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1. 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
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  • [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.

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  • (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
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2. Fritzsche FR, Jung M, Tölle A, Wild P, Hartmann A, Wassermann K, Rabien A, Lein M, Dietel M, Pilarsky C, Calvano D, Grützmann R, Jung K, Kristiansen G: ADAM9 expression is a significant and independent prognostic marker of PSA relapse in prostate cancer. Eur Urol; 2008 Nov;54(5):1097-106
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  • [Title] ADAM9 expression is a significant and independent prognostic marker of PSA relapse in prostate cancer.
  • OBJECTIVES: A disintegrin and metalloprotease (ADAM) 9 has been implicated in tumour progression of prostate cancer.
  • We evaluated the expression of ADAM9 on protein and messenger RNA (mRNA) level in a larger cohort of prostate cancer cases following prostatectomy and correlated the findings with clinicopathological parameters including prostate-specific antigen (PSA) relapse times.
  • METHODS: We immunostained 198 clinicopathologically characterised prostate cancer cases for ADAM9.
  • RESULTS: ADAM9 was significantly upregulated in prostate cancer compared with normal tissue on mRNA and protein level.
  • ADAM9 protein expression was significantly associated with shortened PSA relapse-free survival in univariate and multivariate analyses, particularly in patients who had received prior androgen ablation.
  • CONCLUSIONS: ADAM9 is overexpressed in prostate cancer cases and is an independent prognostic marker of PSA relapse-free survival following radical prostatectomy.
  • Further studies are needed to verify its role as a predictive marker of response to androgen ablation.
  • [MeSH-major] ADAM Proteins / genetics. Gene Expression Regulation, Neoplastic. Membrane Proteins / genetics. Neoplasm Recurrence, Local / genetics. Prostate-Specific Antigen / blood. Prostatic Neoplasms / genetics. RNA, Neoplasm / genetics


3. 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
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  • [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


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4. Chuan YC, Iglesias-Gato D, Fernandez-Perez L, Cedazo-Minguez A, Pang ST, Norstedt G, Pousette A, Flores-Morales A: Ezrin mediates c-Myc actions in prostate cancer cell invasion. Oncogene; 2010 Mar 11;29(10):1531-42
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  • [Title] Ezrin mediates c-Myc actions in prostate cancer cell invasion.
  • The forced overexpression of c-Myc in mouse prostate and in normal human prostate epithelial cells results in tumor transformation with an invasive phenotype.
  • In this study, we have investigated the interplay of c-Myc and androgens in the regulation of prostate cancer cell invasion.
  • We found that c-Myc induces cell invasion and anchorage-independent growth by regulating ezrin protein expression in the presence of androgens.
  • These effects are achieved through androgen-induced changes in ezrin phosphorylation, which results in the regulation of downstream signals.
  • In summary, we have shown a key role for ezrin as a mediator of c-Myc-induced tumorigenesis in prostate cancer cells.
  • [MeSH-minor] Binding Sites / genetics. Blotting, Western. Cell Line, Tumor. Fluorescent Antibody Technique. Gene Expression Regulation, Neoplastic / drug effects. Glycogen Synthase Kinase 3 / metabolism. Humans. Male. Metribolone / pharmacology. Neoplasm Invasiveness. Phosphorylation. Promoter Regions, Genetic / genetics. Protein Binding. Proto-Oncogene Proteins c-akt / metabolism. RNA Interference. Reverse Transcriptase Polymerase Chain Reaction


5. Arencibia JM, Del Rio M, Bonnin A, Lopes R, Lemoine NR, López-Barahona M: Doxazosin induces apoptosis in LNCaP prostate cancer cell line through DNA binding and DNA-dependent protein kinase down-regulation. Int J Oncol; 2005 Dec;27(6):1617-23
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  • [Title] Doxazosin induces apoptosis in LNCaP prostate cancer cell line through DNA binding and DNA-dependent protein kinase down-regulation.
  • Doxazosin is a quinazoline-based compound acting as an alpha-1-adrenergic inhibitor shown to induce apoptosis in prostate cancer cell lines via an alpha-1-adrenergic receptor-independent mechanism.
  • To better understand the mechanism of doxazosin-induced apoptosis in prostate cancer, we performed cDNA microarray to analyze gene expression changes produced by doxazosin in the androgen-dependent human prostate cancer cell line, LNCaP.
  • These facts, together with the demonstration of the ability of doxazosin to bind DNA, allowed us to propose a novel mechanism of action for doxazosin in prostate cancer cells that implies DNA-damage mediated apoptosis by down-regulation of XRCC5 and PRKDC genes.
  • [MeSH-major] Apoptosis / drug effects. DNA, Neoplasm / metabolism. DNA-Activated Protein Kinase / genetics. Doxazosin / pharmacology

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  • (PMID = 16273218.001).
  • [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 / Adrenergic alpha-Antagonists; 0 / DNA, Neoplasm; 0 / DNA, Superhelical; EC 2.7.11.1 / DNA-Activated Protein Kinase; NW1291F1W8 / Doxazosin
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6. 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
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  • [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.

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  • (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
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7. 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
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  • [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

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  • (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
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8. 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
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  • [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


9. Mashima T, Okabe S, Seimiya H: Pharmacological targeting of constitutively active truncated androgen receptor by nigericin and suppression of hormone-refractory prostate cancer cell growth. Mol Pharmacol; 2010 Nov;78(5):846-54
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  • [Title] Pharmacological targeting of constitutively active truncated androgen receptor by nigericin and suppression of hormone-refractory prostate cancer cell growth.
  • In prostate cancer, blockade of androgen receptor (AR) signaling confers a therapeutic benefit.
  • Nevertheless, this standard therapy allows relapse of hormone-refractory prostate cancer (HRPC) with a poor prognosis.
  • HRPC cells often express variant ARs, such as point-mutated alleles and splicing isoforms, resulting in androgen-independent cell growth and resistance to antiandrogen (e.g., flutamide).
  • Here, we established a reporter system that monitors AR-mediated activation of a prostate-specific antigen (PSA) promoter.
  • Our chemical library screening revealed that the antibiotic nigericin inhibits AR-mediated activation of the PSA promoter and PSA production in prostate cancer cells.
  • Nigericin suppressed the androgen-dependent LNCaP cell growth even though the cells expressed a flutamide-resistant mutant AR.
  • In HRPC 22Rv1 cells, which express the full-length AR and the constitutively active, truncated ARs lacking the carboxyl-terminal ligand-binding domain, small interfering RNA-mediated knockdown of both AR isoforms efficiently suppressed the androgen-independent cell growth, whereas knockdown of the full-length AR alone had no significant effect.
  • [MeSH-major] Androgen Receptor Antagonists / pharmacology. Antibiotics, Antineoplastic / pharmacology. Nigericin / pharmacology. Prostatic Neoplasms / pathology. Receptors, Androgen / physiology
  • [MeSH-minor] Cell Line, Tumor. Cell Proliferation / drug effects. Drug Resistance, Neoplasm. Drug Screening Assays, Antitumor. Gene Knockdown Techniques. Genes, Reporter. Humans. Male. Promoter Regions, Genetic. Prostate-Specific Antigen / biosynthesis. Prostate-Specific Antigen / genetics. Protein Isoforms / biosynthesis. Protein Isoforms / genetics. Protein Isoforms / physiology. Protein Processing, Post-Translational. RNA, Messenger / biosynthesis. RNA, Small Interfering / genetics. Signal Transduction / drug effects

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  • (PMID = 20709811.001).
  • [ISSN] 1521-0111
  • [Journal-full-title] Molecular pharmacology
  • [ISO-abbreviation] Mol. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgen Receptor Antagonists; 0 / Antibiotics, Antineoplastic; 0 / Protein Isoforms; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / Receptors, Androgen; EC 3.4.21.77 / Prostate-Specific Antigen; RRU6GY95IS / Nigericin
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10. 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
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  • [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


11. Sasaki T, Komiya A, Suzuki H, Shimbo M, Ueda T, Akakura K, Ichikawa T: Changes in chromogranin a serum levels during endocrine therapy in metastatic prostate cancer patients. Eur Urol; 2005 Aug;48(2):224-9; discussion 229-30
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  • [Title] Changes in chromogranin a serum levels during endocrine therapy in metastatic prostate cancer patients.
  • INTRODUCTION: The concept of neuroendocrine (NE) differentiation in prostate cancer has become more widely recognized as its diagnostic, prognostic, and therapeutic usefulness.
  • PATIENTS AND METHODS: We enrolled 38 patients with stage D prostate cancer who underwent endocrine therapy by medical or surgical castration and oral antiandrogen.
  • (1) pre-treatment, (2) complete response (CR), (3) a nadir level of PSA, (4) PSA failure or hormone independent progression.
  • CONCLUSION: During endocrine therapy in metastatic prostate cancer patients, serum CGA values were not related to serum PSA levels, and increased as treatment periods became longer.
  • It is suggested that CGA velocity has potential to predict androgen independent progression after endocrine therapy.
  • [MeSH-major] Adenocarcinoma / blood. Adenocarcinoma / drug therapy. Androgen Antagonists / therapeutic use. Antineoplastic Agents, Hormonal / therapeutic use. Chromogranins / blood. Prostatic Neoplasms / blood. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Aged. Aged, 80 and over. Analysis of Variance. Biomarkers, Tumor / blood. Disease Progression. Humans. Male. Middle Aged. Neoplasm Metastasis. Neoplasm Staging. Prostate-Specific Antigen / blood. Statistics, Nonparametric


12. 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
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  • [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

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  • (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
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13. 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
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  • [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

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  • (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
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14. Mukherjee S, Bhattacharya RK, Roy M: Targeting protein kinase C (PKC) and telomerase by phenethyl isothiocyanate (PEITC) sensitizes PC-3 cells towards chemotherapeutic drug-induced apoptosis. J Environ Pathol Toxicol Oncol; 2009;28(4):269-82
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  • Prostate cancer is the leading cause of cancer-related death in men, incidences of which are increasing gradually in India.
  • Protein kinase C (PKC), an enzyme, gets overexpressed in prostate cancer and results in a resistance to chemotherapy.
  • Telomerase, a reverse transcriptase, is highly activated in prostate cancer cells.
  • Both of these enzymes can be considered as potential molecular markers for prostate cancer.
  • The present study investigates the effects of natural isothiocyanate phenethyl isothiocyanate (PEITC) in modulating the activities of PKC and telomerase in the androgen-independent human prostate adenocarcinoma (PC-3) cell line.
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / pharmacology. Biomarkers, Tumor / metabolism. Caspases / metabolism. Cell Line, Tumor. Cytochromes c / metabolism. Down-Regulation / drug effects. Doxorubicin / pharmacology. Drug Resistance, Neoplasm. Etoposide / pharmacology. Humans. Male

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  • (PMID = 20102325.001).
  • [ISSN] 2162-6537
  • [Journal-full-title] Journal of environmental pathology, toxicology and oncology : official organ of the International Society for Environmental Toxicology and Cancer
  • [ISO-abbreviation] J. Environ. Pathol. Toxicol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / Isothiocyanates; 6PLQ3CP4P3 / Etoposide; 6U7TFK75KV / phenethyl isothiocyanate; 80168379AG / Doxorubicin; 9007-43-6 / Cytochromes c; EC 2.7.11.13 / Protein Kinase C; EC 2.7.7.49 / Telomerase; EC 3.4.22.- / Caspases
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15. Devilard E, Bladou F, Ramuz O, Karsenty G, Dalès JP, Gravis G, Nguyen C, Bertucci F, Xerri L, Birnbaum D: FGFR1 and WT1 are markers of human prostate cancer progression. BMC Cancer; 2006;6:272
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  • [Title] FGFR1 and WT1 are markers of human prostate cancer progression.
  • BACKGROUND: Androgen-independent prostate adenocarcinomas are responsible for about 6% of overall cancer deaths in men.
  • METHODS: We used DNA microarrays to identify genes related to the transition between androgen-dependent and androgen-independent stages in the LuCaP 23.1 xenograft model of prostate adenocarcinoma.
  • The expression of the proteins encoded by these genes was then assessed by immunohistochemistry on tissue microarrays (TMA) including human prostate carcinoma samples issued from 85 patients who had undergone radical prostatectomy.
  • RESULTS: FGFR1, TACC1 and WT1 gene expression levels were associated with the androgen-independent stage in xenografts and human prostate carcinoma samples.
  • CONCLUSION: Our results suggest that each of these four genes may play a role, or at least reflect a stage of prostate carcinoma growth/development/progression.
  • [MeSH-minor] Animals. Antigens, Neoplasm / metabolism. Disease Progression. Fetal Proteins / metabolism. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. MART-1 Antigen. Male. Mice. Microtubule-Associated Proteins / metabolism. Middle Aged. Models, Biological. Neoplasm Proteins / metabolism. Neoplasm Staging / methods. Nuclear Proteins / metabolism. Oligonucleotide Array Sequence Analysis. Xenograft Model Antitumor Assays

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  • (PMID = 17137506.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / Fetal Proteins; 0 / MART-1 Antigen; 0 / MLANA protein, human; 0 / Microtubule-Associated Proteins; 0 / Mlana protein, mouse; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / TACC1 protein, human; 0 / WT1 Proteins; EC 2.7.10.1 / Receptor, Fibroblast Growth Factor, Type 1
  • [Other-IDs] NLM/ PMC1698935
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16. Colabufo NA, Pagliarulo V, Berardi F, Contino M, Inglese C, Niso M, Ancona P, Albo G, Pagliarulo A, Perrone R: Bicalutamide failure in prostate cancer treatment: involvement of Multi Drug Resistance proteins. Eur J Pharmacol; 2008 Dec 28;601(1-3):38-42
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  • [Title] Bicalutamide failure in prostate cancer treatment: involvement of Multi Drug Resistance proteins.
  • Prolonged bicalutamide treatment induced pathology regression although relapses with a more aggressive form of prostate cancer have been observed.
  • This failure could be due to androgen receptor mutation.
  • In the present work we hypothesized an alternative mechanism responsible for bicalutamide failure involving activity of ATP-binding cassette (ABC) pumps such as P-glycoprotein, Breast Cancer Receptor Protein (BCRP), and Multi Resistant Proteins (MRPs) that extrude the androgen antagonist from the cell membrane.
  • As experimental models androgen-dependent (LnCap) and androgen-independent (PC-3) prostate cancer cell lines have been employed.
  • [MeSH-major] Androgen Antagonists / pharmacology. Anilides / pharmacology. Drug Resistance, Neoplasm. Nitriles / pharmacology. Prostatic Neoplasms / drug therapy. Tosyl Compounds / pharmacology
  • [MeSH-minor] ATP Binding Cassette Transporter, Sub-Family G, Member 2. ATP-Binding Cassette Transporters / metabolism. ATP-Binding Cassette, Sub-Family B, Member 1 / metabolism. Androgens / metabolism. Animals. Cell Line. Cell Line, Tumor. Cell Proliferation / drug effects. Dogs. Dose-Response Relationship, Drug. Humans. Male. Multidrug Resistance-Associated Proteins / metabolism. Neoplasm Proteins / metabolism. Protein Binding

