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1. Stanworth RD, Jones TH: Testosterone in obesity, metabolic syndrome and type 2 diabetes. Front Horm Res; 2009;37:74-90
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  • Low testosterone levels are now being recognised as an independent risk factors for these conditions.
  • Findings from men undergoing androgen suppression as treatment for prostate cancer confirm that the hypogonadal state increases body fat mass and serum insulin and there is a high rate of developing new diabetes in this population.
  • [MeSH-minor] Adipose Tissue / drug effects. Clinical Trials as Topic. Hormone Replacement Therapy. Humans. Insulin Resistance. Receptors, Androgen / genetics. Risk Factors. Trinucleotide Repeats


2. Liu H, Liu YQ, Liu YQ, Xu AH, Young CY, Yuan HQ, Lou HX: A novel anticancer agent, retigeric acid B, displays proliferation inhibition, S phase arrest and apoptosis activation in human prostate cancer cells. Chem Biol Interact; 2010 Dec 5;188(3):598-606
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  • [Title] A novel anticancer agent, retigeric acid B, displays proliferation inhibition, S phase arrest and apoptosis activation in human prostate cancer cells.
  • Here, we observed that RB inhibited prostate cancer cell proliferation and induced cell death in a dose-dependent manner, but exerted very little inhibitory effect on noncancerous prostate epithelial cell viability.
  • Treatment of androgen-independent PC-3 cells with RB caused a moderate increase in p21(Cip1), and enforced the cell cycle arrest in the S phase.
  • However, pretreatment with the pan-caspase inhibitor z-VAD-fmk only partially alleviated RB-triggered apoptosis in PC-3 cells, suggesting the involvement of both caspase-dependent and caspase-independent pathways.
  • Additionally, treatment of androgen-sensitive LNCaP cells with RB led to a reduction in the expression of androgen receptor (AR), and subsequently decreased the transactivity of AR.
  • These observations help to support the search for promising candidates to treat prostate cancer.
  • [MeSH-minor] Cell Line, Tumor. Cell Proliferation / drug effects. Gene Expression Regulation, Neoplastic / drug effects. Humans. Inhibitory Concentration 50. Male. Receptors, Androgen / metabolism. Transcription, Genetic / drug effects


3. Altundag K, Altundag O, Morandi P, Gunduz M: Imatinib mesylate and zoledronic acid in androgen-independent prostate cancer. Urology; 2005 Jan;65(1):211-2; author reply 212
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  • [Title] Imatinib mesylate and zoledronic acid in androgen-independent prostate cancer.

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  • [CommentOn] Urology. 2004 May;63(5):934-9 [15134984.001]
  • (PMID = 15667906.001).
  • [ISSN] 1527-9995
  • [Journal-full-title] Urology
  • [ISO-abbreviation] Urology
  • [Language] eng
  • [Publication-type] Comment; Letter
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / Diphosphonates; 0 / Imidazoles; 0 / Neoplasm Proteins; 0 / Piperazines; 0 / Pyrimidines; 6XC1PAD3KF / zoledronic acid; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Receptors, Platelet-Derived Growth Factor
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4. Mimeault M, Johansson SL, Vankatraman G, Moore E, Henichart JP, Depreux P, Lin MF, Batra SK: Combined targeting of epidermal growth factor receptor and hedgehog signaling by gefitinib and cyclopamine cooperatively improves the cytotoxic effects of docetaxel on metastatic prostate cancer cells. Mol Cancer Ther; 2007 Mar;6(3):967-78
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  • [Title] Combined targeting of epidermal growth factor receptor and hedgehog signaling by gefitinib and cyclopamine cooperatively improves the cytotoxic effects of docetaxel on metastatic prostate cancer cells.
  • The epidermal growth factor receptor (EGFR) and hedgehog cascades provide a critical role in prostate cancer progression and contribute to the resistance to clinical therapies and disease relapse.
  • Therefore, we evaluated, for the first time, the antiproliferative and cytotoxic effects induced by a combination of selective inhibitors of EGFR tyrosine kinase and smoothened hedgehog signaling element, gefitinib and cyclopamine, with a current chemotherapeutic drug used in the clinics, docetaxel, on some metastatic prostate cancer cell lines.
  • Immunohistochemical analyses revealed that sonic hedgehog (SHH) expression was enhanced in 39% of primary prostatic adenocarcinomas (Gleason scores 4-10) compared with the corresponding normal tissues of the same prostate gland from 32 prostate cancer patients.
  • Moreover, the results revealed that the drugs, alone or in combination, at lower concentrations inhibited the growth of EGF plus SHH-stimulated and serum-stimulated androgen-responsive LNCaP-C33 and androgen-independent LNCaP-C81, DU145, and PC3 cells.
  • Importantly, the combined docetaxel, gefitinib, and cyclopamine also caused a higher rate of apoptotic death of prostate cancer cells compared with individual agents.
  • These findings indicate that the combined use of inhibitors of EGF-EGFR and hedgehog signaling with docetaxel could represent a more promising strategy for treatment in patients with metastatic and androgen-independent prostate cancer.

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  • (PMID = 17363490.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA138791; United States / NCI NIH HHS / CA / CA 88184
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hedgehog Proteins; 0 / Quinazolines; 0 / SHH protein, human; 0 / Taxoids; 0 / Veratrum Alkaloids; 15H5577CQD / docetaxel; 9007-43-6 / Cytochromes c; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; S65743JHBS / gefitinib; ZH658AJ192 / cyclopamine
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5. 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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6. Wetherill YB, Fisher NL, Staubach A, Danielsen M, de Vere White RW, Knudsen KE: Xenoestrogen action in prostate cancer: pleiotropic effects dependent on androgen receptor status. Cancer Res; 2005 Jan 1;65(1):54-65
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  • [Title] Xenoestrogen action in prostate cancer: pleiotropic effects dependent on androgen receptor status.
  • Androgen is critical for prostate development, growth, and survival.
  • Therapies for advanced prostate cancer aim to block androgen receptor (AR) action.
  • We have shown previously that a known xenoestrogen, bisphenol A (BPA), activates a tumor-derived AR mutant (T877A), leading to androgen-independent prostate cancer cell proliferation.
  • Here, we show that BPA cooperates with androgen to activate AR-T877A as shown by both reporter assays and increased levels of prostate-specific antigen expression.
  • Further investigations using both yeast and mammalian model systems revealed that multiple AR alleles are responsive to BPA, thus expanding the potential influence of xenoestrogens on prostate cancer.
  • We also show that higher concentrations of BPA block proliferation of AR-positive, androgen-dependent prostate adenocarcinoma cells (LNCaP and LAPC-4), with a more modest inhibitory effect on androgen-independent cells (22Rv-1).
  • By contrast, AR-negative prostate cancer cells failed to show growth inhibition after exposure to high BPA dose.
  • Together, these data show that BPA can serve as a potential "hormone sensitizer" of the mutant ARs present in advanced prostate adenocarcinomas, thereby possibly contributing toward therapeutic relapse in advanced prostate cancer patients and supporting the notion that nonsteroidal environmental compounds can alter the function of nuclear receptor complexes.
  • [MeSH-major] Estrogens, Non-Steroidal / pharmacology. Phenols / pharmacology. Prostatic Neoplasms / pathology. Receptors, Androgen / genetics

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  • (PMID = 15665279.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NIEHS NIH HHS / ES / E30-ES--06096; United States / NIEHS NIH HHS / ES / ES-07250-16; United States / NCI NIH HHS / CA / R01-CA 093404-03
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzhydryl Compounds; 0 / Estrogens, Non-Steroidal; 0 / Phenols; 0 / Receptors, Androgen; 08J2K08A3Y / Dihydrotestosterone; EC 1.13.12.- / Luciferases; MLT3645I99 / bisphenol A
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7. Kurisu T, Tanaka T, Ishii J, Matsumura K, Sugimura K, Nakatani T, Kawashima H: Expression and function of human steroid receptor RNA activator in prostate cancer cells: role of endogenous hSRA protein in androgen receptor-mediated transcription. Prostate Cancer Prostatic Dis; 2006;9(2):173-8
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  • [Title] Expression and function of human steroid receptor RNA activator in prostate cancer cells: role of endogenous hSRA protein in androgen receptor-mediated transcription.
  • Later, we demonstrated that SRA needs to be translated in order to co-activate androgen receptor (AR).
  • Western blot showed that SRA protein was expressed at a higher level in PC-3 than in LNCaP cells, suggesting that SRA may be related to hormone-independent growth of prostate cancer.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Prostatic Neoplasms / genetics. RNA, Untranslated / genetics. Receptors, Androgen / physiology

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  • (PMID = 16607388.001).
  • [ISSN] 1365-7852
  • [Journal-full-title] Prostate cancer and prostatic diseases
  • [ISO-abbreviation] Prostate Cancer Prostatic Dis.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AR protein, human; 0 / Biomarkers, Tumor; 0 / RNA, Long Noncoding; 0 / RNA, Neoplasm; 0 / RNA, Untranslated; 0 / Receptors, Androgen; 0 / steroid receptor RNA activator
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8. Takahara K, Azuma H, Sakamoto T, Kiyama S, Inamoto T, Ibuki N, Nishida T, Nomi H, Ubai T, Segawa N, Katsuoka Y: Conversion of prostate cancer from hormone independency to dependency due to AMACR inhibition: involvement of increased AR expression and decreased IGF1 expression. Anticancer Res; 2009 Jul;29(7):2497-505
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  • [Title] Conversion of prostate cancer from hormone independency to dependency due to AMACR inhibition: involvement of increased AR expression and decreased IGF1 expression.
  • Androgen-independent prostate cancer eventually develops metastasis, and radical treatment may not be possible for patients at this stage.
  • In this study, we examined the gene-expression profiles of two prostate cancer cell lines, LNCaP (androgen-dependent) and C4-2 (androgen-independent), using cDNA-microarray hybridization.
  • We focused on the expression of alpha-methylacyl-CoA racemase (AMACR), whose expression is much higher in C4-2 than in LNCaP, and investigated its biological role in acquisition of androgen-independent cancer growth.
  • Inhibition of AMACR expression using AMACR-siRNA induced an increase in the expression of androgen receptor (AR) and B-cell translocation gene 1, along with a decrease in the expression of genes associated with cancer progression, including insulin-like growth factor I and platelet-derived growth factor alpha, in C4-2 with compared to non-treated C4-2.
  • BrdU analysis and MTT assay demonstrated that AMACR inhibition induced a significant decrease of cell viability in C4-2 when cultured in androgen-depleted serum, becoming consistent with that of LNCaP, suggesting that AMACR inhibition may induce an increase in the expression of AR and characteristic conversion of prostate cancer cells from hormone independency to hormone dependency.
  • We suggest that AMACR inhibition may be a new strategy for treatment of patients with hormone-refractory prostate cancer.
  • [MeSH-major] Insulin-Like Growth Factor I / metabolism. Neoplasms, Hormone-Dependent / metabolism. Prostatic Neoplasms / pathology. Racemases and Epimerases / antagonists & inhibitors. Receptors, Androgen / metabolism

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  • (PMID = 19596919.001).
  • [ISSN] 1791-7530
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / RNA, Small Interfering; 0 / Receptors, Androgen; 67763-96-6 / Insulin-Like Growth Factor I; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
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9. Srinivas S, Krishnan AV, Colocci N, Feldman D: Phase II study evaluating oral triamcinolone in patients with androgen-independent prostate cancer. Urology; 2006 May;67(5):1001-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase II study evaluating oral triamcinolone in patients with androgen-independent prostate cancer.
  • OBJECTIVES: To assess the effect of triamcinolone administration on the serum prostate-specific antigen (PSA) response and the time to progression in patients with androgen-independent prostate cancer (AIPC).
  • [MeSH-minor] Aged. Aged, 80 and over. Androgen Antagonists / administration & dosage. Disease Progression. Humans. Hydrocortisone / blood. Male. Middle Aged. Point Mutation. Prospective Studies. Prostate-Specific Antigen / blood. Receptors, Androgen / genetics. Receptors, Androgen / metabolism


10. 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.

