplantation. Neoplasms, Hormone-Dependent / genetics. Neoplasms, Hormone-Dependent / metabolism. Neoplasms, Hormone-Dependent / pathology. Phenotype. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Receptors, Androgen / biosynthesis. Receptors, Androgen / genetics. Receptors, TNF-Related Apoptosis-Inducing Ligand / metabolism. Transplantation, Heterologous

  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • (PMID = 18512241.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Core Binding Factor Alpha 1 Subunit; 0 / RNA, Messenger; 0 / RUNX2 protein, human; 0 / Receptors, Androgen; 0 / Receptors, TNF-Related Apoptosis-Inducing Ligand
  •  go-up   go-down


99. Hermans KG, van Marion R, van Dekken H, Jenster G, van Weerden WM, Trapman J: TMPRSS2:ERG fusion by translocation or interstitial deletion is highly relevant in androgen-dependent prostate cancer, but is bypassed in late-stage androgen receptor-negative prostate cancer. Cancer Res; 2006 Nov 15;66(22):10658-63
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] TMPRSS2:ERG fusion by translocation or interstitial deletion is highly relevant in androgen-dependent prostate cancer, but is bypassed in late-stage androgen receptor-negative prostate cancer.
  • Recently, a unique fusion between the prostate-specific, androgen-regulated TMPRSS2 gene and the ETS genes ERG, ETV1, or ETV4 has been described in clinical prostate cancer.
  • We investigated mechanisms of expression of four ETS genes, ERG, ETV1, ETV4, and FLI1, in 11 xenografts representing different stages of prostate cancer.
  • All five androgen-dependent xenografts showed as major transcript overexpression of two splice variants of TMPRSS2:ERG, linking TMPRSS2 exon 1 or 2 sequences to ERG exon 4.
  • In one of two androgen-sensitive xenografts, fusion transcripts of TMPRSS2 and ETV1 were detected.
  • Importantly, TMPRSS2 to ERG fusions were also observed in three of four androgen-independent, androgen receptor (AR)-negative xenografts and in two AR-negative clinical prostate cancer specimens; however, the fusion gene was not expressed.
  • Combined, our observations indicate a key role of fusion of TMPRSS2 and ETS genes in most androgen-regulated prostate cancers, which might be bypassed by androgen-independent expression of wild-type ETS factors in late-stage disease.
  • [MeSH-minor] Animals. Down-Regulation. Humans. Male. Mice. Mice, Nude. Neoplasm Staging. Polymerase Chain Reaction. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Receptors, Androgen / biosynthesis. Receptors, Androgen / deficiency. Translocation, Genetic. Transplantation, Heterologous

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • 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 = 17108102.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / ERG protein, human; 0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; 0 / Receptors, Androgen; 0 / Trans-Activators; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.- / TMPRSS2 protein, human
  •  go-up   go-down


100. Park YH, Hwang IS, Jeong CW, Kim HH, Lee SE, Kwak C: Prostate specific antigen half-time and prostate specific antigen doubling time as predictors of response to androgen deprivation therapy for metastatic prostate cancer. J Urol; 2009 Jun;181(6):2520-4; discussion 2525
MedlinePlus Health Information. consumer health - Prostate Cancer Screening.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prostate specific antigen half-time and prostate specific antigen doubling time as predictors of response to androgen deprivation therapy for metastatic prostate cancer.
  • PURPOSE: We determined the clinical significance of prostate specific antigen half-time and prostate specific antigen doubling time after the prostate specific antigen nadir as predictors of the response to androgen deprivation therapy for metastatic prostate cancer.
  • MATERIALS AND METHODS: A total of 131 patients with metastatic prostate cancer treated with androgen deprivation were included in this analysis.
  • Clinicopathological features and cancer specific survival were compared among the patients who were divided according to prostate specific antigen half-time and prostate specific antigen doubling time after the prostate specific antigen nadir.
  • Baseline and nadir prostate specific antigen did not differ between the patients with a short prostate specific antigen half-time (1 month or less) and those with a long prostate specific antigen half-time (longer than 1 month).
  • Patients with a short prostate specific antigen half-time had a higher Gleason score, shorter nadir duration and shorter cancer specific survival.
  • No differences were found between the patients with a short (6 months or less) and those with a long (longer than 6 months) prostate specific antigen doubling time after the prostate specific antigen nadir in terms of baseline prostate specific antigen, nadir prostate specific antigen, biopsy Gleason score and prostate specific antigen half-time.
  • A short prostate specific antigen doubling time after the prostate specific antigen nadir was associated with shorter nadir duration and poorer median cancer specific survival.
  • On multivariate analysis Gleason score, nadir prostate specific antigen and prostate specific antigen half-time remained independent predictors of an increase in prostate specific antigen after androgen deprivation therapy.
  • Nadir prostate specific antigen, prostate specific antigen half-time and prostate specific antigen doubling time after the prostate specific antigen nadir were prognostic factors for cancer specific survival.
  • CONCLUSIONS: The results of our study suggest that prostate specific antigen half-time and prostate specific antigen doubling time after the prostate specific antigen nadir are independent prognostic indicators for an increase in prostate specific antigen after androgen deprivation therapy and cancer related death in patients with metastatic prostate cancer treated with androgen deprivation.
  • [MeSH-major] Prostate-Specific Antigen / blood. Prostatic Neoplasms / blood. Prostatic Neoplasms / therapy
  • [MeSH-minor] Aged. Androgen Antagonists / therapeutic use. Castration. Gonadotropin-Releasing Hormone / agonists. Humans. Male. Neoplasm Metastasis. Predictive Value of Tests. Time Factors

  • Genetic Alliance. consumer health - Prostate cancer.
  • Genetic Alliance. consumer health - Metastatic cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19371894.001).
  • [ISSN] 1527-3792
  • [Journal-full-title] The Journal of urology
  • [ISO-abbreviation] J. Urol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgen Antagonists; 33515-09-2 / Gonadotropin-Releasing Hormone; EC 3.4.21.77 / Prostate-Specific Antigen
  •  go-up   go-down






Advertisement