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  • (PMID = 18992739.001).
  • [ISSN] 1879-0712
  • [Journal-full-title] European journal of pharmacology
  • [ISO-abbreviation] Eur. J. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / ABCG2 protein, human; 0 / ATP Binding Cassette Transporter, Sub-Family G, Member 2; 0 / ATP-Binding Cassette Transporters; 0 / ATP-Binding Cassette, Sub-Family B, Member 1; 0 / Androgen Antagonists; 0 / Androgens; 0 / Anilides; 0 / Multidrug Resistance-Associated Proteins; 0 / Neoplasm Proteins; 0 / Nitriles; 0 / Tosyl Compounds; A0Z3NAU9DP / bicalutamide; Y49M64GZ4Q / multidrug resistance-associated protein 1
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17. 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
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  • [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

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  • (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
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18. Ma S, Guan XY, Beh PS, Wong KY, Chan YP, Yuen HF, Vielkind J, Chan KW: The significance of LMO2 expression in the progression of prostate cancer. J Pathol; 2007 Feb;211(3):278-85
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  • [Title] The significance of LMO2 expression in the progression of prostate cancer.
  • This study has investigated LMO2 expression in human prostatic tissue specimens, prostate cancer cell lines, and xenografts; and has assessed the possible role and mechanism of LMO2 in prostate carcinogenesis.
  • Immunohistochemical analysis on a tissue microarray consisting of 91 human prostate specimens, including normal, prostatic hyperplasia, high-grade prostatic intraepithelial neoplasia, and invasive carcinoma, revealed that overexpression of LMO2 was significantly associated with advanced tumour stage, as measured by Gleason score (p = 0.012), as well as with the development of distant metastasis (p = 0.018).
  • These data were supported by quantitative real-time PCR experiments, where LMO2 mRNA levels were found to be significantly higher in prostate tumour specimen than in normal epithelium (p = 0.037).
  • The expression of LMO2 in cell lines and xenografts representing androgen-dependent (AD) and androgen-independent (AI) prostate cancer stages was further studied.
  • Taken together, these findings provide the first evidence to support the hypothesis that LMO2 may play an important role in prostate cancer progression, possibly via repression of E-cadherin expression.
  • [MeSH-minor] Adaptor Proteins, Signal Transducing. Aged. Aged, 80 and over. Blotting, Western / methods. Cell Line, Tumor. Chi-Square Distribution. Gene Expression Profiling. Humans. Immunohistochemistry / methods. LIM Domain Proteins. Male. Middle Aged. Neoplasm Staging. Oligonucleotide Array Sequence Analysis. Prognosis. Proto-Oncogene Proteins. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction

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  • [Copyright] Copyright 2006 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
  • (PMID = 17167821.001).
  • [ISSN] 0022-3417
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / DNA-Binding Proteins; 0 / LIM Domain Proteins; 0 / LMO2 protein, human; 0 / Metalloproteins; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger
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19. Dondi D, Piccolella M, Biserni A, Della Torre S, Ramachandran B, Locatelli A, Rusmini P, Sau D, Caruso D, Maggi A, Ciana P, Poletti A: Estrogen receptor beta and the progression of prostate cancer: role of 5alpha-androstane-3beta,17beta-diol. Endocr Relat Cancer; 2010 Sep;17(3):731-42
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  • [Title] Estrogen receptor beta and the progression of prostate cancer: role of 5alpha-androstane-3beta,17beta-diol.
  • Prostate cancer (PC) develops in response to an abnormal activation of androgen receptor induced by circulating androgens and, in its initial stages, is pharmacologically controlled by androgen blockade.
  • However, androgen ablation therapy often allows androgen-independent PC development, generally characterized by increased invasiveness.
  • In vivo, continuous administration of 3beta-Adiol reduces growth of established tumors and counteracts metastasis formation when PC3-Luc cells are engrafted s.c. in nude mice or are orthotopically injected into the prostate.
  • [MeSH-minor] Animals. Apoptosis / drug effects. Blotting, Western. Cell Adhesion / drug effects. Cell Line, Tumor. Cell Movement / drug effects. Collagen / metabolism. Drug Combinations. Humans. Laminin / metabolism. Male. Mice. Mice, Inbred BALB C. Neoplasm Invasiveness. Proteoglycans / metabolism. Receptors, Androgen / metabolism. Survival Rate. Xenograft Model Antitumor Assays

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  • (PMID = 20562232.001).
  • [ISSN] 1479-6821
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Grant] Italy / Telethon / / GGP07063
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anabolic Agents; 0 / Drug Combinations; 0 / Estrogen Receptor beta; 0 / Laminin; 0 / Proteoglycans; 0 / Receptors, Androgen; 119978-18-6 / matrigel; 25126-76-5 / Androstane-3,17-diol; 9007-34-5 / Collagen
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20. Jennbacken K, Tesan T, Wang W, Gustavsson H, Damber JE, Welén K: N-cadherin increases after androgen deprivation and is associated with metastasis in prostate cancer. Endocr Relat Cancer; 2010 Jun;17(2):469-79
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  • [Title] N-cadherin increases after androgen deprivation and is associated with metastasis in prostate cancer.
  • Androgen-deprivation therapy (ADT) is the standard treatment for metastatic prostate cancer.
  • In this study, we investigated if the expression of N-cadherin was influenced by androgen deprivation and was associated with metastasis in prostate cancer.
  • The effect of androgen deprivation on N-cadherin expression was initially studied in androgen-dependent (AD) LNCaP and androgen-independent (AI) LNCaP-19 and PC-3 prostate cancer cell lines.
  • Expression of N-cadherin increased in the absence of androgens in AI LNCaP-19 primary tumors and metastases and also in vitro, but not in AI PC-3 tumors, indicating a possible involvement of the androgen receptor in the regulation of N-cadherin.
  • In addition, N-cadherin was evaluated by immunohistochemistry in human prostate tumors.
  • Furthermore, increased N-cadherin was detected in prostate cancer biopsies already 3 months after initiation of ADT when tumors were in a regressed state.
  • In summary the results indicate that androgen deprivation induces N-cadherin in prostate tumors.
  • [MeSH-minor] Animals. Cell Line, Tumor. Gene Expression Regulation, Neoplastic / drug effects. Humans. Male. Mice. Mice, Inbred BALB C. Mice, Nude. Neoplasm Metastasis. Receptors, Androgen / metabolism. Receptors, Androgen / physiology. Transplantation, Heterologous. Treatment Failure. Up-Regulation / drug effects. Up-Regulation / genetics

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  • (PMID = 20233707.001).
  • [ISSN] 1479-6821
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Androgens; 0 / Antigens, CD; 0 / CDH2 protein, human; 0 / Cadherins; 0 / Receptors, Androgen
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21. 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
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  • [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


22. Koike H, Ito K, Takezawa Y, Oyama T, Yamanaka H, Suzuki K: Insulin-like growth factor binding protein-6 inhibits prostate cancer cell proliferation: implication for anticancer effect of diethylstilbestrol in hormone refractory prostate cancer. Br J Cancer; 2005 Apr 25;92(8):1538-44
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  • [Title] Insulin-like growth factor binding protein-6 inhibits prostate cancer cell proliferation: implication for anticancer effect of diethylstilbestrol in hormone refractory prostate cancer.
  • Diethylstilbestrol (DES) is a synthetic oestrogen, and its anticancer effects are exerted in androgen-dependent prostate cancer.
  • However, in androgen-independent prostate cancer patients, who are already orchiectomised, the administration of DES improves symptoms and decreases prostate-specific antigen (PSA).
  • We assessed the gene expression profiles of prostate cancer cells treated with DES, and investigated direct inhibitory effects of DES.
  • From the immunohistochemical analysis of IGFBP-6 using biopsy samples from androgen-independent prostate cancer, we found IGFBP-6 expression in androgen independent prostate cancer, and that DES treatment increased the IGFBP-6 staining intensity of the cancer cells in one sample.
  • These findings suggested that DES induces IGFBP-6, which inhibits cell proliferation in an androgen-independent prostate cancer cell line, PC-3.
  • IGFBP-6 therefore might be involved in the direct effects of DES in androgen-independent prostate cancer.
  • [MeSH-minor] Apoptosis / drug effects. Blotting, Western. Cell Line, Tumor. Dose-Response Relationship, Drug. Drug Resistance, Neoplasm. Gene Expression. Gene Expression Profiling. Hormones / therapeutic use. Humans. Immunohistochemistry. Male. Oligonucleotide Array Sequence Analysis. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 15846301.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Hormones; 0 / Insulin-Like Growth Factor Binding Protein 6; 0 / RNA, Messenger; 731DCA35BT / Diethylstilbestrol
  • [Other-IDs] NLM/ PMC2362003
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23. 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
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  • [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

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  • (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
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24. Kaarbø M, Klokk TI, Saatcioglu F: Androgen signaling and its interactions with other signaling pathways in prostate cancer. Bioessays; 2007 Dec;29(12):1227-38
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  • [Title] Androgen signaling and its interactions with other signaling pathways in prostate cancer.
  • Prostate cancer is the most frequently diagnosed non-skin cancer and the third leading cause of cancer mortality in men.
  • In the initial stages, prostate cancer is dependent on androgens for growth, which is the basis for androgen ablation therapy.
  • However, in most cases, prostate cancer progresses to a hormone refractory phenotype for which there is no effective therapy available at present.
  • The androgen receptor (AR) is required for prostate cancer growth in all stages, including the relapsed, "androgen-independent" tumors in the presence of very low levels of androgens.
  • This review focuses on AR function and AR-target genes and summarizes the major signaling pathways implicated in prostate cancer progression, their crosstalk with each other and with AR signaling.
  • This complex network of interactions is providing a deeper insight into prostate carcinogenesis and may form the basis for novel diagnostic and therapeutic strategies.
  • [MeSH-minor] Animals. Humans. Male. Neoplasm Proteins / metabolism. Receptor Cross-Talk. Receptors, Androgen / metabolism

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  • [Copyright] 2007 Wiley Periodicals, Inc
  • (PMID = 18008377.001).
  • [ISSN] 0265-9247
  • [Journal-full-title] BioEssays : news and reviews in molecular, cellular and developmental biology
  • [ISO-abbreviation] Bioessays
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Neoplasm Proteins; 0 / Receptors, Androgen
  • [Number-of-references] 116
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25. 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
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  • [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

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  • (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
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26. Chow L, Rezmann L, Imamura K, Wang L, Catt K, Tikellis C, Louis WJ, Frauman AG, Louis SN: Functional angiotensin II type 2 receptors inhibit growth factor signaling in LNCaP and PC3 prostate cancer cell lines. Prostate; 2008 May 1;68(6):651-60
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  • [Title] Functional angiotensin II type 2 receptors inhibit growth factor signaling in LNCaP and PC3 prostate cancer cell lines.
  • BACKGROUND: There is clear evidence of a tissue-based renin-angiotensin system in the prostate and studies to date suggest that AT(1)-receptor blocking drugs inhibit the growth of some prostate cancer cell lines and delay the development of prostate cancer.
  • The present studies examine the action of Ang II in two prostate cancer cell lines and report the presence of functional AT(2)-receptors that regulate the actions of growth factors.
  • METHODS: Immunohistochemistry was used to identify the presence of Ang II and QPCR techniques to examine AT(1)- and AT(2)-receptor mRNA expression in androgen-dependent (LNCaP) and independent (PC3) cell lines.
  • CONCLUSIONS: Functional AT(2)-receptors are present and have the capacity to inhibit EGF-induced prostate cancer cell growth in LNCaP and fast growing androgen-independent PC3 cell lines, whereas functional AT(1)-receptors are found only in LNCaP cells where their activation stimulates DNA synthesis.
  • [MeSH-minor] Cell Line, Tumor. DNA / biosynthesis. DNA / drug effects. Gene Expression Regulation, Neoplastic / drug effects. Gene Expression Regulation, Neoplastic / physiology. Humans. Male. Phosphorylation. RNA, Messenger / metabolism. RNA, Neoplasm / analysis. Receptor, Angiotensin, Type 1 / genetics. Receptor, Angiotensin, Type 1 / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction / drug effects. Signal Transduction / physiology

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  • (PMID = 18288685.001).
  • [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 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Receptor, Angiotensin, Type 1; 0 / Receptor, Angiotensin, Type 2; 62229-50-9 / Epidermal Growth Factor; 9007-49-2 / DNA; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1
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27. Kuo PT, Lin TP, Liu LC, Huang CH, Lin JK, Kao JY, Way TD: Penta-O-galloyl-beta-D-glucose suppresses prostate cancer bone metastasis by transcriptionally repressing EGF-induced MMP-9 expression. J Agric Food Chem; 2009 Apr 22;57(8):3331-9
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  • [Title] Penta-O-galloyl-beta-D-glucose suppresses prostate cancer bone metastasis by transcriptionally repressing EGF-induced MMP-9 expression.
  • Prostate carcinoma is the most frequently diagnosed malignancy and the second leading cause of cancer-related death of men in the United States.
  • Epidermal growth factor (EGF) generated from bone tissue contributes to prostate cancer metastasis through stimulating matrix metalloproteinase (MMP) secretions from prostate cancer cells.
  • The anti-invasive and cytotoxic effects of 5GG were found and evaluated on the human androgen-independent prostate cancer PC-3 cell line by MTT assays and Western blot analyses.
  • These results suggest that 5GG may exert at least part of its anti-invasive effect in androgen-independent prostate cancer by controlling MMP-9 expression through the suppression of the EGFR/JNK pathway.
  • These in vitro and in vivo results suggest that 5GG may be a therapeutic candidate for the treatment of advanced prostate cancer.
  • [MeSH-minor] Animals. Cell Line, Tumor. Humans. Male. Mice. Mice, Nude. Neoplasm Invasiveness / prevention & control. Neoplasm Transplantation. RNA, Messenger / genetics. Receptor, Epidermal Growth Factor / genetics. Transcription, Genetic / drug effects


28. 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
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  • [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

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  • (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
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29. Guan XX, Chen LB: [Current opinions on the treatment of androgen-independent prostate cancer]. Zhonghua Nan Ke Xue; 2006 Nov;12(11):1021-5
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  • [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.