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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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11. Sciarra A, Cardi A, Dattilo C, Mariotti G, Di Monaco F, Di Silverio F: New perspective in the management of neuroendocrine differentiation in prostate adenocarcinoma. Int J Clin Pract; 2006 Apr;60(4):462-70
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  • [Title] New perspective in the management of neuroendocrine differentiation in prostate adenocarcinoma.
  • In this review, we will present some of the information that is known about neuroendocrine (NE) cells and differentiation in the prostate.
  • We will then speculate on the potential role that NE differentiation in prostate carcinoma may play and how this differentiation may be clinically analysed and treated.
  • The androgen-independent growth of prostate cancer can be caused by different mechanisms; one of these is receptor-specific paracrine or autocrine growth modulation of human prostatic cancer cells by neuropeptides secreted by NE cells.
  • Our results affirm that different methods of androgen deprivation can influence the serum chromogranin A (CgA) levels to different extents in prostate cancer.
  • In the light of other evidence that supports a significant relationship between serum CgA levels, tissue CgA expression and NE activity, we hypothesise that bicalutamide may reduce the risk of NE cell hyperactivation in prostate cancer.
  • It is important to determine whether increases in CgA levels and NE cell activation are associated with progression towards hormone-independent prostate cancer.
  • We recently proposed as therapy of NE activation in hormone-independent prostate cancer, a combination of oestrogens and somatostatin analogues.
  • This combination therapy also sustains the novel concept in cancer treatment in which therapies may target not only cancer cells but also its microenvironment in combination, which can confer protection from apoptosis.
  • [MeSH-minor] Adult. Androgen Antagonists / therapeutic use. Anilides / therapeutic use. Antineoplastic Agents / therapeutic use. Cell Transformation, Neoplastic / drug effects. Humans. Immunohistochemistry. Male. Middle Aged. Nitriles. Tosyl Compounds. Treatment Outcome

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  • (PMID = 16620361.001).
  • [ISSN] 1368-5031
  • [Journal-full-title] International journal of clinical practice
  • [ISO-abbreviation] Int. J. Clin. Pract.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Anilides; 0 / Antineoplastic Agents; 0 / Nitriles; 0 / Tosyl Compounds; A0Z3NAU9DP / bicalutamide
  • [Number-of-references] 44
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12. Mitas MC, Chaudhary UB, Marshall DT, Gattoni-Celli S: Detection of circulating tumor cells in the peripheral blood of patients with androgen-independent, advanced or metastatic prostate cancer. Am J Hematol; 2008 Jan;83(1):87
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  • [Title] Detection of circulating tumor cells in the peripheral blood of patients with androgen-independent, advanced or metastatic prostate cancer.


13. 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.

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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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14. Klotz L: Combined androgen blockade: an update. Urol Clin North Am; 2006 May;33(2):161-6, v-vi
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  • [Title] Combined androgen blockade: an update.
  • The use of combined androgen blockade therapy in prostate cancer management remains controversial.
  • This article reviews the effect of the different non-steroid androgens in blocking androgen-independent activation of the androgen receptor in the androgen-depleted environment, and the potential benefit of bicalutamide in comparison to the first generation of anti-androgens (flutamide and nilutamide).
  • [MeSH-major] Androgen Antagonists / therapeutic use. Orchiectomy. Prostatic Neoplasms / therapy

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  • (PMID = 16631454.001).
  • [ISSN] 0094-0143
  • [Journal-full-title] The Urologic clinics of North America
  • [ISO-abbreviation] Urol. Clin. North Am.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Anilides; 0 / Nitriles; 0 / Tosyl Compounds; A0Z3NAU9DP / bicalutamide
  • [Number-of-references] 26
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15. Lehen'kyi V, Flourakis M, Skryma R, Prevarskaya N: TRPV6 channel controls prostate cancer cell proliferation via Ca(2+)/NFAT-dependent pathways. Oncogene; 2007 Nov 15;26(52):7380-5
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  • [Title] TRPV6 channel controls prostate cancer cell proliferation via Ca(2+)/NFAT-dependent pathways.
  • The transient receptor potential channel, subfamily V, member 6 (TRPV6), is strongly expressed in advanced prostate cancer and significantly correlates with the Gleason >7 grading, being undetectable in healthy and benign prostate tissues.
  • However, the role of TRPV6 as a highly Ca(2+)-selective channel in prostate carcinogenesis remains poorly understood.
  • Here, we report that TRPV6 is directly involved in the control of prostate cancer cell (LNCaP cell line) proliferation by decreasing: (i) proliferation rate;.
  • Our results suggest that TRPV6 expression in LNCaP cells is regulated by androgen receptor, however, in a ligand-independent manner.
  • We conclude that the upregulation of TRPV6 Ca(2+) channel in prostate cancer cells may represent a mechanism for maintaining a higher proliferation rate, increasing cell survival and apoptosis resistance as well.

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  • (PMID = 17533368.001).
  • [ISSN] 1476-5594
  • [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 / Calcium Channels; 0 / Enzyme Inhibitors; 0 / NFATC Transcription Factors; 0 / TRPV Cation Channels; 0 / TRPV6 protein, human; 67526-95-8 / Thapsigargin; SY7Q814VUP / Calcium
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16. Li Y, Mizokami A, Izumi K, Narimoto K, Shima T, Zhang J, Dai J, Keller ET, Namiki M: CTEN/tensin 4 expression induces sensitivity to paclitaxel in prostate cancer. Prostate; 2010 Jan 1;70(1):48-60
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  • [Title] CTEN/tensin 4 expression induces sensitivity to paclitaxel in prostate cancer.
  • BACKGROUND: Recently, we established paclitaxel-resistant prostate cancer cell lines (PC-3-TxR and DU145-TxR).
  • METHODS: We investigated how knockdown and overexpression of CTEN in androgen-independent cell lines affect paclitaxel sensitivity by colony formation assay and growth inhibition assay.
  • We also examined the association between expression of CTEN and grade of prostate cancer by immunohistochemistry using tissue microarray analysis.

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  • [Copyright] (c) 2009 Wiley-Liss, Inc.
  • (PMID = 19725034.001).
  • [ISSN] 1097-0045
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Microfilament Proteins; 0 / tensins; P88XT4IS4D / Paclitaxel
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17. Dong Z, Liu Y, Lu S, Wang A, Lee K, Wang LH, Revelo M, Lu S: Vav3 oncogene is overexpressed and regulates cell growth and androgen receptor activity in human prostate cancer. Mol Endocrinol; 2006 Oct;20(10):2315-25
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  • [Title] Vav3 oncogene is overexpressed and regulates cell growth and androgen receptor activity in human prostate cancer.
  • The purpose of this research was to investigate the role of Vav3 oncogene in human prostate cancer.
  • We found that expression of Vav3 was significantly elevated in androgen-independent LNCaP-AI cells in comparison with that in their androgen-dependent counterparts, LNCaP cells.
  • Vav3 expression was also detected in other human prostate cancer cell lines (PC-3, DU145, and 22Rv1) and, by immunohistochemistry analysis, was detected in 32% (26 of 82) of surgical specimens of human prostate cancer.
  • Knockdown expression of Vav3 by small interfering RNA inhibited growth of both androgen-dependent LNCaP and androgen-independent LNCaP-AI cells.
  • In contrast, overexpression of Vav3 promoted androgen-independent growth of LNCaP cells induced by epidermal growth factor.
  • Overexpression of Vav3 enhanced androgen receptor (AR) activity regardless of the presence or absence of androgen and stimulated the promoters of AR target genes.
  • Taken together, our data show that overexpression of Vav3, through the PI3K-Akt pathway, inappropriately activates AR signaling axis and stimulates cell growth in prostate cancer cells.
  • These findings suggest that Vav3 overexpression may be involved in prostate cancer development and progression.
  • [MeSH-major] Gene Expression Regulation, Neoplastic / physiology. Guanine Nucleotide Exchange Factors / metabolism. Prostatic Neoplasms / metabolism. Proto-Oncogene Proteins c-vav / metabolism. Receptors, Androgen / metabolism. Signal Transduction / physiology

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  • (PMID = 16762975.001).
  • [ISSN] 0888-8809
  • [Journal-full-title] Molecular endocrinology (Baltimore, Md.)
  • [ISO-abbreviation] Mol. Endocrinol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Guanine Nucleotide Exchange Factors; 0 / Proto-Oncogene Proteins c-vav; 0 / RNA, Small Interfering; 0 / Receptors, Androgen; 0 / VAV3 protein, human; EC 2.7.1.- / Phosphatidylinositol 3-Kinases
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18. Nagata D, Yoshihiro H, Nakanishi M, Naruyama H, Okada S, Ando R, Tozawa K, Kohri K: Peroxisome proliferator-activated receptor-gamma and growth inhibition by its ligands in prostate cancer. Cancer Detect Prev; 2008;32(3):259-66
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  • [Title] Peroxisome proliferator-activated receptor-gamma and growth inhibition by its ligands in prostate cancer.
  • Ligand-induced PPAR-gamma activation can result in growth inhibition and differentiation in these cancer cells; however, the precise mechanism for the anti-proliferative effect of PPAR-gamma ligands is not clear.
  • METHODS: In this study, we examined the expression of PPAR-gamma in human prostate cancer and the effect of two PPAR-gamma ligands, 15 deoxy-Delta(12,14)-prostaglandin J2 (15d-PGJ2) and troglitazone, on prostate cancer cell growth.
  • RESULTS: PPAR-gamma is frequently over-expressed in androgen independent prostate cancer cell lines and human prostate cancer tissues (22 of 47; 47%).
  • Both 15d-PGJ2 and troglitazone inhibited proliferation and DNA synthesis of prostate cancer cell lines in a dose-dependent manner, and slightly increased the proportion of cells with S-phase DNA content.
  • Prostate specific antigen (PSA) promoter reporter assays showed that troglitazone and 15d-PGJ2 down-regulated androgen stimulated reporter gene activity in prostate cancer cell lines LNCaP.
  • CONCLUSIONS: Taken together, these results suggest that PPAR-gamma ligands may be a useful therapeutic agent for the treatment of prostate cancer.
  • [MeSH-minor] Blotting, Western. Cell Line, Tumor. Cell Proliferation / drug effects. Chromans / pharmacology. Flow Cytometry. Humans. Immunohistochemistry. Ligands. Male. Promoter Regions, Genetic / drug effects. Prostaglandin D2 / analogs & derivatives. Prostaglandin D2 / pharmacology. Prostate-Specific Antigen / biosynthesis. Prostate-Specific Antigen / drug effects. Receptors, Androgen / drug effects. Receptors, Androgen / metabolism. Thiazolidinediones / pharmacology. Transfection