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  • (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
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30. DeNardo SJ, Richman CM, Albrecht H, Burke PA, Natarajan A, Yuan A, Gregg JP, O'Donnell RT, DeNardo GL: Enhancement of the therapeutic index: from nonmyeloablative and myeloablative toward pretargeted radioimmunotherapy for metastatic prostate cancer. Clin Cancer Res; 2005 Oct 1;11(19 Pt 2):7187s-7194s
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  • [Title] Enhancement of the therapeutic index: from nonmyeloablative and myeloablative toward pretargeted radioimmunotherapy for metastatic prostate cancer.
  • PURPOSE: New strategies that target selected molecular characteristics and result in an effective therapeutic index are needed for metastatic, hormone-refractory prostate cancer.
  • EXPERIMENTAL DESIGN: A series of preclinical and clinical studies were designed to increase the therapeutic index of targeted radiation therapy for prostate cancer. (111)In/90Y-monoclonal antibody (mAb), m170, which targets aberrant sugars on abnormal MUC1, was evaluated in androgen-independent prostate cancer patients to determine the maximum tolerated dose and efficacy of nonmyeloablative radioimmunotherapy and myeloablative combined modality radioimmunotherapy with paclitaxel.
  • Anti-MUC1 and anti-DOTA scFvs were conjugated to polyethylene glycol scaffolds tested on DU145 prostate cancer cells and prostate tissue arrays, along with mAbs against MUC1 epitopes.
  • Metastatic prostate cancer was targeted in all 17 patients; mean radiation dose was 10.5 Gy/GBq and pain response occurred in 7 of 13 patients reporting pain.
  • Hypoglycosylated MUC1 epitopes were shown to be abundant in prostate cancer and to increase with disease grade.
  • Anti-MUC1 scFvs binding to prostate cancer tissue and live cells were developed into di-scFv binding modules.
  • CONCLUSIONS: The therapeutic index enhancement for prostate radioimmunotherapy was achieved in clinical studies by the addition of cathepsin cleavable linkers to 90Y-conjugated mAbs and the use of paclitaxel.
  • [MeSH-minor] Antibodies, Monoclonal. Antigens / chemistry. Antigens, Neoplasm. Bone Marrow / metabolism. Cathepsins / chemistry. Combined Modality Therapy. Electrophoresis, Polyacrylamide Gel. Epitopes / chemistry. Glycoproteins / chemistry. Humans. Immunohistochemistry. Male. Maleimides / chemistry. Maximum Tolerated Dose. Models, Chemical. Mucin-1. Mucins / chemistry. Neoplasm Metastasis. Paclitaxel / chemistry. Peptide Library. Peptides / chemistry. Polyethylene Glycols / chemistry. Protein Binding. Radiometry. Yttrium Radioisotopes / chemistry

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  • (PMID = 16203820.001).
  • [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 / CA47829
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens; 0 / Antigens, Neoplasm; 0 / Epitopes; 0 / Glycoproteins; 0 / MUC1 protein, human; 0 / Maleimides; 0 / Mucin-1; 0 / Mucins; 0 / Peptide Library; 0 / Peptides; 0 / Yttrium Radioisotopes; 30IQX730WE / Polyethylene Glycols; 541-59-3 / maleimide; EC 3.4.- / Cathepsins; P88XT4IS4D / Paclitaxel
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31. Yuen HF, Chua CW, Chan YP, Wong YC, Wang X, Chan KW: Id proteins expression in prostate cancer: high-level expression of Id-4 in primary prostate cancer is associated with development of metastases. Mod Pathol; 2006 Jul;19(7):931-41
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  • [Title] Id proteins expression in prostate cancer: high-level expression of Id-4 in primary prostate cancer is associated with development of metastases.
  • A major cause of treatment failure for prostate cancer is the development of androgen-independent metastatic disease.
  • In this study, we examined the expressions of four Id proteins, Id-1, -2, -3 and -4, in 125 clinical prostate cancer specimens as well as 40 nodular hyperplasia specimens by immunohistochemistry.
  • We found that Id proteins were dysregulated in prostate cancer.
  • Id-1 and -2 expressions were elevated while Id-3 and -4 expressions were reduced in prostate cancers compared to nodular hyperplasia.
  • The results indicate that these Id proteins may play a positive role in the development of prostate cancer.
  • In contrast, Id-3 might have an inverse relationship with prostate neoplastic transformation (P=0.002) and cancer progression (P=0.022).
  • We found that Id-4 nuclear overexpression in the primary prostate cancers significantly increased the risks to the development of metastasis in the patients (odds ratio=3.215, 95% confidence interval=1.150-8.987, P=0.026).
  • Our results suggest that in prostate cancer patients, differential Id proteins expressions may be a useful marker for poor prognosis, and Id-4 may be a potential prognostic marker for distant metastasis.
  • [MeSH-minor] Aged. Aged, 80 and over. Cell Nucleus / metabolism. Cell Transformation, Neoplastic / metabolism. Cell Transformation, Neoplastic / pathology. Cytoplasm / metabolism. Humans. Immunohistochemistry. Inhibitor of Differentiation Protein 1 / metabolism. Inhibitor of Differentiation Protein 2 / metabolism. Male. Middle Aged. Neoplasm Metastasis. Neoplasm Proteins / metabolism. Prognosis. Retrospective Studies. Tissue Array Analysis

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  • (PMID = 16575399.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / ID1 protein, human; 0 / ID2 protein, human; 0 / ID4 protein, human; 0 / Inhibitor of Differentiation Protein 1; 0 / Inhibitor of Differentiation Protein 2; 0 / Inhibitor of Differentiation Proteins; 0 / Neoplasm Proteins; 147785-34-0 / ID3 protein, human
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32. Lara PN Jr, Stadler WM, Longmate J, Quinn DI, Wexler J, Van Loan M, Twardowski P, Gumerlock PH, Vogelzang NJ, Vokes EE, Lenz HJ, Doroshow JH, Gandara DR: A randomized phase II trial of the matrix metalloproteinase inhibitor BMS-275291 in hormone-refractory prostate cancer patients with bone metastases. Clin Cancer Res; 2006 Mar 1;12(5):1556-63
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  • [Title] A randomized phase II trial of the matrix metalloproteinase inhibitor BMS-275291 in hormone-refractory prostate cancer patients with bone metastases.
  • We conducted a randomized phase II trial of two doses of BMS-275291 (1,200 versus 2,400 mg) in hormone-refractory prostate cancer (HRPC) patients with bone metastases to probe for a dose-response relationship and to assess differential toxicities.
  • Eligibility criteria included documentation of androgen-independent disease (including anti-androgen withdrawal), skeletal metastasis, adequate end-organ function and performance status, and no more than one prior chemotherapy regimen.
  • There were no responders by prostate-specific antigen or measurable disease to treatment.
  • [MeSH-minor] Aged. Aged, 80 and over. Disease-Free Survival. Drug Administration Schedule. Humans. Male. Middle Aged. Neoplasm Staging. Survival Rate. Treatment Outcome

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  • (PMID = 16533781.001).
  • [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] Clinical Trial, Phase II; Journal Article; Randomized Controlled Trial
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Imidazoles; 0 / Matrix Metalloproteinase Inhibitors; 259188-38-0 / N-((2S)-2-mercapto-1-oxo-4-(3,4,4- trimethyl-2,5-dioxo-1-imidazolidinyl)butyl)-L-leucyl-N,3- dimethyl-L-Valinamide
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33. Davis JN, Wojno KJ, Daignault S, Hofer MD, Kuefer R, Rubin MA, Day ML: Elevated E2F1 inhibits transcription of the androgen receptor in metastatic hormone-resistant prostate cancer. Cancer Res; 2006 Dec 15;66(24):11897-906
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  • [Title] Elevated E2F1 inhibits transcription of the androgen receptor in metastatic hormone-resistant prostate cancer.
  • Previously, we showed that homozygous deletion of Rb in a prostate tissue recombination model exhibits increased E2F activity, activation of E2F-target genes, and increased susceptibility to hormonal carcinogenesis.
  • In this study, we examined the expression of E2F1 in 667 prostate tissue cores and compared it with the expression of the androgen receptor (AR), a marker of prostate epithelial differentiation, using tissue microarray analysis.
  • We show that E2F1 expression is low in benign and localized prostate cancer, modestly elevated in metastatic lymph nodes from hormone-naïve patients, and significantly elevated in metastatic tissues from hormone-resistant prostate cancer patients (P = 0.0006).
  • In contrast, strong AR expression was detected in benign prostate (83%), localized prostate cancer (100%), and lymph node metastasis (80%), but decreased to 40% in metastatic hormone-resistant prostate cancer (P = 0.004).
  • Semiquantitative reverse transcription-PCR analysis showed elevated E2F1 mRNA levels and increased levels of the E2F-target genes dihyrofolate reductase and proliferating cell nuclear antigen in metastatic hormone-independent prostate cancer cases compared with benign tissues.
  • To identify a role of E2F1 in hormone-independent prostate cancer, we examined whether E2F1 can regulate AR expression.
  • We show that exogenous expression of E2F1 significantly inhibited AR mRNA and AR protein levels in prostate epithelial cells.
  • Taken together, these results show that elevated E2F1, through its ability to repress AR transcription, may contribute to the progression of hormone-independent prostate cancer.
  • [MeSH-major] E2F1 Transcription Factor / genetics. Gene Expression Regulation, Neoplastic. Prostatic Neoplasms / genetics. Receptors, Androgen / genetics. Transcription, Genetic / drug effects
  • [MeSH-minor] Autopsy. DNA Primers. Genes, Retinoblastoma. Humans. Immunohistochemistry. Male. Neoplasm Metastasis / prevention & control. RNA, Neoplasm / genetics. RNA, Neoplasm / isolation & purification. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 17178887.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P50-CA69569; United States / NIDDK NIH HHS / DK / R01-DK066610; United States / NIDDK NIH HHS / DK / R01-DK61488
  • [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 / DNA Primers; 0 / E2F1 Transcription Factor; 0 / E2F1 protein, human; 0 / RNA, Neoplasm; 0 / Receptors, Androgen
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34. Culig Z, Steiner H, Bartsch G, Hobisch A: Mechanisms of endocrine therapy-responsive and -unresponsive prostate tumours. Endocr Relat Cancer; 2005 Jun;12(2):229-44
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  • [Title] Mechanisms of endocrine therapy-responsive and -unresponsive prostate tumours.
  • Several options for the endocrine treatment of non-organ-confined prostate cancer are available.
  • The androgen receptor (AR) is, in various tumour models, implicated in the development of therapy resistance but molecular mechanisms that by-pass the receptor have also been described.
  • Adaptation mechanisms relevant to tumour recurrence include up-regulation of AR mRNA and protein, overexpression of AR coactivators, increased activation of mutated receptors by steroids and anti-androgens, and ligand-independent activation.
  • For research studies, sublines that respond to but do not depend on androgen for their proliferation were generated.
  • Coactivators SRC-1, TIF-2, RAC3, p300, CBP, Tip60, and gelsolin are highly expressed in endocrine therapy-resistant prostate cancer.
  • Ligand-independent activation of the AR by HER-2/neu and interleukin-6 is associated with activation of the signalling pathway of mitogen-activated protein kinase.
  • Increased activity of intracellular kinases may affect cellular events in both an AR-dependent and -independent manner.
  • Mitogen-activated protein kinases are strongly phosphorylated in endocrine therapy-resistant prostate tumours.
  • Similarly, activation of the AR by phosphorylated protein kinase B, Akt, has also been reported in prostate cancer.
  • Activation of the Akt pathway contributes to increased survival of prostate tumour cells.
  • [MeSH-major] Androgens / therapeutic use. Neoplasms, Hormone-Dependent / drug therapy. Prostatic Neoplasms / drug therapy. Receptors, Androgen / genetics. Receptors, Androgen / metabolism
  • [MeSH-minor] Animals. Drug Resistance, Neoplasm / genetics. Humans. Male. Mitogen-Activated Protein Kinases / metabolism. Point Mutation. Protein-Serine-Threonine Kinases / metabolism. Proto-Oncogene Proteins / metabolism. Proto-Oncogene Proteins c-akt. Treatment Failure


35. Gilbert DC, Parker C: Docetaxel for the treatment of prostate cancer. Future Oncol; 2005 Jun;1(3):307-14
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  • [Title] Docetaxel for the treatment of prostate cancer.
  • Prostate cancer accounts for 12% of male cancer deaths, amounting to almost 10,000 deaths per year in the UK.
  • Patients that develop metastatic disease may have their prostate cancer controlled for approximately 2 years with androgen deprivation but invariably progress to a castrate-independent state and succumb to metastatic disease.
  • The previous experience of cytotoxic chemotherapy in hormone-refractory prostate cancer has yielded modest improvements in quality of life, with mitoxantrone in widest use.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / therapeutic use. Neoplasm Recurrence, Local / drug therapy. Prostatic Neoplasms / drug therapy. Taxoids / therapeutic use
  • [MeSH-minor] Drug Resistance, Neoplasm. Humans. Male

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  • (PMID = 16556003.001).
  • [ISSN] 1479-6694
  • [Journal-full-title] Future oncology (London, England)
  • [ISO-abbreviation] Future Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Taxoids; 15H5577CQD / docetaxel
  • [Number-of-references] 37
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36. Ligr M, Li Y, Zou X, Daniels G, Melamed J, Peng Y, Wang W, Wang J, Ostrer H, Pagano M, Wang Z, Garabedian MJ, Lee P: Tumor suppressor function of androgen receptor coactivator ARA70alpha in prostate cancer. Am J Pathol; 2010 Apr;176(4):1891-900
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  • [Title] Tumor suppressor function of androgen receptor coactivator ARA70alpha in prostate cancer.
  • Androgen receptor (AR), a member of the steroid receptor family, is a transcription factor that has an important role in the regulation of both prostate cell proliferation and growth suppression.
  • We have shown previously that the internally spliced ARA70 isoform, ARA70beta, promotes prostate cancer cell growth and invasion.
  • Here we report that the full length ARA70alpha, in contrast, represses prostate cancer cell proliferation and anchorage-independent growth in vitro and inhibits tumor growth in nude mice xenograft experiments in vivo.
  • The tumor suppressor function of ARA70alpha is consistent with our previous findings that ARA70alpha expression is decreased in prostate cancer cells compared with benign prostate.
  • Although growth inhibition by ARA70alpha is AR-dependent, the inhibition of cell invasion is an androgen-independent process.