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  • (PMID = 18789607.001).
  • [ISSN] 1525-1500
  • [Journal-full-title] Cancer detection and prevention
  • [ISO-abbreviation] Cancer Detect. Prev.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 15-deoxyprostaglandin J2; 0 / Antineoplastic Agents; 0 / Chromans; 0 / Ligands; 0 / PPAR gamma; 0 / Receptors, Androgen; 0 / Thiazolidinediones; EC 3.4.21.77 / Prostate-Specific Antigen; I66ZZ0ZN0E / troglitazone; RXY07S6CZ2 / Prostaglandin D2
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19. Katsogiannou M, El Boustany C, Gackiere F, Delcourt P, Athias A, Mariot P, Dewailly E, Jouy N, Lamaze C, Bidaux G, Mauroy B, Prevarskaya N, Slomianny C: Caveolae contribute to the apoptosis resistance induced by the alpha(1A)-adrenoceptor in androgen-independent prostate cancer cells. PLoS One; 2009;4(9):e7068
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  • [Title] Caveolae contribute to the apoptosis resistance induced by the alpha(1A)-adrenoceptor in androgen-independent prostate cancer cells.
  • BACKGROUND: During androgen ablation prostate cancer cells' growth and survival become independent of normal regulatory mechanisms.
  • These androgen-independent cells acquire the remarkable ability to adapt to the surrounding microenvironment whose factors, such as neurotransmitters, influence their survival.
  • Although findings are becoming evident about the expression of alpha(1A)-adrenoceptors in prostate cancer epithelial cells, their exact functional role in androgen-independent cells has yet to be established.
  • Previous work has demonstrated that membrane lipid rafts associated with key signalling proteins mediate growth and survival signalling pathways in prostate cancer cells.
  • METHODOLOGY/PRINCIPAL FINDINGS: In order to analyze the membrane topology of the alpha(1A)-adrenoceptor we explored its presence by a biochemical approach in purified detergent resistant membrane fractions of the androgen-independent prostate cancer cell line DU145.
  • Further, immunohistofluorescence revealed the relation between high levels of alpha(1A)-adrenoceptor and caveolin-1 expression with advanced stage prostate cancer.
  • CONCLUSIONS/SIGNIFICANCE: In conclusion, we propose that alpha(1A)-adrenoceptor stimulation in androgen-independent prostate cancer cells via caveolae constitutes one of the mechanisms contributing to their protection from TG-induced apoptosis.

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  • (PMID = 19763272.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ADRA1A protein, human; 0 / Neurotransmitter Agents; 0 / Receptors, Adrenergic, alpha-1; 0 / Sphingomyelins; 67526-95-8 / Thapsigargin; 97C5T2UQ7J / Cholesterol
  • [Other-IDs] NLM/ PMC2742726
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20. Wang Y, Kreisberg JI, Ghosh PM: Cross-talk between the androgen receptor and the phosphatidylinositol 3-kinase/Akt pathway in prostate cancer. Curr Cancer Drug Targets; 2007 Sep;7(6):591-604
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cross-talk between the androgen receptor and the phosphatidylinositol 3-kinase/Akt pathway in prostate cancer.
  • Prostate cancer is initially dependent on androgens for growth; hence, recurrent prostate is treated with androgen ablation which may result in progression to androgen independence characterized by a resistance to such therapy.
  • Androgens bind to and activate the androgen receptor (AR), a member of the nuclear steroid receptor family of transcription factors, which regulates prostate cancer cell proliferation and survival in androgen-independent, as well as -dependent, tumors.
  • Here we analyze reports in the literature indicating that these two pathways cooperate to regulate prostate tumor development and progression.
  • This explains why prostate tumors subjected to androgen ablation experience an increase in Akt phosphorylation, and suggest that the tumor compensates for the loss of one pathway with another.
  • [MeSH-major] Phosphatidylinositol 3-Kinases / metabolism. Prostatic Neoplasms / metabolism. Proto-Oncogene Proteins c-akt / metabolism. Receptor Cross-Talk. Receptors, Androgen / metabolism


21. 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.
  • Pln, via glycosaminoglycans in domains I and V, acts as a co-receptor for delivery of heparin binding growth factors (HBGFs) that support cancer growth and vascularization.
  • 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.


22. Wang G, Ahmad KA, Unger G, Slaton JW, Ahmed K: CK2 signaling in androgen-dependent and -independent prostate cancer. J Cell Biochem; 2006 Oct 1;99(2):382-91
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  • [Title] CK2 signaling in androgen-dependent and -independent prostate cancer.
  • CK2 has been found to be dysregulated in all the cancers that have been examined, including prostate cancer.
  • Investigations of CK2 signaling in the prostate were originally initiated in this laboratory, and these studies have identified significant functional activities of CK2 in relation to normal prostate growth and to the pathobiology of androgen-dependent and -independent prostate cancer.
  • We present a brief overview of these developments in the context of prostate biology.
  • An important outcome of these studies is the emerging concept that CK2 can be effectively targeted for cancer therapy.
  • [MeSH-minor] Animals. Apoptosis. Cell Line, Tumor. Cell Proliferation. Humans. Male. Models, Biological. Prostate / metabolism. Signal Transduction

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  • [Copyright] Copyright 2006 Wiley-Liss, Inc.
  • (PMID = 16598768.001).
  • [ISSN] 0730-2312
  • [Journal-full-title] Journal of cellular biochemistry
  • [ISO-abbreviation] J. Cell. Biochem.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-15062
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; EC 2.7.11.1 / Casein Kinase II
  • [Number-of-references] 63
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23. McPherson SJ, Hussain S, Balanathan P, Hedwards SL, Niranjan B, Grant M, Chandrasiri UP, Toivanen R, Wang Y, Taylor RA, Risbridger GP: Estrogen receptor-beta activated apoptosis in benign hyperplasia and cancer of the prostate is androgen independent and TNFalpha mediated. Proc Natl Acad Sci U S A; 2010 Feb 16;107(7):3123-8
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  • [Title] Estrogen receptor-beta activated apoptosis in benign hyperplasia and cancer of the prostate is androgen independent and TNFalpha mediated.
  • Prostate cancer (PCa) and benign prostatic hyperplasia (BPH) are androgen-dependent diseases commonly treated by inhibiting androgen action.
  • However, androgen ablation or castration fail to target androgen-independent cells implicated in disease etiology and recurrence.
  • In PCa, ERbeta causes apoptosis in Gleason Grade 7 xenografted tissues and androgen-independent cells lines (PC3 and DU145) via caspase-8.
  • These data provide evidence of the beneficial effects of ERbeta agonist on epithelium and stroma of BPH, as well as androgen-independent tumor cells implicated in recurrent disease.
  • Our data are indicative of the therapeutic potential of ERbeta agonist for treatment of PCa and/or BPH with or without androgen withdrawal.
  • [MeSH-major] Apoptosis / physiology. Estrogen Receptor beta / metabolism. Hyperplasia / metabolism. Prostate / pathology. Prostatic Neoplasms / metabolism. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 20133657.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Estrogen Receptor beta; 0 / Tumor Necrosis Factor-alpha
  • [Other-IDs] NLM/ PMC2840300
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24. Guo J, Jiang C, Wang Z, Lee HJ, Hu H, Malewicz B, Lee HJ, Lee JH, Baek NI, Jeong JH, Kim DK, Kang KS, Kim SH, Lu J: A novel class of pyranocoumarin anti-androgen receptor signaling compounds. Mol Cancer Ther; 2007 Mar;6(3):907-17
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  • [Title] A novel class of pyranocoumarin anti-androgen receptor signaling compounds.
  • Androgen and the androgen receptor (AR)-mediated signaling are crucial for prostate cancer development.
  • Novel agents that can inhibit AR signaling in ligand-dependent and ligand-independent manners are desirable for the chemoprevention of prostate carcinogenesis and for the treatment of advanced prostate cancer.
  • We have shown recently that the pyranocoumarin compound decursin from the herb Angelica gigas possesses potent anti-AR activities distinct from the anti-androgen bicalutamide.
  • Here, we compared the anti-AR activities and the cell cycle arrest and apoptotic effects of decursin and two natural analogues in the androgen-dependent LNCaP human prostate cancer cell culture model to identify structure-activity relationships and mechanisms.
  • Decursin and its isomer decursinol angelate decreased prostate-specific antigen expression with IC(50) of approximately 1 mumol/L.
  • Both inhibited the androgen-stimulated AR nuclear translocation and transactivation, decreased AR protein abundance through proteasomal degradation, and induced G(0/1) arrest and morphologic differentiation.
  • Furthermore, they lacked the agonist activity of bicalutamide in the absence of androgen and were more potent than bicalutamide for suppressing androgen-stimulated cell growth.
  • In conclusion, decursin and decursinol angelate are members of a novel class of nonsteroidal compounds that exert a long-lasting inhibition of both ligand-dependent and ligand-independent AR signaling.
  • [MeSH-major] Androgen Receptor Antagonists. Benzopyrans / therapeutic use. Butyrates / therapeutic use. Neoplasms, Hormone-Dependent / drug therapy. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Androgens / metabolism. Angelica / chemistry. Apoptosis / drug effects. Cell Cycle Proteins / metabolism. Cell Nucleus / drug effects. Cell Nucleus / metabolism. Cell Proliferation / drug effects. Gene Expression Regulation, Neoplastic. Humans. Ligands. Male. Prostate-Specific Antigen / metabolism. Protein Transport / drug effects. Reactive Oxygen Species / metabolism. Tumor Cells, Cultured / drug effects

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  • (PMID = 17363485.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 95642
  • [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 Receptor Antagonists; 0 / Androgens; 0 / Benzopyrans; 0 / Butyrates; 0 / Cell Cycle Proteins; 0 / Ligands; 0 / Reactive Oxygen Species; 5928-25-6 / decursin; EC 3.4.21.77 / Prostate-Specific Antigen
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25. Ren A, Yan G, You B, Sun J: Down-regulation of mammalian sterile 20-like kinase 1 by heat shock protein 70 mediates cisplatin resistance in prostate cancer cells. Cancer Res; 2008 Apr 1;68(7):2266-74
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  • [Title] Down-regulation of mammalian sterile 20-like kinase 1 by heat shock protein 70 mediates cisplatin resistance in prostate cancer cells.
  • Here, we reported that heat shock protein 70 (Hsp70), which is thought to protect cells against cellular stress, has been identified as an Mst1-interacting protein, in a yeast two-hybrid screen of human adult prostate cDNA library with a dominant-negative Mst1 (K59R) as bait.
  • The interaction of Mst1 with Hsp70 was confirmed by coimmunoprecipitation in both cotransfected HEK293 cells and prostate cancer cells.
  • Most strikingly, in response to the treatment of anticancer drug cisplatin, the induction of Hsp70 expression is higher in the androgen-independent DU145 cells compared with the androgen-dependent LNCaP cells.
  • The higher levels of Hsp70 induction and subsequent Mst1 degradation mediate cisplatin resistance in prostate cancer DU145 cells.
  • Moreover, overexpression of Mst1 sensitizes prostate cancer cells to cisplatin treatment.
  • These findings implicate that Mst1, a downstream target of Hsp70, may be developed as a target for sensitizing hormone-refractory prostate cancers to chemotherapy.

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  • (PMID = 18381433.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / HSP70 Heat-Shock Proteins; EC 2.7.1.- / STK4 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 6.3.2.19 / STUB1 protein, human; EC 6.3.2.19 / Ubiquitin-Protein Ligases; Q20Q21Q62J / Cisplatin
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26. 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).

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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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27. Sissung TM, Baum CE, Deeken J, Price DK, Aragon-Ching J, Steinberg SM, Dahut W, Sparreboom A, Figg WD: ABCB1 genetic variation influences the toxicity and clinical outcome of patients with androgen-independent prostate cancer treated with docetaxel. Clin Cancer Res; 2008 Jul 15;14(14):4543-9
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  • [Title] ABCB1 genetic variation influences the toxicity and clinical outcome of patients with androgen-independent prostate cancer treated with docetaxel.
  • PURPOSE: Polymorphisms that are associated with ABCB1 expression and function may be linked to treatment efficacy and the development of neutropenia and neurotoxicity in patients with androgen-independent prostate cancer receiving docetaxel.
  • EXPERIMENTAL DESIGN: Patients with androgen-independent prostate cancer treated with docetaxel alone (n = 23) or docetaxel and thalidomide (n = 50) were genotyped for the ABCB1 1236C>T, 2677 G>T/A, and 3435 C>T alleles by direct sequencing, and diplotypes were constructed using an EM algorithm.

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  • (PMID = 18628469.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z01 BC010453-06
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ABCB1 protein, human; 0 / Androgens; 0 / Antineoplastic Agents; 0 / P-Glycoprotein; 0 / P-Glycoproteins; 0 / Taxoids; 15H5577CQD / docetaxel; 4Z8R6ORS6L / Thalidomide
  • [Other-IDs] NLM/ NIHMS105257; NLM/ PMC2723795
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28. Andrieu C, Taieb D, Baylot V, Ettinger S, Soubeyran P, De-Thonel A, Nelson C, Garrido C, So A, Fazli L, Bladou F, Gleave M, Iovanna JL, Rocchi P: Heat shock protein 27 confers resistance to androgen ablation and chemotherapy in prostate cancer cells through eIF4E. Oncogene; 2010 Apr 1;29(13):1883-96
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Heat shock protein 27 confers resistance to androgen ablation and chemotherapy in prostate cancer cells through eIF4E.
  • One strategy to improve therapies in advanced prostate cancer (PC) involves targeting genes that are activated by androgen withdrawal to delay the emergence of the androgen-independent (AI) phenotype.
  • Heat shock protein 27 (Hsp27) expression becomes highly upregulated in PC cells after androgen withdrawal or chemotherapy, in which it functions as a cytoprotective chaperone to confer broad-spectrum treatment resistance.
  • Forced overexpression of eIF4E induces resistance to androgen-withdrawal and paclitaxel treatment in the prostate LNCaP cells in vitro.
  • These findings identify Hsp27 as a modulator of eIF4E and establish a potential mechanism for the eIF4E-regulated apoptosis after androgen ablation and chemotherapy.
  • [MeSH-minor] Androgen Antagonists / pharmacology. Antineoplastic Agents, Hormonal / pharmacology. Apoptosis / drug effects. Cell Line, Tumor. Disease Progression. Eukaryotic Initiation Factor-4E. HeLa Cells. Heat-Shock Proteins. Humans. Male. Molecular Chaperones / pharmacology. RNA, Small Interfering / pharmacology. Xenograft Model Antitumor Assays


29. Wu K, Zeng J, Li L, Fan J, Zhang D, Xue Y, Zhu G, Yang L, Wang X, He D: Silibinin reverses epithelial-to-mesenchymal transition in metastatic prostate cancer cells by targeting transcription factors. Oncol Rep; 2010 Jun;23(6):1545-52
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  • [Title] Silibinin reverses epithelial-to-mesenchymal transition in metastatic prostate cancer cells by targeting transcription factors.
  • Silibinin, a naturally occurring flavanone isolated from milk thistle extract, has been shown to possess strong anticancer efficacy against both androgen-dependent and androgen-independent prostate cancer, wherein it inhibits not only cell growth, but also cell invasion and metastasis.
  • Inhibitory effects of silibinin on prostate cancer invasion, motility and migration were previously observed in the highly bone metastatic ARCaP M cell line; however, mechanisms of such efficacy are not completely elucidated.
  • The epithelial-to-mesenchymal transition (EMT) is a crucial step in the progression of prostate cancer, reversal or inhibition of EMT by drugs thus provides a new approach to prostate cancer therapy.
  • Overall these findings demonstrate silibinin was able to reverse EMT to suppress the invasive property of metastatic prostate cancer cells at the transcriptional level.

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  • (PMID = 20428808.001).
  • [ISSN] 1791-2431
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antioxidants; 0 / Keratin-18; 0 / NF-kappa B; 0 / RNA, Messenger; 0 / Silymarin; 0 / Transcription Factors; 0 / Vimentin; 4RKY41TBTF / silybin; EC 3.4.24.24 / Matrix Metalloproteinase 2
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30. Papatsoris AG, Karamouzis MV, Papavassiliou AG: The power and promise of "rewiring" the mitogen-activated protein kinase network in prostate cancer therapeutics. Mol Cancer Ther; 2007 Mar;6(3):811-9
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  • [Title] The power and promise of "rewiring" the mitogen-activated protein kinase network in prostate cancer therapeutics.
  • Prostate cancer is the most frequently diagnosed cancer among men and the second leading cause of male cancer deaths.
  • Initially, tumor growth is androgen dependent and thus responsive to pharmacologic androgen deprivation, but there is a high rate of treatment failure because the disease evolves in an androgen-independent state.
  • Growing evidence suggests that the Ras/mitogen-activated protein kinase (MAPK) signaling cascade represents a pivotal molecular circuitry participating directly or indirectly in prostate cancer evolution.
  • Here, we will delineate the current knowledge regarding the involvement of the Ras/MAPK pathway in prostate carcinogenesis, spotlight ongoing research concerning the development of novel targeted agents such as the Ras/MAPK inhibitors in prostate cancer, and discuss the future perspectives of their therapeutic efficacy.

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  • (PMID = 17363478.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Enzyme Inhibitors; EC 2.7.11.24 / Mitogen-Activated Protein Kinases
  • [Number-of-references] 70
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31. Rabi T, Bishayee A: d -Limonene sensitizes docetaxel-induced cytotoxicity in human prostate cancer cells: Generation of reactive oxygen species and induction of apoptosis. J Carcinog; 2009;8:9
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  • [Title] d -Limonene sensitizes docetaxel-induced cytotoxicity in human prostate cancer cells: Generation of reactive oxygen species and induction of apoptosis.
  • BACKGROUND: Clinical trials have shown that docetaxel combined with other novel agents can improve the survival of androgen-independent prostate cancer patients. d -Limonene, a non-nutrient dietary component, has been found to inhibit various cancer cell growths without toxicity.
  • We sought to characterize whether a non-toxic dose of d -limonene may enhance tumor response to docetaxel in an in vitro model of metastatic prostate cancer.
  • MATERIALS AND METHODS: Human prostate carcinoma DU-145 and normal prostate epithelial PZ-HPV-7 cells were treated with various concentrations of d -limonene, docetaxel or a combination of both, and cell viability was determined by MTT assay.
  • CONCLUSION: Our results show, for the first time, that d -limonene enhanced the antitumor effect of docetaxel against prostate cancer cells without being toxic to normal prostate epithelial cells.
  • The combined beneficial effect could be through the modulation of proteins involved in mitochondrial pathway of apoptosis. d -Limonene could be used as a potent non-toxic agent to improve the treatment outcome of hormone-refractory prostate cancer with docetaxel.

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  • (PMID = 19465777.001).
  • [ISSN] 1477-3163
  • [Journal-full-title] Journal of carcinogenesis
  • [ISO-abbreviation] J Carcinog
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2699604
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32. Cai C, Omwancha J, Hsieh CL, Shemshedini L: Androgen induces expression of the multidrug resistance protein gene MRP4 in prostate cancer cells. Prostate Cancer Prostatic Dis; 2007;10(1):39-45
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  • [Title] Androgen induces expression of the multidrug resistance protein gene MRP4 in prostate cancer cells.
  • Using a gene array analysis, we have identified MRP4 as an androgen receptor (AR)-regulated gene.
  • Dihydrotestosterone induced MRP4 expression in both androgen-dependent and -independent LNCaP cells, whereas there was little detectable expression in PC-3 or normal prostate epithelial cells.
  • Analysis of human tissues showed detectable MRP4 expression only in metastatic prostate cancer.
  • [MeSH-minor] Antimetabolites, Antineoplastic / pharmacology. Drug Resistance, Neoplasm / drug effects. Drug Resistance, Neoplasm / genetics. Gene Deletion. Humans. Male. Methotrexate / pharmacology. Receptors, Androgen / physiology. Tumor Cells, Cultured

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  • (PMID = 17003774.001).
  • [ISSN] 1365-7852
  • [Journal-full-title] Prostate cancer and prostatic diseases
  • [ISO-abbreviation] Prostate Cancer Prostatic Dis.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / ABCC4 protein, human; 0 / Antimetabolites, Antineoplastic; 0 / Multidrug Resistance-Associated Proteins; 0 / Receptors, Androgen; 08J2K08A3Y / Dihydrotestosterone; YL5FZ2Y5U1 / Methotrexate
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33. Dovio A, Sartori ML, De Francia S, Mussino S, Perotti P, Saba L, Abbadessa G, Racca S, Angeli A: Differential expression of determinants of glucocorticoid sensitivity in androgen-dependent and androgen-independent human prostate cancer cell lines. J Steroid Biochem Mol Biol; 2009 Aug;116(1-2):29-36
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  • [Title] Differential expression of determinants of glucocorticoid sensitivity in androgen-dependent and androgen-independent human prostate cancer cell lines.
  • Glucocorticoids (GCs) are widely used for the treatment of hormone refractory prostate cancer.
  • However, few data are available on the expression and regulation of glucocorticoid and mineralocorticoid receptors (GR and MR) and 11beta-hydroxysteroid dehydrogenase (11beta-HSD) 1 and -2 activities in prostate cancer cells.
  • Here we show that GR is expressed in both the androgen-independent PC-3 cell line and, at very low levels, in the androgen-dependent LNCaP cells, and MR is expressed in both cell lines.
  • Inhibition of IL-6 and OPG release by GCs may contribute to the antitumor efficacy in prostate cancer.