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  • (PMID = 20167864.001).
  • [ISSN] 1525-2191
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK058024
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / NCOA4 protein, human; 0 / Nuclear Receptor Coactivators; 0 / Protein Isoforms
  • [Other-IDs] NLM/ PMC2843478
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37. 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
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  • [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

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  • [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
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38. Jariwala U, Prescott J, Jia L, Barski A, Pregizer S, Cogan JP, Arasheben A, Tilley WD, Scher HI, Gerald WL, Buchanan G, Coetzee GA, Frenkel B: Identification of novel androgen receptor target genes in prostate cancer. Mol Cancer; 2007 Jun 06;6:39
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  • [Title] Identification of novel androgen receptor target genes in prostate cancer.
  • BACKGROUND: The androgen receptor (AR) plays critical roles in both androgen-dependent and castrate-resistant prostate cancer (PCa).
  • Whereas the AR occupied the same loci in C4-2B (castrate resistant) and LNCaP (androgen-dependent) PCa cells, differences between the two cell lines were observed in the response of nearby genes to androgens.
  • Another AR target gene, ornithine aminotransferase (OAT), was AR-stimulated in a ligand-independent manner, since it was repressed by AR siRNA knockdown, but not stimulated by DHT.
  • Some of the genes near AR-occupied regions appear to be regulated by the AR in vivo as evidenced by their expression levels in prostate cancer tumors of various stages.

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  • (PMID = 17553165.001).
  • [ISSN] 1476-4598
  • [Journal-full-title] Molecular cancer
  • [ISO-abbreviation] Mol. Cancer
  • [Language] ENG
  • [Grant] United States / NCRR NIH HHS / RR / RR10600-01; United States / NIDDK NIH HHS / DK / DK071122; United States / NCI NIH HHS / CA / P50 CA92629; United States / NIGMS NIH HHS / GM / T 32 GM067587; United States / NCI NIH HHS / CA / C06 CA062528; United States / NCI NIH HHS / CA / P50 CA092629; United States / NIDDK NIH HHS / DK / R01 DK071122; United States / NCI NIH HHS / CA / R01 CA109147; United States / NCRR NIH HHS / RR / RR14514-01; United States / NIDDK NIH HHS / DK / R56 DK071122; United States / NCRR NIH HHS / RR / C06 RR014514; United States / NCI NIH HHS / CA / CA62528-01; United States / NCI NIH HHS / CA / CA109147
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Androgens; 0 / CRELD2 protein, human; 0 / Cell Adhesion Molecules; 0 / Extracellular Matrix Proteins; 0 / Intracellular Signaling Peptides and Proteins; 0 / MRFAP1 protein, human; 0 / MUC6 protein, human; 0 / Mucin-6; 0 / Mucins; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Receptors, Androgen; 0 / TRPV Cation Channels; 0 / TRPV3 protein, human; 08J2K08A3Y / Dihydrotestosterone; EC 1.5.1.- / Pyrroline Carboxylate Reductases; EC 1.5.1.2 / delta-1-pyrroline-5-carboxylate reductase; EC 2.5.1.- / GSTT2 protein, human; EC 2.5.1.18 / Glutathione Transferase; EC 2.6.1.13 / Ornithine-Oxo-Acid Transaminase; EC 2.7.11.13 / PRKCD protein, human; EC 2.7.11.13 / Protein Kinase C-delta
  • [Other-IDs] NLM/ PMC1904239
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39. Minelli A, Bellezza I, Agostini M, Bracarda S, Culig Z: Mechanism of 2-chloroadenosine toxicity to PC3 cell line. Prostate; 2006 Sep 15;66(13):1425-36
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  • METHODS: Androgen-independent (PC3) prostate cancer cells were used in the study and proliferation, cell-cycle progression, and apoptosis analyzed.
  • RESULTS: 2-CADO treatment dramatically reduced the number of prostate cancer cells and permanently stopped cell-cycle progression in the S-phase.
  • The role of 2-CADO in prostate cancer cells is uptake-mediated and followed by sequential phosphorylations to 2-Cl-ATP that irreversibly inhibits several key-enzymes for DNA biosynthesis.
  • [MeSH-minor] Cell Cycle / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. DNA Damage / drug effects. DNA, Neoplasm / biosynthesis. DNA, Neoplasm / drug effects. Drug Screening Assays, Antitumor. Humans. Male

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  • (PMID = 16741921.001).
  • [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 / DNA, Neoplasm; 146-77-0 / 2-Chloroadenosine
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40. Zhang X, Ling MT, Wang X, Wong YC: Inactivation of Id-1 in prostate cancer cells: A potential therapeutic target in inducing chemosensitization to taxol through activation of JNK pathway. Int J Cancer; 2006 Apr 15;118(8):2072-81
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  • [Title] Inactivation of Id-1 in prostate cancer cells: A potential therapeutic target in inducing chemosensitization to taxol through activation of JNK pathway.
  • Resistance to anticancer drugs is the major problem in the treatment of many advanced cancers, including androgen-independent prostate cancer.
  • To test this hypothesis, in this study, by using RNA interfering technology, we inactivated the Id-1 gene in 2 androgen-independent prostate cancer cell lines, DU145 and PC3, and investigated whether downregulation of Id-1 could lead to increased sensitivity to a commonly used anticancer drug, taxol.
  • By using colony forming assay and MTT assay, we found that inactivation of Id-1 resulted in both decreased colony forming ability and cell viability in prostate cancer cells, after taxol treatment.
  • These results indicate that increased Id-1 expression in prostate cancer cells may play a protective role against apoptosis, and downregulation of Id-1 may be a potential target to increase sensitivity of taxol-induced apoptosis in prostate cancer cells.
  • [MeSH-minor] Apoptosis. Cell Survival. Down-Regulation. Drug Resistance, Neoplasm. Enzyme Activation. Gene Expression Profiling. Humans. Male. Tumor Cells, Cultured. Up-Regulation

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  • [Copyright] Copyright (c) 2005 Wiley-Liss, Inc.
  • (PMID = 16287090.001).
  • [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 / Antineoplastic Agents, Phytogenic; 0 / Inhibitor of Differentiation Protein 1; EC 2.7.12.2 / MAP Kinase Kinase 4; P88XT4IS4D / Paclitaxel
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41. Lin SH, Lee YC, Choueiri MB, Wen S, Mathew P, Ye X, Do KA, Navone NM, Kim J, Tu SM, Yu-Lee LY, Logothetis CJ: Soluble ErbB3 levels in bone marrow and plasma of men with prostate cancer. Clin Cancer Res; 2008 Jun 15;14(12):3729-36
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  • [Title] Soluble ErbB3 levels in bone marrow and plasma of men with prostate cancer.
  • PURPOSE: Prostate cancer tends to metastasize to bone and induce osteoblastic lesions.
  • We identified a soluble form of ErbB3 (sErbB3), p45-sErbB3, in bone marrow supernatant from men with prostate cancer bone metastasis and showed that p45-sErbB3 enhances bone formation.
  • EXPERIMENTAL DESIGN: We did ELISAs on marrow from 108 men [34 with androgen-dependent disease, 30 with androgen-independent disease (AI) but negative bone scan (AI/BS-), and 44 with AI and positive bone scan (AI/BS+)], sequential marrow from 5 men during treatment, plasma from 52 men before and after docetaxel treatment, and plasma from 95 men ages > or =70 years old without prostate cancer.
  • Among men with metastatic progression in bone, docetaxel treatment reduced plasma sErbB3 (P < 0.0001) but did not affect bone-specific alkaline phosphatase (P = 0.206) or prostate-specific antigen (P = 0.906).
  • sErbB3 was also detected in men without prostate cancer.
  • CONCLUSIONS: The apparent correlation between higher sErbB3 levels and longer time to bone metastasis suggests that sErbB3 participates in progression in bone of prostate cancer.

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  • (PMID = 18559590.001).
  • [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 / R01 CA111479-03; United States / NCI NIH HHS / CA / P50-CA90270; United States / NCI NIH HHS / CA / R01 CA111479-02; United States / NCI NIH HHS / CA / P50 CA090270; United States / NCI NIH HHS / CA / R01 CA111479; United States / NCI NIH HHS / CA / CA111479-02; United States / NIDDK NIH HHS / DK / DK053176-02; United States / NIDDK NIH HHS / DK / R01 DK053176-02; United States / NCI NIH HHS / CA / CA111479-03; United States / NCI NIH HHS / CA / R01 CA111479-01A1; United States / NIDDK NIH HHS / DK / R01 DK053176; United States / NCI NIH HHS / CA / CA111479-01A1; United States / NCI NIH HHS / CA / R01 CA111479-04; United States / NCI NIH HHS / CA / CA111479-04; United States / NIDDK NIH HHS / DK / DK53176; United States / NCI NIH HHS / CA / CA111479; United States / NCI NIH HHS / CA / P50 CA090270-01; United States / NCI NIH HHS / CA / CA090270-01
  • [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 / Antineoplastic Agents; 0 / Taxoids; 15H5577CQD / docetaxel; EC 2.7.10.1 / Receptor, ErbB-3
  • [Other-IDs] NLM/ NIHMS47853; NLM/ PMC2562877
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42. 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
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  • [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

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  • (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
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43. Yemelyanov A, Gasparian A, Lindholm P, Dang L, Pierce JW, Kisseljov F, Karseladze A, Budunova I: Effects of IKK inhibitor PS1145 on NF-kappaB function, proliferation, apoptosis and invasion activity in prostate carcinoma cells. Oncogene; 2006 Jan 19;25(3):387-98
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  • [Title] Effects of IKK inhibitor PS1145 on NF-kappaB function, proliferation, apoptosis and invasion activity in prostate carcinoma cells.
  • We and others showed previously that NF-kappaB transcription factor was constitutively activated in androgen-independent prostate carcinoma (PC) cell lines due to the upregulated activity of inhibitor of NF-kappaB kinases (IKK).
  • [MeSH-major] Apoptosis / drug effects. Cell Proliferation / drug effects. Enzyme Inhibitors / pharmacology. Heterocyclic Compounds, 3-Ring / pharmacology. I-kappa B Kinase / antagonists & inhibitors. NF-kappa B / physiology. Neoplasm Invasiveness / prevention & control. Prostatic Neoplasms / pathology. Pyridines / pharmacology


44. Ryan CJ, Halabi S, Ou SS, Vogelzang NJ, Kantoff P, Small EJ: Adrenal androgen levels as predictors of outcome in prostate cancer patients treated with ketoconazole plus antiandrogen withdrawal: results from a cancer and leukemia group B study. Clin Cancer Res; 2007 Apr 1;13(7):2030-7
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  • [Title] Adrenal androgen levels as predictors of outcome in prostate cancer patients treated with ketoconazole plus antiandrogen withdrawal: results from a cancer and leukemia group B study.
  • PURPOSE: Adrenal androgens activate the androgen receptor and stimulate prostate cancer growth.
  • Ketoconazole is used as an inhibitor of adrenal androgen synthesis in men with androgen-independent prostate cancer.
  • This study analyzes the relationship between pretreatment androgen levels and outcome following ketoconazole treatment.
  • Regression models (logistic and proportional hazard) were used to assess the prognostic significance of these levels in predicting overall survival and prostate-specific antigen (PSA) response defined by Consensus Criteria.
  • A linear correlation was observed among all androgen levels.
  • These data suggest that therapy with ketoconazole is less effective in patients with low levels of androgen at baseline.
  • [MeSH-major] Androgen Antagonists / therapeutic use. Androgens / blood. Drug Resistance, Neoplasm / physiology. Ketoconazole / therapeutic use. Prostatic Neoplasms / blood
  • [MeSH-minor] Adrenal Glands / drug effects. Aged. Aged, 80 and over. Humans. Male. Middle Aged. Prostate-Specific Antigen / blood. Prostate-Specific Antigen / drug effects. Treatment Outcome

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  • (PMID = 17404083.001).
  • [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 / CA31946
  • [Publication-type] Clinical Trial, Phase III; 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 / Androgen Antagonists; 0 / Androgens; EC 3.4.21.77 / Prostate-Specific Antigen; R9400W927I / Ketoconazole
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45. Shah GV, Muralidharan A, Thomas S, Gokulgandhi M, Mudit M, Khanfar M, El Sayed K: Identification of a small molecule class to enhance cell-cell adhesion and attenuate prostate tumor growth and metastasis. Mol Cancer Ther; 2009 Mar;8(3):509-20
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  • [Title] Identification of a small molecule class to enhance cell-cell adhesion and attenuate prostate tumor growth and metastasis.
  • Expression of calcitonin (CT) and its receptor (CTR) is elevated in advanced prostate cancer, and activated CT-CTR autocrine axis plays a pivotal role in tumorigenicity and metastatic potential of multiple prostate cancer cell lines.
  • Recent studies suggest that CT promotes prostate cancer metastasis by reducing cell-cell adhesion through the disassembly of tight and adherens junctions and activation of beta-catenin signaling.
  • We attempted to identify a class of molecules that enhances cell-cell adhesion of prostate cells and reverses the disruptive actions of CT on tight and adherens junctions.
  • By virtue of its ability to stabilize cell junctions, PMH could reverse the effect of CT on junctional disruption and metastasis, which strengthens the possibility of using PMH as a potential drug candidate for CT-positive androgen-independent prostate cancers.