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  • (PMID = 19406240.001).
  • [ISSN] 1879-1220
  • [Journal-full-title] The Journal of steroid biochemistry and molecular biology
  • [ISO-abbreviation] J. Steroid Biochem. Mol. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Androgens; 0 / Antineoplastic Agents; 0 / Glucocorticoids; 0 / Interleukin-1beta; 0 / Osteoprotegerin; 0 / Receptors, Glucocorticoid; 0 / Receptors, Mineralocorticoid; EC 1.1.1.146 / 11-beta-Hydroxysteroid Dehydrogenase Type 1; EC 1.1.1.146 / 11-beta-Hydroxysteroid Dehydrogenase Type 2
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34. Azuma K, Nakashiro K, Sasaki T, Goda H, Onodera J, Tanji N, Yokoyama M, Hamakawa H: Anti-tumor effect of small interfering RNA targeting the androgen receptor in human androgen-independent prostate cancer cells. Biochem Biophys Res Commun; 2010 Jan 1;391(1):1075-9
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  • [Title] Anti-tumor effect of small interfering RNA targeting the androgen receptor in human androgen-independent prostate cancer cells.
  • Early phase prostate cancer is usually androgen-dependent, with the androgen/androgen receptor (AR) signaling pathway playing a central role.
  • At this stage, the cancer responds well to androgen ablation therapy, but prostate cancers eventually acquire androgen independence and more aggressive phenotypes.
  • To determine if the AR is a plausible therapeutic target, we investigated the anti-tumor effect of small interfering RNAs targeting the AR (siAR) in the human prostate cancer cells, LNCaP and 22Rv1, which express mutated AR.
  • These results suggest that the AR is still a key therapeutic target even in androgen-independent prostate cancer (AIPC).
  • [MeSH-major] Androgen Receptor Antagonists. Prostatic Neoplasms / therapy. RNA Interference. RNA, Small Interfering / genetics
  • [MeSH-minor] Androgens / genetics. Androgens / metabolism. Base Sequence. Cell Line, Tumor. Gene Knockdown Techniques. Humans. Male. Receptors, Androgen / genetics

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  • [Copyright] Copyright 2009 Elsevier Inc. All rights reserved.
  • (PMID = 20004643.001).
  • [ISSN] 1090-2104
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgen Receptor Antagonists; 0 / Androgens; 0 / RNA, Small Interfering; 0 / Receptors, Androgen
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35. Huang J, Wu C, di Sant'Agnese PA, Yao JL, Cheng L, Na Y: Function and molecular mechanisms of neuroendocrine cells in prostate cancer. Anal Quant Cytol Histol; 2007 Jun;29(3):128-38
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  • [Title] Function and molecular mechanisms of neuroendocrine cells in prostate cancer.
  • Benign prostate contains luminal epithelial cells, basal cells and a minor component of neuroendocrine cells whose function may be to regulate the growth, differentiation and secretory function of the prostate gland.
  • Neuroendocrine (NE) cells are also present in prostate cancer (PC), and many studies have shown that their number increases in high-grade and high-stage tumors, particularly in hormonally treated and hormone-refractory (androgen independent) PC.
  • Unlike the non-neuroendocrine secretory-type PC cells, NE cells lack androgen receptor and are likely androgen independent.
  • Therefore it is conceivable that hormonal therapy for advanced or metastatic prostate cancer, which consists of inhibiting androgen production or blocking androgen function, will not eliminate NE cancer cells.
  • Instead, these cells may be enriched after the therapy and they may establish paracrine networks to stimulate androgen-independent proliferation of PC, leading to tumor recurrence.
  • This article reviews the major functions of NE cells in PC, including stimulation of cancer proliferation and invasion, apoptosis resistance and angiogenesis.

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  • (PMID = 17672372.001).
  • [ISSN] 0884-6812
  • [Journal-full-title] Analytical and quantitative cytology and histology
  • [ISO-abbreviation] Anal. Quant. Cytol. Histol.
  • [Language] ENG
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 126
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36. Gaughan L, Logan IR, Neal DE, Robson CN: Regulation of androgen receptor and histone deacetylase 1 by Mdm2-mediated ubiquitylation. Nucleic Acids Res; 2005;33(1):13-26
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  • [Title] Regulation of androgen receptor and histone deacetylase 1 by Mdm2-mediated ubiquitylation.
  • The androgen receptor (AR) is a member of the nuclear hormone receptor family of transcription factors and plays a critical role in regulating the expression of genes involved in androgen-dependent and -independent tumour formation.
  • Using chromatin immunoprecipitation (ChIP) and re-ChIP analyses, we show that Mdm2 associates with AR and HDAC1 at the active androgen-responsive PSA promoter in LNCaP prostate cancer cells.
  • [MeSH-major] Histone Deacetylases / metabolism. Nuclear Proteins / physiology. Proto-Oncogene Proteins / physiology. Receptors, Androgen / metabolism. Ubiquitins / metabolism

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  • (PMID = 15640443.001).
  • [ISSN] 1362-4962
  • [Journal-full-title] Nucleic acids research
  • [ISO-abbreviation] Nucleic Acids Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Androgens; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins; 0 / Receptors, Androgen; 0 / Ubiquitins; EC 2.7.10.2 / Proto-Oncogene Proteins c-abl; EC 3.5.1.98 / Histone Deacetylases; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2
  • [Other-IDs] NLM/ PMC546130
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37. Funao K, Matsuyama M, Kawahito Y, Sano H, Chargui J, Touraine JL, Nakatani T, Yoshimura R: Telmisartan is a potent target for prevention and treatment in human prostate cancer. Oncol Rep; 2008 Aug;20(2):295-300
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  • [Title] Telmisartan is a potent target for prevention and treatment in human prostate cancer.
  • Recent studies have reported that ARBs have the potential to inhibit the growth of prostate cancer (PC) cells.
  • We used normal prostate stromal cell (NPC), human hormone-refractory PC (PC3), androgen-independent PC (DU-145) and androgen-dependent PC (LNCaP) cell lines.
  • [MeSH-minor] Flow Cytometry. Humans. Male. PPAR gamma / agonists. Prostate / metabolism. Tumor Cells, Cultured

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  • (PMID = 18636189.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Angiotensin II Type 1 Receptor Blockers; 0 / Benzimidazoles; 0 / Benzoates; 0 / PPAR gamma; U5SYW473RQ / telmisartan
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38. Wallner L, Dai J, Escara-Wilke J, Zhang J, Yao Z, Lu Y, Trikha M, Nemeth JA, Zaki MH, Keller ET: Inhibition of interleukin-6 with CNTO328, an anti-interleukin-6 monoclonal antibody, inhibits conversion of androgen-dependent prostate cancer to an androgen-independent phenotype in orchiectomized mice. Cancer Res; 2006 Mar 15;66(6):3087-95
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  • [Title] Inhibition of interleukin-6 with CNTO328, an anti-interleukin-6 monoclonal antibody, inhibits conversion of androgen-dependent prostate cancer to an androgen-independent phenotype in orchiectomized mice.
  • Initially, prostate cancer is androgen dependent.
  • However, most cases progress to an androgen-independent state through unknown mechanisms.
  • Interleukin-6 (IL-6) has been associated with prostate cancer progression including activation of the androgen receptor (AR).
  • To determine if IL-6 plays a role in the conversion of prostate cancer from androgen dependent to androgen independent, we established androgen-dependent LuCaP 35 human prostate cancer xenografts in nude mice, castrated the mice, and blocked IL-6 activity using a neutralizing antibody (CNT0328) for a period of 18 weeks.
  • IL-6 inhibition increased survival of mice and inhibited tumor growth, as reflected by decreased tumor volume and prostate-specific antigen levels, compared with that in mice receiving isotype control antibody.
  • To test the effect of IL-6 inhibition on the conversion from androgen dependent to androgen independent, tumor cells from the treated mice were assessed for their androgen dependence both in vitro and by implanting them into sham-operated or orchiectomized mice.
  • Tumor cells derived from the isotype-treated animals converted to androgen-independent state, whereas tumor cells from the anti-IL-6 antibody-treated mice were still androgen dependent in vitro and in vivo.
  • Although there was no difference in AR levels between the androgen-independent and androgen-dependent tumors, IL-6 inhibition promoted both apoptosis and inhibited cell proliferation in tumors and blocked the orchiectomy-induced expression of histone acetylases, p300 and CBP, which are AR cofactors.
  • These data show that IL-6 contributes to the development of androgen independence in prostate cancer and suggest that it mediates this effect, in part, through modulation of p300 and CBP.


39. Pai HH, Eldridge B, Bishop D, Alexander A, Lesperance M, Blood P, Lim J, Ludgate C: Does neoadjuvant hormone therapy improve outcome in prostate cancer patients receiving radiotherapy after radical prostatectomy? Can J Urol; 2009 Apr;16(2):4541-52
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  • [Title] Does neoadjuvant hormone therapy improve outcome in prostate cancer patients receiving radiotherapy after radical prostatectomy?
  • PURPOSE: To assess outcome and predictive factors in men with prostate cancer who receive post radical prostatectomy (RP) radiotherapy (RT) either in the adjuvant or salvage setting, with or without neoadjuvant androgen deprivation therapy (NADT).
  • METHODS: A retrospective analysis was performed on 175 patients with clinically localized prostate cancer treated with RP who subsequently received RT (dose range 50 Gy-68 Gy).
  • Outcome was assessed by biochemical disease free survival (BDFS), prostate cancer specific survival and overall survival (OS).
  • Significant independent predictive factors of improved BDFS were pre-RT PSA < or = 0.2 ng/ml, low Gleason score and positive surgical margins.
  • Age and Gleason score were independent predictors of OS.
  • [MeSH-major] Adenocarcinoma / drug therapy. Adenocarcinoma / surgery. Androgen Antagonists / therapeutic use. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / surgery
  • [MeSH-minor] Aged. Humans. Male. Middle Aged. Neoadjuvant Therapy. Prostate-Specific Antigen / blood. Prostatectomy. Radiotherapy Dosage. Radiotherapy, Adjuvant. Salvage Therapy. Treatment Outcome

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  • (PMID = 19364426.001).
  • [ISSN] 1195-9479
  • [Journal-full-title] The Canadian journal of urology
  • [ISO-abbreviation] Can J Urol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Canada
  • [Chemical-registry-number] 0 / Androgen Antagonists; EC 3.4.21.77 / Prostate-Specific Antigen
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40. Liao CP, Zhong C, Saribekyan G, Bading J, Park R, Conti PS, Moats R, Berns A, Shi W, Zhou Z, Nikitin AY, Roy-Burman P: Mouse models of prostate adenocarcinoma with the capacity to monitor spontaneous carcinogenesis by bioluminescence or fluorescence. Cancer Res; 2007 Aug 1;67(15):7525-33
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  • [Title] Mouse models of prostate adenocarcinoma with the capacity to monitor spontaneous carcinogenesis by bioluminescence or fluorescence.
  • The application of Cre/loxP technology has resulted in a new generation of conditional mouse models of prostate cancer.
  • Here, we describe the improvement of the conditional Pten deletion model of prostate adenocarcinoma by combining it with either a conditional luciferase or enhanced green fluorescent protein reporter line.
  • In the luciferase reporter model, the growth of the primary cancer can be followed noninvasively by bioluminescence imaging (BLI).
  • When castrated animals are maintained, the emergence of androgen depletion-independent cancer is detected using BLI at times varying from 7 to 28 weeks postcastration.
  • By comparing the distribution of phenotypically distinct populations of epithelial cells in cancer tissues, we noted that the degree of hyperplasia of cells with neuroendocrine differentiation significantly increases in the recurrent cancer relative to the primary cancer, a characteristic which may parallel the appearance of a neuroendocrine phenotype in human androgen depletion-independent cancer.
  • The enhanced green fluorescent protein model, at necropsy, can provide an opportunity to locate or assess tumor volume or to isolate enriched populations of cancer cells from tumor tissues via fluorescence-based technologies.
  • These refined models should be useful in the elucidation of mechanisms of prostate cancer progression, and for the development of approaches to preclinical intervention.