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  • (PMID = 19276166.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA096534; United States / NCRR NIH HHS / RR / P20 RR016456; United States / NCI NIH HHS / CA / R56 CA096534-05A1; United States / NCRR NIH HHS / RR / P20RR16456; United States / NCI NIH HHS / CA / R56 CA096534; United States / NCI NIH HHS / CA / CA096534-05A1; United States / NCI NIH HHS / CA / R01CA96534
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Hydantoins; 0 / Small Molecule Libraries
  • [Other-IDs] NLM/ NIHMS99731; NLM/ PMC2748671
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46. Jäger T, Rübben H, Börgermann C: [Differential therapy of prostate cancer]. Internist (Berl); 2007 Dec;48(12):1382-7
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  • [Title] [Differential therapy of prostate cancer].
  • Prostate cancer has become the most common malignancy in males worldwide.
  • Standard therapy in local confined prostate cancer with curative intent is a radical ablation of the gland.
  • In cases of advanced disease androgen deprivation is applied to eliminate testosterone which is the natural stimulator of tumor growth.
  • The application of chemotherapy is limited to androgen-independent disease without curative intention.
  • Both early detection and aftercare are based on measurement of prostate-specific antigen.
  • [MeSH-minor] Aged. Androgen Antagonists / adverse effects. Androgen Antagonists / therapeutic use. Biomarkers, Tumor / blood. Biopsy. Combined Modality Therapy. Early Diagnosis. Endosonography. Humans. Male. Middle Aged. Neoplasm Staging. Orchiectomy. Palliative Care. Prognosis. Prostate / pathology. Prostate-Specific Antigen / blood. Prostatectomy. Taxoids / adverse effects. Taxoids / therapeutic use

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  • (PMID = 17965846.001).
  • [ISSN] 0020-9554
  • [Journal-full-title] Der Internist
  • [ISO-abbreviation] Internist (Berl)
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Biomarkers, Tumor; 0 / Taxoids; 15H5577CQD / docetaxel; EC 3.4.21.77 / Prostate-Specific Antigen
  • [Number-of-references] 33
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47. Malinowska K, Neuwirt H, Cavarretta IT, Bektic J, Steiner H, Dietrich H, Moser PL, Fuchs D, Hobisch A, Culig Z: Interleukin-6 stimulation of growth of prostate cancer in vitro and in vivo through activation of the androgen receptor. Endocr Relat Cancer; 2009 Mar;16(1):155-69
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  • [Title] Interleukin-6 stimulation of growth of prostate cancer in vitro and in vivo through activation of the androgen receptor.
  • It is hypothesized that ligand-independent activation of the androgen receptor is one of the mechanisms implicated in tumour progression.
  • However, supportive evidence is limited to the effect of HER-2/neu that stimulates prostate cancer progression through activation of the androgen receptor.
  • In the present study, we have asked whether the proinflammatory cytokine interleukin-6 (IL-6), which is known to stimulate androgen receptor activity and expression of its downstream target genes, may also induce growth of androgen-sensitive cells.
  • In MDA PCa 2b cells, growth stimulation by IL-6 was reversed by administration of either the non-steroidal anti-androgen bicalutamide or the inhibitor of the mitogen-activated protein kinase pathway PD98059.
  • Interestingly, the treatment of those prostate cancer cells did not increase phosphorylation of STAT3.
  • The effect of IL-6 on stimulation of androgen receptor activity in MDA PCa 2b cells was lower than that of androgen, comparable with findings reported by other researchers.
  • Taken together, data in the present study demonstrate that IL-6 may cause growth of androgen receptor-positive tumours in vitro and in vivo through activation of the androgen receptor.
  • [MeSH-major] Interleukin-6 / metabolism. Prostatic Neoplasms / metabolism. Prostatic Neoplasms / pathology. Receptors, Androgen / metabolism
  • [MeSH-minor] Anilides / pharmacology. Animals. Antineoplastic Agents / pharmacology. Cell Division / drug effects. Cell Division / physiology. Cell Line, Tumor. Humans. In Vitro Techniques. Male. Mice. Mice, Inbred BALB C. Mice, Nude. Mitogen-Activated Protein Kinases / metabolism. Neoplasm Transplantation. Nitriles / pharmacology. Orchiectomy. Phosphorylation / drug effects. Phosphorylation / physiology. RNA, Messenger / metabolism. Receptors, Interleukin-6 / genetics. Receptors, Interleukin-6 / metabolism. STAT3 Transcription Factor / metabolism. Signal Transduction / drug effects. Signal Transduction / physiology. Tosyl Compounds / pharmacology

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  • (PMID = 19011039.001).
  • [ISSN] 1351-0088
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anilides; 0 / Antineoplastic Agents; 0 / IL6 protein, human; 0 / Interleukin-6; 0 / Nitriles; 0 / RNA, Messenger; 0 / Receptors, Androgen; 0 / Receptors, Interleukin-6; 0 / STAT3 Transcription Factor; 0 / STAT3 protein, human; 0 / Tosyl Compounds; A0Z3NAU9DP / bicalutamide; EC 2.7.11.24 / Mitogen-Activated Protein Kinases
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48. 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
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  • [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

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  • (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
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49. Schalken JA: Molecular aspects of hormone-independent prostate cancer. BJU Int; 2007 Jul;100 Suppl 2:52-5
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  • [Title] Molecular aspects of hormone-independent prostate cancer.
  • [MeSH-major] Androgens / metabolism. Oncogenes / physiology. Prostatic Neoplasms / metabolism. Receptors, Androgen / metabolism
  • [MeSH-minor] Humans. Male. Neoplasm Recurrence, Local / metabolism

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  • (PMID = 17594361.001).
  • [ISSN] 1464-4096
  • [Journal-full-title] BJU international
  • [ISO-abbreviation] BJU Int.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Androgens; 0 / Receptors, Androgen
  • [Number-of-references] 18
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50. 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
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  • [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

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  • (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
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51. 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
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  • [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

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  • (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
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52. Dagvadorj A, Collins S, Jomain JB, Abdulghani J, Karras J, Zellweger T, Li H, Nurmi M, Alanen K, Mirtti T, Visakorpi T, Bubendorf L, Goffin V, Nevalainen MT: Autocrine prolactin promotes prostate cancer cell growth via Janus kinase-2-signal transducer and activator of transcription-5a/b signaling pathway. Endocrinology; 2007 Jul;148(7):3089-101
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  • [Title] Autocrine prolactin promotes prostate cancer cell growth via Janus kinase-2-signal transducer and activator of transcription-5a/b signaling pathway.
  • The molecular mechanisms that promote progression of localized prostate cancer to hormone-refractory and disseminated disease are poorly understood.
  • Prolactin (Prl) is a local growth factor produced in high-grade prostate cancer, and exogenously added Prl in tissue or explant cultures of normal and malignant prostate is a strong mitogen and survival factor for prostate epithelium.
  • The key signaling proteins that mediate the biological effects of Prl in prostate cancer are Signal Transducer and Activator of Transcription (Stat)-5a/5b via activation of Janus kinase-2.
  • Importantly, inhibition of Stat5a/b in prostate cancer cells induces apoptotic death.
  • Using a specific Prl receptor antagonist (Delta1-9G129R-hPRL), we demonstrate here for the first time that autocrine Prl in androgen-independent human prostate cancer cells promotes cell viability via Stat5 signaling pathway.
  • Furthermore, we examined a unique clinical material of human hormone refractory prostate cancers and metastases and show that autocrine Prl is expressed in 54% of hormone-refractory clinical human prostate cancers and 62% prostate cancer metastases.
  • Finally, we demonstrate that autocrine Prl is expressed from both the proximal and distal promoters of the Prl gene in clinical human prostate cancers and in vivo and in vitro human prostate cancer models, independently of pituitary transcription factor-1 (Pit-1).
  • Collectively, the data provide novel evidence for the concept that autocrine Prl signaling pathway is involved in growth of hormone-refractory and metastatic prostate cancer.
  • The study also provides support for the use of Prl receptor antagonists or other therapeutic strategies to block the Prl-Janus kinase-2-Stat5 signaling pathway in advanced prostate cancer.
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Survival / drug effects. Gene Expression Regulation, Neoplastic / drug effects. Humans. Immunoblotting. Male. Mice. Mice, Nude. Neoplasm Metastasis. Neoplasms, Experimental / genetics. Neoplasms, Experimental / metabolism. Neoplasms, Experimental / pathology. Oligodeoxyribonucleotides, Antisense / genetics. Phosphorylation / drug effects. Promoter Regions, Genetic / genetics. Reverse Transcriptase Polymerase Chain Reaction. Transcription, Genetic / drug effects. Transplantation, Heterologous. Tumor Suppressor Proteins. Tyrphostins / pharmacology

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  • (PMID = 17412813.001).
  • [ISSN] 0013-7227
  • [Journal-full-title] Endocrinology
  • [ISO-abbreviation] Endocrinology
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1R01CA113580-01A1; United States / NCI NIH HHS / CA / CA56036-08
  • [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 / Oligodeoxyribonucleotides, Antisense; 0 / STAT5 Transcription Factor; 0 / STAT5A protein, human; 0 / Tumor Suppressor Proteins; 0 / Tyrphostins; 0 / alpha-cyano-(3,4-dihydroxy)-N-benzylcinnamide; 9002-62-4 / Prolactin; EC 2.7.10.2 / Janus Kinase 2
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53. Burdick MJ, Reddy CA, Ulchaker J, Angermeier K, Altman A, Chehade N, Mahadevan A, Kupelian PA, Klein EA, Ciezki JP: Comparison of biochemical relapse-free survival between primary Gleason score 3 and primary Gleason score 4 for biopsy Gleason score 7 prostate cancer. Int J Radiat Oncol Biol Phys; 2009 Apr 1;73(5):1439-45
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  • [Title] Comparison of biochemical relapse-free survival between primary Gleason score 3 and primary Gleason score 4 for biopsy Gleason score 7 prostate cancer.
  • PURPOSE: To determine whether the primary grade (PG) of biopsy Gleason score (GS) 7 prostate cancer (CaP) was predictive for biochemical relapse-free survival (bRFS).
  • METHODS AND MATERIALS: We reviewed the data from 705 patients with biopsy GS7 CaP, from a prospectively maintained database, who had been treated at our institution between September 1996 and March 2005 with radical prostatectomy (n = 310), external beam radiotherapy (n = 268), or prostate radioactive seed implantation (n = 127).
  • Cox proportional hazards regression analysis was used for univariate and multivariate analyses examining these factors in relation to bRFS: PG of biopsy GS, initial prostate-specific antigen level, clinical T stage, use of androgen deprivation, risk group (high or intermediate), and treatment modality.
  • Comparing PG3 and PG4 within treatment modalities, only prostate implantation patients had a significant difference in the 5-year bRFS rate, 88% vs. 76%, respectively (p = 0.0231).
  • On multivariate analysis, the PG of biopsy GS remained an independent predictor of bRFS, with PG3 having better bRFS than PG4 (relative risk, 0.655; 95% confidence interval, 0.472-0.909; p = 0.0113).
  • [MeSH-major] Prostate / pathology. Prostate-Specific Antigen / blood. Prostatic Neoplasms
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biopsy. Disease-Free Survival. Humans. Male. Middle Aged. Neoplasm Staging / methods. Proportional Hazards Models. Regression Analysis


54. Chen KC, Hsieh CL, Peng CC, Hsieh-Li HM, Chiang HS, Huang KD, Peng RY: Brain derived metastatic prostate cancer DU-145 cells are effectively inhibited in vitro by guava (Psidium gujava L.) leaf extracts. Nutr Cancer; 2007;58(1):93-106
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  • [Title] Brain derived metastatic prostate cancer DU-145 cells are effectively inhibited in vitro by guava (Psidium gujava L.) leaf extracts.
  • At 1.0 mg/mL, PE reduced the viability of PCa DU-145 (the androgen independent PCa cells) to 36.1 and 3.59%, respectively after 48 h and 72 h of incubations.
  • [MeSH-minor] Apoptosis / drug effects. Caspases / metabolism. Cell Cycle / drug effects. Cell Survival / drug effects. Dose-Response Relationship, Drug. Flow Cytometry. Humans. In Situ Nick-End Labeling. Male. Neoplasm Invasiveness. Neoplasm Metastasis. Time Factors. Tumor Cells, Cultured


55. Silvestris N, Leone B, Numico G, Lorusso V, De Lena M: Present status and perspectives in the treatment of hormone-refractory prostate cancer. Oncology; 2005;69(4):273-82
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  • [Title] Present status and perspectives in the treatment of hormone-refractory prostate cancer.
  • The cornerstone in the treatment of de novo or recurrent metastatic prostate cancer is androgen deprivation.
  • Unfortunately, nearly all patients will develop androgen-independent ('hormone-refractory') disease with progressive clinical deterioration and ultimately death.
  • [MeSH-minor] Bone Density Conservation Agents / therapeutic use. Chemotherapy, Adjuvant. Clinical Trials, Phase III as Topic. Diphosphonates / therapeutic use. Humans. Male. Neoplasm Recurrence, Local / drug therapy. Palliative Care / methods. Prostate-Specific Antigen / blood. Radiopharmaceuticals / therapeutic use. Radiotherapy, Adjuvant. Survival Analysis. Taxoids / administration & dosage. Treatment Outcome

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  • [Copyright] Copyright (c) 2005 S. Karger AG, Basel.
  • (PMID = 16282706.001).
  • [ISSN] 0030-2414
  • [Journal-full-title] Oncology
  • [ISO-abbreviation] Oncology
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Androgens; 0 / Bone Density Conservation Agents; 0 / Diphosphonates; 0 / Radiopharmaceuticals; 0 / Taxoids; 15H5577CQD / docetaxel; EC 3.4.21.77 / Prostate-Specific Antigen
  • [Number-of-references] 77
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56. Song HZ, Chen LB: [Targeted therapies for hormone-refractory prostate cancer]. Zhonghua Nan Ke Xue; 2010 Dec;16(12):1108-12
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  • [Title] [Targeted therapies for hormone-refractory prostate cancer].
  • Prostate cancer is one of the most common type of cancer among men after middle age.
  • Androgen withdrawal can delay its progression in the initial stage, but it finally becomes independent of androgens in almost all the cases.
  • The combination of docetaxel with prednisone is currently a standard first-line treatment for patients with hormone-refractory prostate cancer (HRPC), but hitherto there is no established second-line therapy.
  • [MeSH-minor] Drug Resistance, Neoplasm. Hormones / pharmacology. Humans. Male

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  • (PMID = 21348204.001).
  • [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; Review
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Hormones
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57. 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
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  • [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

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  • (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
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58. Li Y, Chen HQ, Chen MF, Liu HZ, Dai YQ, Lv H, Bing Zu X, Qi L: Neuroendocrine differentiation is involved in chemoresistance induced by EGF in prostate cancer cells. Life Sci; 2009 Jun 19;84(25-26):882-7
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  • [Title] Neuroendocrine differentiation is involved in chemoresistance induced by EGF in prostate cancer cells.
  • We hypothesize that neuroendocrine differentiation (NED), a common phenomenon in prostate cancer, is related to chemoresistance in prostate cancer.
  • MAIN METHODS: Androgen-independent human prostate cancer DU145 and PC-3 cells were exposed to epidermal growth factor (EGF).
  • SIGNIFICANCE: NED in prostate cancer is involved in the chemoresistance induced by EGF.
  • EGF and/or the EGF receptor may be potential targets for medical intervention in chemo-resistant prostate cancer.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Cell Differentiation / drug effects. Cisplatin / pharmacology. Drug Resistance, Neoplasm. Epidermal Growth Factor / metabolism. Neuroendocrine Cells / cytology. Prostatic Neoplasms / metabolism

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  • (PMID = 19356736.001).
  • [ISSN] 1879-0631
  • [Journal-full-title] Life sciences
  • [ISO-abbreviation] Life Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / RNA, Messenger; 62229-50-9 / Epidermal Growth Factor; EC 4.2.1.11 / Phosphopyruvate Hydratase; Q20Q21Q62J / Cisplatin
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59. Lebret T, Méjean A: [Management of metastatic androgeno-independent prostate cancer]. Prog Urol; 2008 Nov;18 Suppl 7:S343-8
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  • [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

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  • (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
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60. Kleeberger W, Bova GS, Nielsen ME, Herawi M, Chuang AY, Epstein JI, Berman DM: Roles for the stem cell associated intermediate filament Nestin in prostate cancer migration and metastasis. Cancer Res; 2007 Oct 1;67(19):9199-206
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  • [Title] Roles for the stem cell associated intermediate filament Nestin in prostate cancer migration and metastasis.
  • Nestin mRNA was detected in cell lines from small cell lung, and breast cancers, and particularly elevated in cell lines derived from prostate cancer metastases.
  • Whereas the androgen-independent lines PC3, 22RV1, and DU145 all expressed Nestin transcripts under standard culture conditions, the androgen-dependent line LnCaP expressed Nestin only on androgen withdrawal.
  • We confirmed associations of Nestin expression, androgen withdrawal, and metastatic potential by immunohistochemical analysis of samples from 254 prostate cancer patients.
  • Cytoplasmic Nestin protein was readily identifiable in prostate cancer cells from 75% of patients with lethal androgen-independent disease, even in cancer sampled from the prostate itself.
  • However, Nestin expression was undetectable in localized androgen-deprived tumors and in metastases without prior androgen deprivation.
  • To address its function, we reduced Nestin levels with short hairpin RNAs, markedly inhibiting in vitro migration and invasion in prostate cancer cells but leaving cell growth intact.
  • These results specify a function for Nestin in cell motility and identify a novel pathway for prostate cancer metastasis.
  • Activity of this pathway may be selected by the extraprostatic environment or, as supported by our data, may originate within the prostate after androgen deprivation.

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  • (PMID = 17909025.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA058236; United States / NCI NIH HHS / CA / P30 CA006973; United States / NIDDK NIH HHS / DK / DK05937; United States / NCI NIH HHS / CA / P50 CA58236; United States / NCI NIH HHS / CA / P50 CA058236-13
  • [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 / Intermediate Filament Proteins; 0 / NES protein, human; 0 / Nerve Tissue Proteins; 0 / Nes protein, mouse; 0 / Nestin
  • [Other-IDs] NLM/ NIHMS43631; NLM/ PMC3072059
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61. Cao P, Deng Z, Wan M, Huang W, Cramer SD, Xu J, Lei M, Sui G: MicroRNA-101 negatively regulates Ezh2 and its expression is modulated by androgen receptor and HIF-1alpha/HIF-1beta. Mol Cancer; 2010 May 17;9:108
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  • [Title] MicroRNA-101 negatively regulates Ezh2 and its expression is modulated by androgen receptor and HIF-1alpha/HIF-1beta.
  • BACKGROUND: In prostate cancer (PCa), the common treatment involving androgen ablation alleviates the disease temporarily, but results in the recurrence of highly aggressive and androgen-independent metastatic cancer.
  • It is known that aberrant epigenetics contributes to prostate malignancy.
  • In this report, we present our study showing that microRNA-101 (miR-101) inhibits Ezh2 expression and differentially regulates prostate cancer cells.
  • In addition, the expression of miR-101 alters upon androgen treatment and HIF-1alpha/HIF-1beta induction.
  • In addition, the expression of miR-101 is regulated by androgen receptor and HIF-1alpha/HIF-1beta.
  • MiR-101 differentially regulates prostate cell proliferation.
  • Meanwhile, the expression of miR-101 is also modulated at different physiological conditions, such as androgen stimulation and HIF-1alpha/HIF-1beta induction.

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  • (PMID = 20478051.001).
  • [ISSN] 1476-4598
  • [Journal-full-title] Molecular cancer
  • [ISO-abbreviation] Mol. Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / T32 CA079448; United States / NCI NIH HHS / CA / 5T32CA079448-09
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / ARNT protein, human; 0 / DNA-Binding Proteins; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / MIRN101 microRNA, human; 0 / MIRN26A microRNA, human; 0 / MicroRNAs; 0 / Receptors, Androgen; 0 / Transcription Factors; 138391-32-9 / Aryl Hydrocarbon Receptor Nuclear Translocator; EC 2.1.1.43 / EZH2 protein, human; EC 2.1.1.43 / Polycomb Repressive Complex 2
  • [Other-IDs] NLM/ PMC2881117
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62. Donovan MJ, Khan FM, Fernandez G, Mesa-Tejada R, Sapir M, Zubek VB, Powell D, Fogarasi S, Vengrenyuk Y, Teverovskiy M, Segal MR, Karnes RJ, Gaffey TA, Busch C, Haggman M, Hlavcak P, Freedland SJ, Vollmer RT, Albertsen P, Costa J, Cordon-Cardo C: Personalized prediction of tumor response and cancer progression on prostate needle biopsy. J Urol; 2009 Jul;182(1):125-32
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  • [Title] Personalized prediction of tumor response and cancer progression on prostate needle biopsy.
  • PURPOSE: To our knowledge in patients with prostate cancer there are no available tests except clinical variables to determine the likelihood of disease progression.
  • We also investigated whether biopsy androgen receptor levels predict a durable response to therapy after secondary treatment.
  • MATERIALS AND METHODS: We evaluated paraffin embedded prostate needle biopsy tissue from 1,027 patients with cT1c-T3 prostate cancer treated with surgery and followed a median of 8 years.
  • Validation in an independent cohort of 341 patients (total of 44 progression events) yielded 76% sensitivity, 64% specificity, a C index of 0.73 and a HR of 3.47.
  • Increased androgen receptor in tumor cells in the biopsy highly significantly predicted resistance to therapy, ie androgen ablation with or without salvage radiotherapy, and clinical failure (p <0.0001).
  • When combined with biomarker data, it adds to the hematoxylin and eosin analysis, and prostate specific antigen values currently used to assess outcome at diagnosis.
  • Biopsy androgen receptor levels predict the likelihood of a response to therapy after recurrence and may guide future treatment decisions.
  • [MeSH-major] Biopsy, Needle / methods. Neoplasm Recurrence, Local / pathology. Prostate-Specific Antigen / blood. Prostatic Neoplasms / pathology. Prostatic Neoplasms / surgery
  • [MeSH-minor] Aged. Analysis of Variance. Cohort Studies. Disease Progression. Follow-Up Studies. Humans. Immunohistochemistry. Male. Middle Aged. Neoplasm Invasiveness / pathology. Neoplasm Staging. Paraffin Embedding / methods. Predictive Value of Tests. Probability. Prostatectomy / methods. Retrospective Studies. Risk Assessment. Sensitivity and Specificity. Survival Analysis. Time Factors. Treatment Outcome

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  • (PMID = 19450827.001).
  • [ISSN] 1527-3792
  • [Journal-full-title] The Journal of urology
  • [ISO-abbreviation] J. Urol.
  • [Language] eng
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't; Validation Studies
  • [Publication-country] United States
  • [Chemical-registry-number] EC 3.4.21.77 / Prostate-Specific Antigen
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63. Hammacher A, Thompson EW, Williams ED: Interleukin-6 is a potent inducer of S100P, which is up-regulated in androgen-refractory and metastatic prostate cancer. Int J Biochem Cell Biol; 2005 Feb;37(2):442-50
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  • [Title] Interleukin-6 is a potent inducer of S100P, which is up-regulated in androgen-refractory and metastatic prostate cancer.
  • Elevated circulating interleukin-6 (IL6) and up-regulated S100P in prostate cancer (PCa) specimens correlate independently with progression to androgen-independent and metastatic PCa.
  • Determination of mRNA and protein levels by real-time PCR and Western blotting revealed that IL6 is a more potent inducer of S100P than the synthetic androgen, R1881, in the LNCaP/C4-2B model of PCa progression.
  • IL6 did not require androgen to induce S100P in these cells, which express a functional androgen receptor (AR).
  • Epidermal growth factor (EGF), which like IL6 is a non-androgen activator of the AR, did not induce S100P.
  • A link between elevated IL6 and up-regulated S100P in androgen-refractory and metastatic PCa is postulated.
  • [MeSH-major] Calcium-Binding Proteins / biosynthesis. Gene Expression Regulation, Neoplastic / drug effects. Interleukin-6 / pharmacology. Neoplasm Proteins / biosynthesis. Prostatic Neoplasms / metabolism. Up-Regulation / drug effects
  • [MeSH-minor] Androgens / metabolism. Cell Line, Tumor. Humans. Male. Metribolone / pharmacology. Neoplasm Metastasis / pathology. RNA, Messenger / biosynthesis. Receptors, Androgen / metabolism. Transcriptional Activation


64. Abramjuk C, Lein M, Rothaug W, Krell HW, Loening SA, Jung K: Enhanced inhibitory effect of the matrix metalloproteinase inhibitor Ro 28-2653 in combination with estramustine and etoposide on the prostate carcinoma in the rat Dunning orthotopic tumor model. Cancer Chemother Pharmacol; 2007 Feb;59(2):275-82
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  • [Title] Enhanced inhibitory effect of the matrix metalloproteinase inhibitor Ro 28-2653 in combination with estramustine and etoposide on the prostate carcinoma in the rat Dunning orthotopic tumor model.
  • We hypothesized that the inhibitor effect of Ro 28-2653 on the tumor growth could be improved by combination with chemotherapeutic drugs and examined therefore the effect of Ro 28-2653 alone and in combination with etoposide or estramustine in the MatLyLu Dunning R-3327 rat tumor model characteristic for the androgen-independent prostate cancer (PCa).
  • [MeSH-minor] Animals. Body Weight / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Disease Models, Animal. Drug Resistance, Neoplasm. Drug Screening Assays, Antitumor / methods. Drug Synergism. Estramustine / administration & dosage. Etoposide / administration & dosage. Humans. Injections, Intraperitoneal. Male. Neoplasm Invasiveness / prevention & control. Neoplasm Transplantation. Piperazines / administration & dosage. Pyrimidines / administration & dosage. Rats. Time Factors. Tissue Inhibitor of Metalloproteinases / administration & dosage

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  • (PMID = 16758188.001).
  • [ISSN] 0344-5704
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Piperazines; 0 / Pyrimidines; 0 / Ro 28-2653; 0 / Tissue Inhibitor of Metalloproteinases; 35LT29625A / Estramustine; 6PLQ3CP4P3 / Etoposide
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65. Hayashi N, Asano K, Suzuki H, Yamamoto T, Tanigawa N, Egawa S, Manome Y: Adenoviral infection of survivin antisense sensitizes prostate cancer cells to etoposide in vivo. Prostate; 2005 Sep 15;65(1):10-9
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  • [Title] Adenoviral infection of survivin antisense sensitizes prostate cancer cells to etoposide in vivo.
  • BACKGROUND: We aimed to investigate whether use of a survivin antisense fragment carried by an adenovirus vector (Ad.survivin-AS) could enhance the therapeutic efficacy of chemotherapy for androgen-independent prostate cancer.
  • [MeSH-major] Adenoviridae / genetics. Antisense Elements (Genetics) / pharmacology. Etoposide / pharmacology. Microtubule-Associated Proteins / antagonists & inhibitors. Neoplasm Proteins / antagonists & inhibitors. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Animals. Apoptosis. Cell Line, Tumor. Cell Proliferation. Humans. Inhibitor of Apoptosis Proteins. Male. Mice. Mice, Inbred BALB C. Neoplasm Transplantation. Taxoids / pharmacology. Transplantation, Heterologous

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  • (PMID = 15799033.001).
  • [ISSN] 0270-4137
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antisense Elements (Genetics); 0 / BIRC5 protein, human; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / Taxoids; 15H5577CQD / docetaxel; 6PLQ3CP4P3 / Etoposide
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66. 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
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  • [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

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  • (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
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67. Chen JQ, Litton J, Xiao L, Zhang HZ, Warneke CL, Wu Y, Shen X, Wu S, Sahin A, Katz R, Bondy M, Hortobagyi G, Berinstein NL, Murray JL, Radvanyi L: Quantitative immunohistochemical analysis and prognostic significance of TRPS-1, a new GATA transcription factor family member, in breast cancer. Horm Cancer; 2010 Feb;1(1):21-33
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  • TRPS-1 was also shown to be expressed in prostate cancer where it was shown to play a proapoptotic function during androgen withdrawal possibly through regulating antioxidant metabolism.
  • The role of TRPS-1 and its prognostic significance in hormone-dependent and hormone-independent BC however is not known.
  • [MeSH-minor] Breast Neoplasms, Male / genetics. Breast Neoplasms, Male / pathology. Female. Humans. Kaplan-Meier Estimate. Male. Middle Aged. Neoplasm Staging. Prognosis. Proportional Hazards Models