41. Lin Y, Fukuchi J, Hiipakka RA, Kokontis JM, Xiang J: Up-regulation of Bcl-2 is required for the progression of prostate cancer cells from an androgen-dependent to an androgen-independent growth stage. Cell Res; 2007 Jun;17(6):531-6
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  • [Title] Up-regulation of Bcl-2 is required for the progression of prostate cancer cells from an androgen-dependent to an androgen-independent growth stage.
  • However, the role of Bcl-2 in the progression of prostate cancer is not clear.
  • Here we report that Bcl-2 is required for the progression of LNCaP prostate cancer cells from an androgen-dependent to an androgen-independent growth stage.
  • The mRNA and protein levels of Bcl-2 are significantly increased in androgen-independent prostate cancer cells. shRNA-mediated gene silencing of Bcl-2 in androgen-independent prostate cancer cells promotes UV-induced apoptosis and suppresses the growth of prostate tumors in vivo.
  • Growing androgen-dependent cells under androgen-deprivation conditions results in formation of androgen-independent colonies; and the transition from androgen-dependent to androgen-independent growth is blocked by ectopic expression of the Bcl-2 antagonist Bax or Bcl-2 shRNA.
  • Thus, our results demonstrate that Bcl-2 is not only critical for the survival of androgen-independent prostate cancer cells, but is also required for the progression of prostate cancer cells from an androgen-dependent to an androgen-independent growth stage.

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  • (PMID = 17404601.001).
  • [ISSN] 1748-7838
  • [Journal-full-title] Cell research
  • [ISO-abbreviation] Cell Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / K01CA090516
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Androgens; 0 / Proto-Oncogene Proteins c-bcl-2
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42. Titus MA, Schell MJ, Lih FB, Tomer KB, Mohler JL: Testosterone and dihydrotestosterone tissue levels in recurrent prostate cancer. Clin Cancer Res; 2005 Jul 1;11(13):4653-7
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  • [Title] Testosterone and dihydrotestosterone tissue levels in recurrent prostate cancer.
  • PURPOSE: Prostate cancer eventually recurs during androgen deprivation therapy despite castrate levels of serum androgens.
  • Expression of androgen receptor and androgen receptor-regulated proteins suggests androgen receptor activation in recurrent prostate cancer.
  • Many groups have pursued mechanisms of ligand-independent androgen receptor activation but we found high levels of testicular androgens in recurrent prostate cancer tissue using RIA.
  • EXPERIMENTAL DESIGNS: Prostate specimens from 36 men were procured preserving blood flow to prevent ischemia and cyropreserved immediately.
  • Recurrent prostate cancer specimens from 18 men whose cancer recurred locally during androgen deprivation therapy and androgen-stimulated benign prostate specimens from 18 men receiving no hormonal treatments were studied.
  • RESULTS: Testosterone levels were similar in recurrent prostate cancer (3.75 pmol/g tissue) and androgen-stimulated benign prostate (2.75 pmol/g tissue, Wilcoxon two-sided, P=0.30).
  • Dihydrotestosterone levels decreased 91% in recurrent prostate cancer (1.25 pmol/g tissue) compared with androgen-stimulated benign prostate (13.7 pmol/g tissue; Wilcoxon two-sided, P < 0.0001) although dihydrotestosterone levels in most specimens of recurrent prostate cancer were sufficient for androgen receptor activation.
  • CONCLUSIONS: Recurrent prostate cancer may develop the capacity to biosynthesize testicular androgens from adrenal androgens or cholesterol.
  • This surprising finding suggests intracrine production of dihydrotestosterone and should be exploited for novel treatment of recurrent prostate cancer.


43. Sikand K, Slane SD, Shukla GC: Intrinsic expression of host genes and intronic miRNAs in prostate carcinoma cells. Cancer Cell Int; 2009;9:21
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  • [Title] Intrinsic expression of host genes and intronic miRNAs in prostate carcinoma cells.
  • BACKGROUND: Recent data show aberrant and altered expression of regulatory noncoding micro (mi) RNAs in prostate cancer (PCa).
  • Furthermore, whether expression of a subset of miRNAs is distinct in androgen-responsive and androgen-independent cells is not clear.
  • RESULTS: The expression profiling of miRNAs and host genes was performed in androgen-sensitive MDA PCa 2b and LNCaP as well as in androgen-refractory PC-3 and DU 145 cell culture models of PCa.
  • Androgen-sensitive MDA PCa 2b cells exhibited the highest level of expression of most miRNAs studied in this report.
  • The expressions of C13orf25 and miR 17-92 cluster as well as MCM7 and miR 106b-25 cluster did not reveal statistically significant correlation, thus suggesting that host genes and resident miRNAs may be expressed independent of each other.

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  • (PMID = 19674469.001).
  • [ISSN] 1475-2867
  • [Journal-full-title] Cancer cell international
  • [ISO-abbreviation] Cancer Cell Int.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2739157
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44. Eigl BJ, Eggener SE, Baybik J, Ettinger S, Chi KN, Nelson C, Wang Z, Gleave ME: Timing is everything: preclinical evidence supporting simultaneous rather than sequential chemohormonal therapy for prostate cancer. Clin Cancer Res; 2005 Jul 1;11(13):4905-11
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  • [Title] Timing is everything: preclinical evidence supporting simultaneous rather than sequential chemohormonal therapy for prostate cancer.
  • PURPOSE: Androgen ablation is the mainstay of systemic therapy for prostate cancer, with cytotoxic therapies reserved for hormone-refractory disease.
  • We explored the hypothesis that stress-induced gene expression changes after chemotherapy can induce a hormone-independent phenotype.
  • Gene expression and reverse transcription-PCR studies confirmed that several genes known to play a role in androgen independence were up-regulated in response to paclitaxel exposure.
  • CONCLUSIONS: In laboratory models of prostate cancer, simultaneous androgen deprivation plus paclitaxel is more effective than sequential treatments.
  • These findings provide preclinical proof-of-principle for ongoing clinical trials addressing the role and timing of systemic therapies in prostate cancer.

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  • (PMID = 16000589.001).
  • [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] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Antineoplastic Agents, Phytogenic; 0 / RNA, Messenger; P88XT4IS4D / Paclitaxel
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45. Berruti A, Mosca A, Tucci M, Terrone C, Torta M, Tarabuzzi R, Russo L, Cracco C, Bollito E, Scarpa RM, Angeli A, Dogliotti L: Independent prognostic role of circulating chromogranin A in prostate cancer patients with hormone-refractory disease. Endocr Relat Cancer; 2005 Mar;12(1):109-17
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  • [Title] Independent prognostic role of circulating chromogranin A in prostate cancer patients with hormone-refractory disease.
  • The presence of neuroendocrine (NE) differentiation in the context of predominantly exocrine prostate cancer may play a key role in androgen-independent tumor growth.
  • The prognostic significance of plasma chromogranin A (CgA) was assessed in a series of consecutive prostate cancer patients with hormone-refractory disease.
  • One hundred and eight patients with newly diagnosed hormone-refractory prostate cancer entered the study.
  • Plasma CgA levels and other biochemical parameters, such as serum prostate specific antigen, serum alkaline phosphatase, serum lactate dehydrogenase, serum albumin and hemoglobin concentration, were measured at baseline (i.e. when hormone refractoriness occurred) and their prognostic role was evaluated together with patient performance status, Gleason score (at diagnosis of prostate cancer) and the presence of visceral metastases.
  • Elevated plasma CgA levels are frequently observed in prostate cancer patients with hormone-refractory disease and correlate with poor prognosis.
  • [MeSH-minor] Aged. Aged, 80 and over. Albumins / metabolism. Alkaline Phosphatase / blood. Bone Neoplasms / blood. Bone Neoplasms / secondary. Cell Differentiation. Chromogranin A. Hemoglobins / metabolism. Humans. L-Lactate Dehydrogenase / blood. Liver Neoplasms / blood. Liver Neoplasms / secondary. Lung Neoplasms / blood. Lung Neoplasms / secondary. Male. Middle Aged. Neoplasm Staging. Prognosis. Prospective Studies. Prostate-Specific Antigen / blood. Survival Rate

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  • (PMID = 15788643.001).
  • [ISSN] 1351-0088
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Albumins; 0 / Biomarkers, Tumor; 0 / CHGA protein, human; 0 / Chromogranin A; 0 / Chromogranins; 0 / Hemoglobins; EC 1.1.1.27 / L-Lactate Dehydrogenase; EC 3.1.3.1 / Alkaline Phosphatase; EC 3.4.21.77 / Prostate-Specific Antigen
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46. Wang J, Eltoum IE, Lamartiniere CA: Genistein chemoprevention of prostate cancer in TRAMP mice. J Carcinog; 2007 Mar 16;6:3
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  • [Title] Genistein chemoprevention of prostate cancer in TRAMP mice.
  • Epidemiological studies suggest an inverse association between soy intake and prostate cancer risk.
  • To determine the most effective period for genistein chemoprevention, the Transgenic adenocarcinoma mouse prostate (TRAMP) model was used.
  • In a separate experiment in castrated TRAMP mice, dietary genistein suppressed the development of advanced prostate cancer by 35% compared with controls.
  • ICI 182,780 (ICI), genistein and estrogen down-regulated androgen receptor (AR), estrogen receptor alpha (ER-alpha) and progesterone receptor (PR) in the prostates of C57BL/6 mice, and act independently of ER.
  • Our data obtained in intact and castrated transgenic mice suggest that genistein may be a promising chemopreventive agent against androgen-dependent and independent prostate cancers.

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  • (PMID = 17367528.001).
  • [ISSN] 1477-3163
  • [Journal-full-title] Journal of carcinogenesis
  • [ISO-abbreviation] J Carcinog
  • [Language] ENG
  • [Grant] United States / NIEHS NIH HHS / ES / R01 ES011743
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Other-IDs] NLM/ PMC1832183
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47. Liu X, Gao R, Dong Y, Gao L, Zhao Y, Zhao L, Zhao X, Zhang H: Survivin gene silencing sensitizes prostate cancer cells to selenium growth inhibition. BMC Cancer; 2010 Aug 10;10:418
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  • [Title] Survivin gene silencing sensitizes prostate cancer cells to selenium growth inhibition.
  • BACKGROUND: Prostate cancer is a leading cause of cancer-related death in men worldwide.
  • Survivin is a member of the inhibitor of apoptosis (IAP) protein family that is expressed in the majority of human tumors including prostate cancer, but is barely detectable in terminally differentiated normal cells.
  • Downregulation of survivin could sensitize prostate cancer cells to chemotherapeutic agents in vitro and in vivo.
  • Several studies have shown that selenium compounds inhibit the growth of prostate cancer cells.
  • The objective of this study is to investigate whether survivin gene silencing in conjunction with selenium treatment could enhance the therapeutic efficacy for prostate cancer and to elucidate the underlying mechanisms.
  • In vitro studies were conducted in PC-3M, C4-2B, and 22Rv1 prostate cancer cells.
  • RESULTS: We found that survivin was undetectable in normal prostatic tissues but was highly expressed in prostate cancers.
  • Survivin knockdown or selenium treatment inhibited the growth of prostate cancer cells, but the selenium effect was modest.
  • In contrast to what have been observed in other cell lines, selenium treatment had little or no effect on survivin expression in several androgen-independent prostate cancer cell lines.
  • CONCLUSIONS: Selenium could inhibit the growth of hormone-refractory prostate cancer cells both in vitro and in vivo, but the effects were modest.