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  • (PMID = 21761348.001).
  • [ISSN] 1868-8500
  • [Journal-full-title] Hormones & cancer
  • [ISO-abbreviation] Horm Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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68. Xin DQ, Zhu XH, Lai YQ, You R, Na YQ, Guo YL, Mao ZB: [Regulation of expression of pituitary tumor transforming gene 1 (PTTG1) by androgen in prostate cancer]. Beijing Da Xue Xue Bao; 2005 Dec 18;37(6):638-40
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  • [Title] [Regulation of expression of pituitary tumor transforming gene 1 (PTTG1) by androgen in prostate cancer].
  • OBJECTIVE: To identify the androgen-responsive genes in prostate and screen the molecular targets for further studying human prostate cancer.
  • METHODS: The potential androgen-responsive gene pituitary tumor transforming gene 1 (PTTG1) was selected which had been previously screened by cDNA microarray in rat prostate and its mRNA level was detected by Northern blot in the castrated rat prostate with and without replacement of Mibolerone.
  • Immunohistochemistry was performed to determine the expression and location of PTTG1 in human prostate tissues.
  • Then human androgen-dependent prostate cancer cells LNCaP were used as a model to study the regulation of PTTG1 by Mibolerone.
  • RESULTS: PTTG1 mRNA was hardly detectable in the prostate of 7-day castrated rats, while it was up-regulated dramatically in the prostate of 7-day castrated rats treated with Mibolerone for 2 days.
  • It was showed that high expression of PTTG1 was localized to the epithelial cells of human prostate cancer but not to the stromal cells with Immunohistochemistry.
  • The basic expression of PTTG1 in human androgen-independent prostate cancer cell lines PC3 or DU145 was even higher than that in the human androgen-dependent prostate cancer cells LNCaP treated with Mibolerone.
  • CONCLUSION: Androgen can up-regulate the PTTG1 expression in castrated rat prostate and human prostate cancer cell LNCaP.
  • It suggests that PTTG1 is potential to play an important role in human prostate cancer progression.
  • [MeSH-major] Gene Expression / drug effects. Nandrolone / analogs & derivatives. Neoplasm Proteins / genetics. Prostate / metabolism

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  • (PMID = 16378119.001).
  • [ISSN] 1671-167X
  • [Journal-full-title] Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences
  • [ISO-abbreviation] Beijing Da Xue Xue Bao
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / Securin; 0 / Testosterone Congeners; 0 / pituitary tumor-transforming protein 1, human; 6PG9VR430D / Nandrolone; 9OGY4BOR8D / mibolerone
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69. Dong Z, Liu Y, Scott KF, Levin L, Gaitonde K, Bracken RB, Burke B, Zhai QJ, Wang J, Oleksowicz L, Lu S: Secretory phospholipase A2-IIa is involved in prostate cancer progression and may potentially serve as a biomarker for prostate cancer. Carcinogenesis; 2010 Nov;31(11):1948-55
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  • [Title] Secretory phospholipase A2-IIa is involved in prostate cancer progression and may potentially serve as a biomarker for prostate cancer.
  • The majority of prostate cancers are indolent, whereas a significant portion of patients will require systemic treatment during the course of their disease.
  • To date, only high Gleason scores are best associated with a poor prognosis in prostate cancer.
  • Previous studies showed that secretory phospholipase A2-IIa (sPLA2-IIa) is overexpressed in almost all human prostate cancer specimens and its elevated levels are correlated with high tumor grade.
  • Here, we found that sPLA2-IIa is overexpressed in androgen-independent prostate cancer LNCaP-AI cells relative to their androgen-dependent LNCaP cell counterparts.
  • Blocking sPLA2-IIa function compromises androgen-independent cell growth.
  • More importantly, we demonstrated elevated serum sPLA2-IIa levels in prostate cancer patients.
  • Increased sPLA2-IIa expression was confirmed in prostate cancer cells, but not in normal epithelium and stroma by immunohistochemistry analysis.
  • We showed that elevated signaling of the HER/HER2-PI3K-Akt-NF-κB pathway contributes to sPLA2-IIa overexpression and secretion by prostate cancer cells.
  • Given that sPLA2-IIa overexpression is associated with prostate development and progression, serum sPLA2-IIa may serve as a prognostic biomarker for prostate cancer and a potential surrogate prostate biomarker indicative of tumor burden.

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  • (PMID = 20837598.001).
  • [ISSN] 1460-2180
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA131137; United States / NCI NIH HHS / CA / R01 CA119935
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / NF-kappa B; 0 / RNA, Messenger; 0 / RNA, Small Interfering; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / ERBB2 protein, human; EC 2.7.10.1 / Receptor, ErbB-2; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.1.1.4 / Group II Phospholipases A2
  • [Other-IDs] NLM/ PMC2981059
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70. Li L, Zhang D, Zhang L, Zhu G, Sun Y, Wu K, Wang X, He D: PrLZ expression is associated with the progression of prostate cancer LNCaP cells. Mol Carcinog; 2009 May;48(5):432-40
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  • [Title] PrLZ expression is associated with the progression of prostate cancer LNCaP cells.
  • PrLZ is a novel recent isolated gene and specific expression in prostate tissues.
  • PrLZ expression was specifically elevated in prostate embryonic tissues and androgen independent prostate cancer cells, suggesting it might be association with the embryonic development and malignancy progression.
  • However, the function and mechanism of PrLZ during the progression of prostate cancer remain blurred.
  • Our present studies showed PrLZ expression might enhance the proliferation and invasion capability in vitro and also increase the tumorigenicity in situ prostate cancer animal model, which is indicated PrLZ expression contributed to the malignancy progression of prostate cancer.
  • In addition, PrLZ also might up regulate androgen receptor (AR) expression and increase the PSA expression, a putative downstream target gene of AR, which indicated PrLZ mediated the malignancy progression of prostate cancer was associated with androgen signals.
  • [MeSH-major] Neoplasm Proteins / genetics. Prostatic Neoplasms / pathology
  • [MeSH-minor] Animals. Base Sequence. DNA Primers. Disease Progression. Humans. Male. Matrix Metalloproteinase 2 / metabolism. Mice. Mice, Inbred BALB C. Mice, Nude. Prostate-Specific Antigen / metabolism. Reverse Transcriptase Polymerase Chain Reaction


71. 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
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  • [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


72. Gardner ER, Ahlers CM, Shukla S, Sissung TM, Ockers SB, Price DK, Hamada A, Robey RW, Steinberg SM, Ambudkar SV, Dahut WL, Figg WD: Association of the ABCG2 C421A polymorphism with prostate cancer risk and survival. BJU Int; 2008 Dec;102(11):1694-9
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  • [Title] Association of the ABCG2 C421A polymorphism with prostate cancer risk and survival.
  • OBJECTIVE: To determine if the C421A single nucleotide polymorphism (SNP) in the ATP-binding cassette transporter ABCG2 increases prostate cancer risk or affects survival.
  • PATIENTS, SUBJECTS AND METHODS: Numerous studies have suggested that dietary, hormonal and environmental factors all play a role in the initiation in prostate cancer; among these, the carcinogenic heterocyclic amine 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP), a known substrate of the ABCG2.
  • Due to the expression of ABCG2 in the prostate, together with the purported role of dietary carcinogens and steroids in the development and progression of prostate cancer, 311 individuals were genotyped for the ABCG2 C421A SNP, 170 patients with androgen-independent prostate cancer (AIPC) and 141 'healthy' controls.
  • RESULTS: There were no significant differences in the prevalence of prostate cancer based on ABCG2 genetic variation in this population.
  • CONCLUSION: Increased exposure to PhIP may decrease survival, but the ABCG2 C421A polymorphism does not appear to increase the risk of prostate cancer.
  • [MeSH-major] ATP-Binding Cassette Transporters / metabolism. Neoplasm Proteins / metabolism. Polymorphism, Single Nucleotide / genetics. Prostatic Neoplasms / genetics

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  • [Cites] Clin Cancer Res. 2004 Sep 1;10(17):5889-94 [15355921.001]
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  • (PMID = 18710444.001).
  • [ISSN] 1464-410X
  • [Journal-full-title] BJU international
  • [ISO-abbreviation] BJU Int.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z99 CA999999; United States / Intramural NIH HHS / / NIH0011335962; United States / Intramural NIH HHS / / Z01 BC010627-04; United States / NCI NIH HHS / CO / N01 CO012400; United States / Intramural NIH HHS / / Z01 BC010453-06; United States / NCI NIH HHS / CA / N01CO12400
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / ABCG2 protein, human; 0 / ATP Binding Cassette Transporter, Sub-Family G, Member 2; 0 / ATP-Binding Cassette Transporters; 0 / Androgens; 0 / Neoplasm Proteins
  • [Other-IDs] NLM/ NIHMS88477; NLM/ PMC2605573
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73. Donovan MJ, Hamann S, Clayton M, Khan FM, Sapir M, Bayer-Zubek V, Fernandez G, Mesa-Tejada R, Teverovskiy M, Reuter VE, Scardino PT, Cordon-Cardo C: Systems pathology approach for the prediction of prostate cancer progression after radical prostatectomy. J Clin Oncol; 2008 Aug 20;26(24):3923-9
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  • [Title] Systems pathology approach for the prediction of prostate cancer progression after radical prostatectomy.
  • PURPOSE: For patients with prostate cancer treated by radical prostatectomy, no current personalized tools predict clinical failure (CF; metastasis and/or androgen-independent disease).
  • We developed such a tool through integration of clinicopathologic data with image analysis and quantitative immunofluorescence of prostate cancer tissue.
  • PATIENTS AND METHODS: A prospectively designed algorithm was applied retrospectively to a cohort of 758 patients with clinically localized or locally advanced prostate cancer.
  • A model predicting distant metastasis and/or androgen-independent recurrence was derived from features selected through supervised multivariate learning.
  • The model includes androgen receptor (AR) levels, dominant prostatectomy Gleason grade, lymph node involvement, and three quantitative characteristics from hematoxylin and eosin staining of prostate tissue.
  • Model validation on an independent cohort of 385 patients with 29 CF events yielded a CI of 0.84, sensitivity of 84%, and specificity of 85%.
  • High levels of AR predicted shorter time to castrate prostate-specific antigen increase after androgen deprivation therapy (ADT).
  • [MeSH-major] Neoplasm Recurrence, Local / pathology. Prostatic Neoplasms / pathology. Prostatic Neoplasms / surgery
  • [MeSH-minor] Algorithms. Cohort Studies. Disease Progression. Fluorescent Antibody Technique. Humans. Male. Models, Statistical. Predictive Value of Tests. Prostate-Specific Antigen / metabolism. Prostatectomy. Receptors, Androgen / metabolism. Treatment Outcome

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  • [CommentIn] J Clin Oncol. 2008 Aug 20;26(24):3916-7 [18711177.001]
  • (PMID = 18711180.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Androgen; EC 3.4.21.77 / Prostate-Specific Antigen
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74. Koochekpour S, Zhuang YJ, Beroukhim R, Hsieh CL, Hofer MD, Zhau HE, Hiraiwa M, Pattan DY, Ware JL, Luftig RB, Sandhoff K, Sawyers CL, Pienta KJ, Rubin MA, Vessella RL, Sellers WR, Sartor O: Amplification and overexpression of prosaposin in prostate cancer. Genes Chromosomes Cancer; 2005 Dec;44(4):351-64
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  • [Title] Amplification and overexpression of prosaposin in prostate cancer.
  • We identified prosaposin (PSAP) as a secreted protein expressed in androgen-independent (AI) prostate cancer cells by cloning/sequencing, after probing a PC-3 cDNA library expressed in the lambdaTriplEx phagemid expression vector with a polyclonal rabbit antibody generated against pooled human seminal plasma.
  • PSAP is a neurotrophic molecule; its deficiency or inactivation has proved to be lethal in man and mice, and in mice, it leads to abnormal development and atrophy of the prostate gland, despite normal testosterone levels.
  • We used Southern hybridization, quantitative real-time polymerase chain reaction, and/or single nucleotide polymorphism (SNP) array analysis, and we now report the genomic amplification of PSAP in the metastatic AI prostate cancer cell lines, PC-3, DU-145, MDA-PCa 2b, M-12, and NCI-H660.
  • In addition, by using SNP arrays and a set of 25 punch biopsy samples of human prostate cancer xenografts (LAPC3, LuCaP 23.1, 35, 49, 58, 73, 77, 81, 86.2, 92.1, 93, 96, 105, and 115), lymph nodes, and visceral-organ metastases, we detected amplification of the PSAP locus (10q22.1) in LuCaP 58 and 96 xenografts and two lymph node metastases.
  • In addition, AI metastatic prostate cancer cell lines C4-2B and IA8-ARCaP over-expressed PSAP mRNA without evidence of genomic amplification.
  • Taken together with prior data that demonstrated the growth-, migration-, and invasion-promoting activities, the activation of multiple signal transduction pathways, and the antiapoptotic effect of PSAP (or one of its active domains, saposin C) in prostate cancer cells, our current observation of PSAP amplification or overexpression in prostate cancer suggests, for the first time, a role for this molecule in the process of carcinogenesis or cancer progression in the prostate.

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  • [Copyright] (c) 2005 Wiley-Liss, Inc.
  • (PMID = 16080200.001).
  • [ISSN] 1045-2257
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / T32 CA009172; United States / NCI NIH HHS / CA / 5T32CA09172-30; United States / NCI NIH HHS / CA / P01 CA85859
  • [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.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / PSAP protein, human; 0 / Saposins
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75. Shah RB, Ghosh D, Elder JT: Epidermal growth factor receptor (ErbB1) expression in prostate cancer progression: correlation with androgen independence. Prostate; 2006 Sep 15;66(13):1437-44
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  • [Title] Epidermal growth factor receptor (ErbB1) expression in prostate cancer progression: correlation with androgen independence.
  • BACKGROUND: The role of the epidermal growth factor receptor (ErbB1) in the progression of prostate cancer is incompletely understood.
  • METHODS: Tissue microarrays from hormone-naive and advanced androgen-independent tumors were used to investigate the role of ErbB1 in prostate cancer progression.
  • However, ErbB1 overexpression was not a statistically significant covariate in a multivariate proportional hazards model for biochemical failure of hormone-naïve prostate cancer.
  • CONCLUSIONS: These findings are consistent with a model in which ErbB1 expression increases during the development of the androgen-independent state, and suggest that drugs targeted toward ErbB signaling could be of therapeutic relevance in the management of advanced prostatic carcinoma.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cell Transformation, Neoplastic / genetics. Cell Transformation, Neoplastic / pathology. Disease Progression. Gene Expression Regulation, Neoplastic. Humans. Male. Middle Aged. Multivariate Analysis. Neoplasm Metastasis / genetics. Neoplasm Metastasis / pathology. Neoplasm Staging. Receptors, Androgen / genetics. Receptors, Androgen / metabolism


76. Gong J, Lee J, Akio H, Schlegel PN, Shen R: Attenuation of apoptosis by chromogranin A-induced Akt and survivin pathways in prostate cancer cells. Endocrinology; 2007 Sep;148(9):4489-99
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  • [Title] Attenuation of apoptosis by chromogranin A-induced Akt and survivin pathways in prostate cancer cells.
  • Multiple studies indicate that neuroendocrine (NE) differentiation in prostate cancer (PC) contributes to androgen-independent progression.
  • [MeSH-major] Apoptosis / drug effects. Chromogranin A / pharmacology. Microtubule-Associated Proteins / genetics. Neoplasm Proteins / genetics. Proto-Oncogene Proteins c-akt / genetics

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  • (PMID = 17584963.001).
  • [ISSN] 0013-7227
  • [Journal-full-title] Endocrinology
  • [ISO-abbreviation] Endocrinology
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA80240; United States / NIDDK NIH HHS / DK / R01 DK060908-02
  • [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 / BIRC5 protein, human; 0 / Chromogranin A; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / Recombinant Proteins; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
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77. Falci C, Morello E, Droz JP: Treatment of prostate cancer in unfit senior adult patients. Cancer Treat Rev; 2009 Oct;35(6):522-7
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  • [Title] Treatment of prostate cancer in unfit senior adult patients.
  • Prostate cancer is a disease typical of the elderly with a peak of incidence at 80 years.
  • As most patients aged > or = 70 years show impairment of physical and/or cognitive performance, a complete geriatric assessment should be mandatory before planning any oncological treatment, in order to remove treatable conditions and to estimate the individual cancer-independent survival probability.
  • In unfit patients with early prostate cancer watchful waiting represent the best strategy when the chance of living <10 years and the benefit from any upfront active treatment would be poor.
  • Radiotherapy should be sometimes offered to vulnerable patients having high risk prostate cancer.
  • Even in locally advanced prostate cancer active treatment could be deferred in asymptomatic patients, with short individual cancer-independent survival and well or moderately differentiated tumour.
  • At the present a number of issues about prostate cancer in unfit senior adults patients are still unsolved and should be debated in the light of results from dedicate prospective trials.
  • [MeSH-minor] Aged. Androgen Antagonists / adverse effects. Frail Elderly. Geriatric Assessment. Humans. Male. Neoplasm Staging


78. 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
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  • [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

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  • (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
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79. 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
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  • [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


80. Degraff DJ, Aguiar AA, Sikes RA: Disease evidence for IGFBP-2 as a key player in prostate cancer progression and development of osteosclerotic lesions. Am J Transl Res; 2009 Jan 20;1(2):115-30
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  • [Title] Disease evidence for IGFBP-2 as a key player in prostate cancer progression and development of osteosclerotic lesions.
  • Additionally, they contribute to hormonal insensitivity in adenocarcinomas such as those derived from prostate and breast.
  • Increased expression of insulin-like growth factor binding protein 2 (IGFBP-2) is found in advanced cancers of the ovary, breast, stomach, adrenal gland, bladder, CNS, and prostate.
  • Further, IGFBP-2 seemingly has ligand-independent effects that participate in the development and dissemination of advanced cancer cells.
  • While several reports have shown an important role for IGFBP-2 in the development of androgen insensitivity and the proliferation of AI PCa cells in vivo, these studies have not tested a role for IGFBP-2 in the metastatic spread of AI PCa cells.

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  • (PMID = 19956425.001).
  • [ISSN] 1943-8141
  • [Journal-full-title] American journal of translational research
  • [ISO-abbreviation] Am J Transl Res
  • [Language] ENG
  • [Grant] United States / NCRR NIH HHS / RR / P20 RR016472
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2776314
  • [Keywords] NOTNLM ; Insulin-like growth factor, IGF / androgen insensitivity, AI / androgen sensitive, AS / neoplasm, bone, metastasis / prostate cancer, PCa
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81. Marques RB, van Weerden WM, Erkens-Schulze S, de Ridder CM, Bangma CH, Trapman J, Jenster G: The human PC346 xenograft and cell line panel: a model system for prostate cancer progression. Eur Urol; 2006 Feb;49(2):245-57
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  • [Title] The human PC346 xenograft and cell line panel: a model system for prostate cancer progression.
  • OBJECTIVE: Prostate cancer (PC) model systems that reflect the different disease stages are essential for studying the development and progression of PC and for testing new treatment modalities.
  • METHODS: The PC346 model was derived from the transurethral resection of a primary prostate tumor.
  • RESULTS: The PC346 panel includes sublines with hormone-response characteristics that range from androgen-sensitive to androgen-independent (AI) growth.
  • In vivo and in vitro selection of androgen-sensitive lines under androgen-depleted conditions replicated the clinically relevant relapse phenomenon, and resulted in a series of modifications in the androgen-receptor (AR) pathway: AR mutation, overexpression, and downregulation.
  • [MeSH-minor] Animals. Biomarkers, Tumor / blood. Disease Progression. Humans. Male. Neoplasm Staging. Prostate-Specific Antigen / blood. Receptors, Androgen / metabolism. Signal Transduction

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  • (PMID = 16413664.001).
  • [ISSN] 0302-2838
  • [Journal-full-title] European urology
  • [ISO-abbreviation] Eur. Urol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Receptors, Androgen; EC 3.4.21.77 / Prostate-Specific Antigen
  • [Number-of-references] 69
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82. Savorè C, Zhang C, Muir C, Liu R, Wyrwa J, Shu J, Zhau HE, Chung LW, Carson DD, Farach-Carson MC: Perlecan knockdown in metastatic prostate cancer cells reduces heparin-binding growth factor responses in vitro and tumor growth in vivo. Clin Exp Metastasis; 2005;22(5):377-90
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  • [Title] Perlecan knockdown in metastatic prostate cancer cells reduces heparin-binding growth factor responses in vitro and tumor growth in vivo.
  • The contribution of Pln to prostate cancer growth was tested using a ribozyme approach to knockdown Pln expression levels.
  • Transfection into the androgen-independent, bone targeted prostate cancer line, C4-2B, and efficient stable knockdown of Pln was demonstrated by quantitative PCR, immunohistochemistry and immunoblotting.
  • Anchorage-independent growth assays showed reduced colony size and cohesiveness by all Pln deficient subclones compared to parental C4-2B cells.
  • We conclude that Pln is an essential ECM component involved in growth responses of metastatic prostate cancer cells to HBGFs deposited in local and metastatic microenvironment.
  • [MeSH-major] Heparan Sulfate Proteoglycans / genetics. Heparan Sulfate Proteoglycans / physiology. Neoplasm Metastasis / physiopathology. Prostatic Neoplasms / genetics. Prostatic Neoplasms / pathology


83. Yamaguchi K, Uzzo RG, Pimkina J, Makhov P, Golovine K, Crispen P, Kolenko VM: Methylseleninic acid sensitizes prostate cancer cells to TRAIL-mediated apoptosis. Oncogene; 2005 Sep 1;24(38):5868-77
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  • [Title] Methylseleninic acid sensitizes prostate cancer cells to TRAIL-mediated apoptosis.
  • Recent studies establish a critical role of selenium in prostate cancer prevention in vitro and in vivo.
  • Here, we demonstrate that concomitant administration of TRAIL and methylseleninic acid (MSA) produces synergistic effects on the induction of apoptosis in androgen-dependent LNCaP and androgen-independent DU-145 prostate cancer cells.
  • These results suggest that selenium-based dietary compounds may help to overcome resistance to TRAIL-mediated apoptosis in prostate cancer cells.
  • [MeSH-minor] Apoptosis Regulatory Proteins. Blotting, Western. Caspase 8. Caspases / drug effects. Caspases / metabolism. Cell Line, Tumor. Drug Resistance, Neoplasm. Drug Synergism. Flow Cytometry. Humans. Male. Membrane Potentials / drug effects. Mitochondria / drug effects. Mitochondria / metabolism. Mitochondria / pathology. Phosphorylation / drug effects. TNF-Related Apoptosis-Inducing Ligand

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  • (PMID = 15897871.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Apoptosis Regulatory Proteins; 0 / Membrane Glycoproteins; 0 / Organoselenium Compounds; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFSF10 protein, human; 0 / Tumor Necrosis Factor-alpha; 28274-57-9 / methylselenic acid; EC 3.4.22.- / CASP8 protein, human; EC 3.4.22.- / Caspase 8; EC 3.4.22.- / Caspases
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84. Kim J, Roh M, Abdulkadir SA: Pim1 promotes human prostate cancer cell tumorigenicity and c-MYC transcriptional activity. BMC Cancer; 2010 Jun 01;10:248
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  • [Title] Pim1 promotes human prostate cancer cell tumorigenicity and c-MYC transcriptional activity.
  • BACKGROUND: The serine/threonine kinase PIM1 has been implicated as an oncogene in various human cancers including lymphomas, gastric, colorectal and prostate carcinomas.
  • However, there has been limited analysis of the tumorigenic potential of Pim1 overexpression in benign and malignant human prostate cancer cells in vivo.
  • METHODS: We overexpressed Pim1 in three human prostate cell lines representing different disease stages including benign (RWPE1), androgen-dependent cancer (LNCaP) and androgen-independent cancer (DU145).
  • However, Pim1 expression enhanced the in vitro and in vivo tumorigenic potentials of the human prostate cancer cell lines LNCaP and DU145.
  • The c-MYC inhibitor 10058-F4 suppressed the tumorigenicity of Pim1-expressing prostate cancer cells.
  • CONCLUSION: Our results suggest an in vivo role of Pim1 in promoting prostate tumorigenesis although it displayed distinct oncogenic activities depending on the disease stage of the cell line.

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  • (PMID = 20515470.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01CA123484
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 5-(4-ethylbenzylidene)-2-thioxothiazolidin-4-one; 0 / AR protein, human; 0 / MYC protein, human; 0 / Proto-Oncogene Proteins c-myc; 0 / RNA, Messenger; 0 / Receptors, Androgen; 0 / Thiazoles; EC 2.7.11.1 / Proto-Oncogene Proteins c-pim-1
  • [Other-IDs] NLM/ PMC2886047
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85. Lainakis G, Nikos A, Gerassimos A, Michael C, Iraklis M, Konstantinos L, Ioannis V, Harilaos K, Dimopoulos MA, Bamias A: Biweekly doxorubicin/ketoconazole as second-line treatment in docetaxel-resistant, hormone-refractory prostate cancer. Urology; 2008 Jun;71(6):1181-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Biweekly doxorubicin/ketoconazole as second-line treatment in docetaxel-resistant, hormone-refractory prostate cancer.
  • OBJECTIVES: Docetaxel is an effective first-line treatment for hormone-refractory prostate cancer.
  • METHODS: A total of 34 patients with androgen-independent prostate cancer received doxorubicin, 30 mg/m(2), every 2 weeks and ketoconazole daily, 400 mg orally every 8 hours.
  • RESULTS: Of the 32 evaluable patients, 13 (43.7%, 95% confidence interval [CI] 26.3% to 62.3%) had a prostate-specific antigen (PSA) response, and 4 (28%, 95% CI 8.4% to 58.1%) of 14 patients with measurable disease had a response to therapy.
  • CONCLUSIONS: The combination of biweekly doxorubicin and ketoconazole is an effective, well-tolerated, second-line therapy for hormone-refractory prostate cancer.
  • [MeSH-major] Antibiotics, Antineoplastic / administration & dosage. Antifungal Agents / administration & dosage. Doxorubicin / administration & dosage. Drug Resistance, Neoplasm. Ketoconazole / administration & dosage. Prostatic Neoplasms / drug therapy

  • Genetic Alliance. consumer health - Prostate cancer.
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  • Hazardous Substances Data Bank. DOCETAXEL .
  • Hazardous Substances Data Bank. DOXORUBICIN .
  • Hazardous Substances Data Bank. KETOCONAZOLE .
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  • (PMID = 18400264.001).
  • [ISSN] 1527-9995
  • [Journal-full-title] Urology
  • [ISO-abbreviation] Urology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antifungal Agents; 0 / Antineoplastic Agents; 0 / Taxoids; 15H5577CQD / docetaxel; 80168379AG / Doxorubicin; R9400W927I / Ketoconazole
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86. 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
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  • [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

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  • (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
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87. Callen DF, Ricciardelli C, Butler M, Stapleton A, Stahl J, Kench JG, Horsfall DJ, Tilley WD, Schulz R, Nesland JM, Neilsen PM, Kumar R, Holm R: Co-expression of the androgen receptor and the transcription factor ZNF652 is related to prostate cancer outcome. Oncol Rep; 2010 Apr;23(4):1045-52
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Co-expression of the androgen receptor and the transcription factor ZNF652 is related to prostate cancer outcome.
  • ZNF652, a DNA binding transcription factor, was previously suggested to be differentially expressed in prostate cancer.
  • This study investigated if the expressions of ZNF652 and androgen receptor (AR) in prostate cancer are associated with prostate specific antigen (PSA) defined relapse.
  • ZNF652 and AR immunoreactivity were evaluated in prostate tissues from a cohort of 121 patients with prostate cancer and associations with disease outcome determined.
  • To assess if ZNF652 can influence AR expression, or vice versa, levels of expression of ZNF652, AR and PSA were determined in the prostate cell line LNCaP following induction of AR activity by 5alpha-dihydrotestosterone, or knockdown of ZNF652 expression.
  • Two thirds of prostate tumors retained high levels of ZNF652 (71/109 cases) and 50% of tumors high levels of AR (57/113).
  • There was a significant decrease (p=0.005) in relapse-free survival of patients with high expression levels of both ZNF652 and AR and this was independent of preoperative PSA and seminal vesicle involvement.
  • High levels of expression of both AR and ZNF652 in clinically organ-defined prostate cancer are associated with a statistically increased risk of relapse.
  • [MeSH-major] Biomarkers, Tumor / analysis. DNA-Binding Proteins / biosynthesis. Prostatic Neoplasms / metabolism. Receptors, Androgen / biosynthesis
  • [MeSH-minor] Adult. Aged. Blotting, Western. Gene Expression. Gene Expression Profiling. Humans. Immunohistochemistry. Kaplan-Meier Estimate. Male. Middle Aged. Neoplasm Recurrence, Local / genetics. Neoplasm Recurrence, Local / metabolism. Neoplasm Recurrence, Local / pathology. Neoplasm Staging. Prostate-Specific Antigen / blood. Tissue Array Analysis