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  • (PMID = 20698994.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / K01 CA114252
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Birc5 protein, mouse; 0 / Inhibitor of Apoptosis Proteins; 0 / Organoselenium Compounds; 0 / RNA, Messenger; 0 / Repressor Proteins; 0CH9049VIS / Selenocysteine; 28274-57-9 / methylselenic acid; K848JZ4886 / Cysteine; TWK220499Z / selenomethylselenocysteine
  • [Other-IDs] NLM/ PMC2928796
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48. Lukacs RU, Lawson DA, Xin L, Zong Y, Garraway I, Goldstein AS, Memarzadeh S, Witte ON: Epithelial stem cells of the prostate and their role in cancer progression. Cold Spring Harb Symp Quant Biol; 2008;73:491-502
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  • [Title] Epithelial stem cells of the prostate and their role in cancer progression.
  • Prostate cancer is a leading cause of cancer-related death in adult men.
  • It can regress dramatically upon antihormonal therapy, but it often recurs in a more aggressive, androgen-independent form.
  • Defining the prostate tissue stem cells (PrSCs) and their involvement in cancer initiation and maintenance may lead to better therapeutics.
  • Using a tissue-regeneration model in which dissociated prostate epithelial cells mixed with inductive mesenchyme give rise to prostatic tubules, we have identified a small population of prostate cells that contains multiple stem cell characteristics.
  • In this system, prostate cancer can be initiated by autocrine or paracrine growth factor signaling and intracellular overexpression of genes often found mutated in human prostate cancer.
  • Using an in vitro prostate sphere assay, we further defined the PrSC population and demonstrated their self-renewal and multilineage differentiation capabilities.
  • Microarray analyses of the stem- and non-stem-cell populations have assisted us in finding and evaluating additional markers that can better define the PrSC population and further delineate the different cell types of the prostate, including those that serve as the target cell for tumor initiation.
  • [MeSH-major] Adult Stem Cells / cytology. Neoplastic Stem Cells / pathology. Prostate / cytology. Prostatic Neoplasms / pathology

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  • (PMID = 19022743.001).
  • [ISSN] 1943-4456
  • [Journal-full-title] Cold Spring Harbor symposia on quantitative biology
  • [ISO-abbreviation] Cold Spring Harb. Symp. Quant. Biol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1K99CA125937; United States / NCI NIH HHS / CA / K12-CA076905-09; United States / Howard Hughes Medical Institute / /
  • [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.; Review
  • [Publication-country] United States
  • [Number-of-references] 110
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49. Cocciadiferro L, Miceli V, Kang KS, Polito LM, Trosko JE, Carruba G: Profiling cancer stem cells in androgen-responsive and refractory human prostate tumor cell lines. Ann N Y Acad Sci; 2009 Feb;1155:257-62
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  • [Title] Profiling cancer stem cells in androgen-responsive and refractory human prostate tumor cell lines.
  • In this study, we investigated androgen metabolism in two different human prostate cancer cell lines, the androgen-responsive LNCaP cells and the nonresponsive PC3 cells.
  • Following 24-h and 72-h incubation with either testosterone (T) or androstenedione (Ad) used as precursor, divergent patterns and rates of androgen metabolism were observed.
  • Given the recent interest in the multiple uses of embryonic and adult stem cells for basic and applied research, we compared the expression of three presumptive stem cell markers (Oct-4, SUZ-12, and Cripto-1), along with connexin 43 (Cx43), Cx32, and androgen receptor (AR), used as cell differentiation gene markers.
  • In anchorage-independent cell growth conditions, the expression levels of candidate markers of cancer stem cells initially increased (days 2-4) but drastically fell thereafter (day 6) in both cell lines.
  • Our data suggest that both androgen-responsive and androgen-nonresponsive prostate tumor cell lines contain a presumptive cancer stem cell population that can be identified using a panel of selected gene markers, including Oct-4, SUZ-12, and Cripto-1.

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  • (PMID = 19250213.001).
  • [ISSN] 1749-6632
  • [Journal-full-title] Annals of the New York Academy of Sciences
  • [ISO-abbreviation] Ann. N. Y. Acad. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Biomarkers; 0 / DNA Primers
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50. Zhang YY, Wu LC, Wang ZP, Wang ZX, Jia Q, Jiang GS, Zhang WD: Anti-proliferation Effect of Polypeptide Extracted from Scorpion Venom on Human Prostate Cancer Cells in vitro. J Clin Med Res; 2009 Apr;1(1):24-31
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  • [Title] Anti-proliferation Effect of Polypeptide Extracted from Scorpion Venom on Human Prostate Cancer Cells in vitro.
  • BACKGROUND: Prostate cancer is a major cause of cancer-related death in men.
  • Polypeptide extracted from scorpion venom (PESV), originally obtained from the East-Asian scorpion Buthus martensi Karsch (BmK), is being studied for both prevention and treatment of various human malignancies including prostate cancer.
  • METHODS: The present study was to investigate the effect of PESV on cell proliferation, cell cycle, and apoptosis in human androgen-independent prostate cancer cells DU-145 in vitro.
  • CONCLUSIONS: These results suggest that PESV modulates the expression of cell cycle-related and apoptosis-related proteins and induces growth inhibition and apoptosis of DU145 cells, providing a strong rationale for future studies to evaluate prevention or/and intervention strategies for PESV in pre-clinical prostate cancer models.
  • KEYWORDS: Prostate cancer, PESV, cell proliferation, cell cycle, apoptosis.

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  • (PMID = 22505961.001).
  • [ISSN] 1918-3003
  • [Journal-full-title] Journal of clinical medicine research
  • [ISO-abbreviation] J Clin Med Res
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Canada
  • [Other-IDs] NLM/ PMC3318865
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51. Smith MR: Osteoclast targeted therapy for prostate cancer: bisphosphonates and beyond. Urol Oncol; 2008 Jul-Aug;26(4):420-5
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  • [Title] Osteoclast targeted therapy for prostate cancer: bisphosphonates and beyond.
  • Bone metastases are a major cause of morbidity for men with prostate cancer.
  • Although typical bone metastases from prostate cancer appear osteoblastic by radiographic imaging, excess number and activity of both osteoblasts and osteoclasts characterize most "osteoblastic" bone metastases.
  • Zoledronic acid, a potent intravenous bisphosphonate, reduces markers of osteoclast activity and significantly decreases the risk of skeletal complications in men with androgen-independent prostate cancer and bone metastases.
  • Three ongoing pivotal studies involving more than 4,500 subjects will evaluate the role of denosumab for prevention of treatment-related fractures, bone metastases, and disease-related skeletal complications in men with prostate cancer.

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  • (PMID = 18593621.001).
  • [ISSN] 1078-1439
  • [Journal-full-title] Urologic oncology
  • [ISO-abbreviation] Urol. Oncol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA121990-03; United States / NCI NIH HHS / CA / K24 CA121990; United States / NCI NIH HHS / CA / K24 CA121990-02; United States / NCI NIH HHS / CA / 1K24CA121990-01A1; United States / NCI NIH HHS / CA / K24 CA121990-03; United States / NCI NIH HHS / CA / CA121990-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Diphosphonates; 0 / RANK Ligand; 0 / TNFSF11 protein, human; 4EQZ6YO2HI / Denosumab
  • [Number-of-references] 27
  • [Other-IDs] NLM/ NIHMS272559; NLM/ PMC3090666
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52. 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.

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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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53. Slack-Davis JK, Hershey ED, Theodorescu D, Frierson HF, Parsons JT: Differential requirement for focal adhesion kinase signaling in cancer progression in the transgenic adenocarcinoma of mouse prostate model. Mol Cancer Ther; 2009 Aug;8(8):2470-7
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  • [Title] Differential requirement for focal adhesion kinase signaling in cancer progression in the transgenic adenocarcinoma of mouse prostate model.
  • Increasing evidence indicates that adhesion signaling plays an important role in the tumor microenvironment, contributing to cancer progression, invasion, and metastasis.
  • Focal adhesion kinase (FAK) is a nonreceptor protein tyrosine kinase that regulates adhesion-dependent cell signaling and has been implicated in mediating steps in cancer progression and metastasis in many human cancers, including prostate.
  • We have investigated the role of FAK in the appearance of adenocarcinoma (atypical epithelial hyperplasia of T antigen) and neuroendocrine carcinomas in the transgenic adenocarcinoma of mouse prostate (TRAMP) model using either Cre-mediated recombination to genetically ablate FAK expression or pharmacologic inhibition of FAK activity with the small-molecule inhibitor, PF-562,271.
  • However, continued FAK expression (and activity) is essential for the androgen-independent formation of neuroendocrine carcinoma.
  • These data indicate that integrin signaling through FAK is an important component of cancer progression in the TRAMP model and suggest that treatment modalities targeting FAK may be an appropriate strategy for patients with castrate-resistant cancer.

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  • (PMID = 19671741.001).
  • [ISSN] 1538-8514
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA040042-230002; United States / NCI NIH HHS / CA / CA 40042; United States / NCI NIH HHS / CA / P01 CA040042-230002; United States / NCI NIH HHS / CA / CA104106-04; United States / NCI NIH HHS / CA / P01 CA104106-04; United States / NCI NIH HHS / CA / CA 104106; United States / NCI NIH HHS / CA / P01 CA104106; United States / NCI NIH HHS / CA / P01 CA040042
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.2 / Focal Adhesion Protein-Tyrosine Kinases
  • [Other-IDs] NLM/ NIHMS128025; NLM/ PMC2728172
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54. Lin FM, Tsai CH, Yang YC, Tu WC, Chen LR, Liang YS, Wang SY, Shyur LF, Chien SC, Cha TL, Hsiao PW: A novel diterpene suppresses CWR22Rv1 tumor growth in vivo through antiproliferation and proapoptosis. Cancer Res; 2008 Aug 15;68(16):6634-42
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  • Androgen receptor (AR) is the main therapeutic target for treatment of metastatic prostate cancers (PCa).
  • As recurrent tumors restore AR activity independent of hormones, new therapies that abolish AR activity have been sought to prevent or delay the emergence of ablation-resistant disease.
  • HDHS treatment of androgen-dependent LNCaP and androgen-responsive 22Rv1 cells induced apoptosis as shown by nucleosome release, activation of caspase-3 and caspase-7, and cleavage of poly(ADP-ribose) polymerase accompanied with concomitant up-regulation of tumor suppressor p53.
  • [MeSH-minor] Administration, Oral. Androgen Receptor Antagonists. Animals. Cryptomeria / chemistry. Cyclin-Dependent Kinases / metabolism. Cyclins / metabolism. G1 Phase / drug effects. Humans. Male. Mice. Mice, Nude. Plant Bark / chemistry. Receptors, Androgen / genetics. Tumor Cells, Cultured. Xenograft Model Antitumor Assays


55. Yan X, Shen H, Jiang H, Zhang C, Hu D, Wang J, Wu X: External Qi of Yan Xin Qigong induces G2/M arrest and apoptosis of androgen-independent prostate cancer cells by inhibiting Akt and NF-kappa B pathways. Mol Cell Biochem; 2008 Mar;310(1-2):227-34
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  • [Title] External Qi of Yan Xin Qigong induces G2/M arrest and apoptosis of androgen-independent prostate cancer cells by inhibiting Akt and NF-kappa B pathways.
  • In order to understand the molecular mechanisms underlying the antitumor effects of YXQG-EQ, we investigate the effects of YXQG-EQ on growth and apoptosis in androgen-independent prostate cancer PC3 cells.
  • These results indicate that YXQG-EQ has profound effects on growth and apoptosis of prostate cancer cells by targeting survival pathways including the Akt and NF-kappa B pathways.


56. Nakamura Y, Suzuki T, Arai Y, Sasano H: Nuclear receptor DAX1 in human prostate cancer: a novel independent biological modulator. Endocr J; 2009;56(1):39-44
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  • [Title] Nuclear receptor DAX1 in human prostate cancer: a novel independent biological modulator.
  • Prostate cancer is also sex steroid-dependent tumor in which androgens play important roles in the pathogenesis and development via androgen receptor (AR).
  • DAX1 is also reported to repress AR activity in human prostate cancer cell line (LNCaP) but its biological roles have remained unclear in the human prostate cancer.
  • The aim of this study is to examine the expression of DAX1 in human prostate cancer using immunohistochemistry in order to evaluate its possible biological and/or clinical significance.
  • In this study, we examined the DAX1 immunoreactivity in human prostate cancer obtained from surgery (n = 40), and correlated the findings with clinicopathological features of the patients.
  • DAX1 immunoreactivity is considered a new biological modulator of human prostate cancer, but independent to the status of sex steroid receptors in human prostate cancer tissues.
  • [MeSH-minor] Aged. Biomarkers, Tumor / metabolism. Biomarkers, Tumor / physiology. DAX-1 Orphan Nuclear Receptor. Disease Progression. Estrogen Receptor beta / metabolism. Female. Humans. Male. Middle Aged. Neoplasm Staging. Receptors, Androgen / metabolism. Receptors, Progesterone / metabolism

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  • (PMID = 18827407.001).
  • [ISSN] 1348-4540
  • [Journal-full-title] Endocrine journal
  • [ISO-abbreviation] Endocr. J.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / AR protein, human; 0 / Biomarkers, Tumor; 0 / DAX-1 Orphan Nuclear Receptor; 0 / DNA-Binding Proteins; 0 / Estrogen Receptor beta; 0 / NR0B1 protein, human; 0 / Receptors, Androgen; 0 / Receptors, Progesterone; 0 / Receptors, Retinoic Acid; 0 / Repressor Proteins
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57. Bryant RJ, Cross NA, Eaton CL, Hamdy FC, Cunliffe VT: EZH2 promotes proliferation and invasiveness of prostate cancer cells. Prostate; 2007 Apr 01;67(5):547-56
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  • [Title] EZH2 promotes proliferation and invasiveness of prostate cancer cells.
  • EZH2 expression in prostate cancer correlates with progression to hormone-refractory and metastatic disease, but it is unknown whether EZH2 plays a specific role in the acquisition of an advanced prostate cancer phenotype.
  • METHODS: Using siRNA knockdown, we investigated the role of EZH2 in maintenance of prostate cancer cell proliferation and invasiveness.
  • RESULTS: Knockdown of endogenous EZH2 reduced proliferation of androgen-responsive and androgen-independent prostate cancer cells.
  • EZH2 knockdown also inhibited prostate cancer cell invasion.
  • However, overexpression of EZH2 in androgen-responsive cancer cells did not appreciably affect either proliferation or invasiveness.
  • CONCLUSIONS: EZH2 promotes proliferation and invasion of prostate cancer cells, which can account for the correlation between EZH2 expression levels and an adverse prostate cancer prognosis.
  • [MeSH-minor] Androgen Antagonists / pharmacology. Anilides / pharmacology. Cell Growth Processes / physiology. Cell Line, Tumor. Enhancer of Zeste Homolog 2 Protein. Histocytochemistry. Humans. Male. Nitriles / pharmacology. Polycomb Repressive Complex 2. RNA, Small Interfering / genetics. Tosyl Compounds / pharmacology. Transcription, Genetic. Transfection

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  • (PMID = 17252556.001).
  • [ISSN] 0270-4137
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G84/6456
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Anilides; 0 / DNA-Binding Proteins; 0 / Nitriles; 0 / RNA, Small Interfering; 0 / Tosyl Compounds; 0 / Transcription Factors; A0Z3NAU9DP / bicalutamide; EC 2.1.1.43 / EZH2 protein, human; EC 2.1.1.43 / Enhancer of Zeste Homolog 2 Protein; EC 2.1.1.43 / Polycomb Repressive Complex 2
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58. Jia RP, Xu LW, Su Q, Zhao JH, Li WC, Wang F, Xu Z: Cyclooxygenase-2 expression is dependent upon epidermal growth factor receptor expression or activation in androgen independent prostate cancer. Asian J Androl; 2008 Sep;10(5):758-64
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  • [Title] Cyclooxygenase-2 expression is dependent upon epidermal growth factor receptor expression or activation in androgen independent prostate cancer.
  • AIM: To investigate the expression of cyclooxygenase-2 (COX-2) and epidermal growth factor receptor (EGFR) and the possible mechanism in the development in androgen independent prostate cancer (AIPC).
  • METHODS: Immunohistochemistry was performed on paraffin-embedded sections with goat polyclonal against COX-2 and mouse monoclonal antibody against EGFR in 30 AIPC and 18 androgen dependent prostate cancer (ADPC) specimens.
  • RESULTS: COX-2 was positively expressed in AIPC and ADPC, which were predominantly in endochylema of prostate cancer (PCa) cells.


59. Amato RJ, Sarao H: A phase I study of paclitaxel/doxorubicin/ thalidomide in patients with androgen- independent prostate cancer. Clin Genitourin Cancer; 2006 Mar;4(4):281-6
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  • [Title] A phase I study of paclitaxel/doxorubicin/ thalidomide in patients with androgen- independent prostate cancer.
  • PURPOSE: The antiangiogenic and immunomodulatory effects of thalidomide induce responses in patients with androgen-independent prostate cancer (AIPC).
  • A phase I dose-escalation study was conducted to evaluate the use of these agents in combination to enhance the chemotherapeutic effects of treatment for refractory cancer.
  • PATIENTS AND METHODS: Twelve men with AIPC (mean age, 64.5 years) and a median prostate-specific antigen (PSA) level of 30 ng/mL were enrolled.
  • [MeSH-minor] Aged. Androgens / physiology. Angiogenesis Inhibitors / administration & dosage. Angiogenesis Inhibitors / adverse effects. Antibiotics, Antineoplastic / administration & dosage. Antibiotics, Antineoplastic / adverse effects. Antineoplastic Agents, Phytogenic / administration & dosage. Antineoplastic Agents, Phytogenic / adverse effects. Dose-Response Relationship, Drug. Doxorubicin / administration & dosage. Doxorubicin / adverse effects. Humans. Immunologic Factors / administration & dosage. Immunologic Factors / adverse effects. Male. Middle Aged. Paclitaxel / administration & dosage. Paclitaxel / adverse effects. Prostate-Specific Antigen / blood. Thalidomide / administration & dosage. Thalidomide / adverse effects. Treatment Outcome

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  • (PMID = 16729912.001).
  • [ISSN] 1558-7673
  • [Journal-full-title] Clinical genitourinary cancer
  • [ISO-abbreviation] Clin Genitourin Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase I; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Angiogenesis Inhibitors; 0 / Antibiotics, Antineoplastic; 0 / Antineoplastic Agents, Phytogenic; 0 / Immunologic Factors; 4Z8R6ORS6L / Thalidomide; 80168379AG / Doxorubicin; EC 3.4.21.77 / Prostate-Specific Antigen; P88XT4IS4D / Paclitaxel
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60. Lange CA, Gioeli D, Hammes SR, Marker PC: Integration of rapid signaling events with steroid hormone receptor action in breast and prostate cancer. Annu Rev Physiol; 2007;69:171-99
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  • [Title] Integration of rapid signaling events with steroid hormone receptor action in breast and prostate cancer.
  • Steroid hormone receptors (SRs) are ligand-activated transcription factors and sensors for growth factor-initiated signaling pathways in hormonally regulated tissues, such as the breast or prostate.
  • Alternatively, SR-activated kinase cascades provide additional avenues for SR-regulated gene expression independent of SR nuclear action.
  • We provide an overview of SR and signaling cross talk in breast and prostate cancers, using the human progesterone receptor (PR) and androgen receptor (AR) as models.
  • Cross talk between SR and membrane-initiated signaling events suggests a mechanism for coordinate regulation of gene subsets by mitogenic stimuli in hormonally responsive normal tissues; such cross talk is suspected to contribute to cancer biology.
  • [MeSH-minor] Androgens / physiology. Female. Humans. Male. Receptor Cross-Talk / physiology. Receptors, Androgen / physiology. Receptors, Progesterone / physiology

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  • (PMID = 17037979.001).
  • [ISSN] 0066-4278
  • [Journal-full-title] Annual review of physiology
  • [ISO-abbreviation] Annu. Rev. Physiol.
  • [Language] eng
  • [Grant] United States / NIA NIH HHS / AG / AG024278; United States / NCI NIH HHS / CA / CA123763; United States / NIDDK NIH HHS / DK / DK069662; United States / NIDDK NIH HHS / DK / DK53825; United States / NIDDK NIH HHS / DK / DK59913
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Receptors, Androgen; 0 / Receptors, Progesterone; 0 / Receptors, Steroid
  • [Number-of-references] 151
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61. Shanmugam R, Jayaprakasan V, Gokmen-Polar Y, Kelich S, Miller KD, Yip-Schneider M, Cheng L, Bhat-Nakshatri P, Sledge GW Jr, Nakshatri H, Zheng QH, Miller MA, DeGrado T, Hutchins GD, Sweeney CJ: Restoring chemotherapy and hormone therapy sensitivity by parthenolide in a xenograft hormone refractory prostate cancer model. Prostate; 2006 Oct 1;66(14):1498-511
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  • [Title] Restoring chemotherapy and hormone therapy sensitivity by parthenolide in a xenograft hormone refractory prostate cancer model.
  • METHODS: The in vitro effects of P were assessed using the androgen independent cell line, CWR22Rv1, and human umbilical endothelial cells (HUVECs).
  • The in vivo activity of P as a single agent and its ability to augment the efficacy of docetaxel and the anti-androgen, bicalutamide, were determined using the CWR22Rv1 xenograft model.
  • Parthenolide also augmented the in vivo efficacy of docetaxel and restored sensitivity to anti-androgen therapy.
  • [MeSH-minor] Androgen Antagonists / pharmacology. Anilides / pharmacology. Animals. Antineoplastic Agents, Phytogenic / pharmacology. Bridged Compounds / pharmacology. Cell Line, Tumor. Drug Synergism. Endothelium, Vascular / cytology. Endothelium, Vascular / drug effects. Fibroblast Growth Factor 2 / metabolism. Humans. JNK Mitogen-Activated Protein Kinases / metabolism. Male. Mice. Mice, Nude. NF-kappa B / metabolism. Nitriles. TNF Receptor-Associated Factor 1 / metabolism. TNF Receptor-Associated Factor 2 / metabolism. Taxoids / pharmacology. Tosyl Compounds. Umbilical Veins / cytology. Vascular Endothelial Growth Factor A / metabolism

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  • [Copyright] (c) 2006 Wiley-Liss, Inc.
  • (PMID = 16921510.001).
  • [ISSN] 0270-4137
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P20 CA86350
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Anilides; 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Antineoplastic Agents, Phytogenic; 0 / Bridged Compounds; 0 / NF-kappa B; 0 / Nitriles; 0 / Sesquiterpenes; 0 / TNF Receptor-Associated Factor 1; 0 / TNF Receptor-Associated Factor 2; 0 / Taxoids; 0 / Tosyl Compounds; 0 / Vascular Endothelial Growth Factor A; 103107-01-3 / Fibroblast Growth Factor 2; 15H5577CQD / docetaxel; 1605-68-1 / taxane; 2RDB26I5ZB / parthenolide; A0Z3NAU9DP / bicalutamide; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases
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62. Helley D, Banu E, Bouziane A, Banu A, Scotte F, Fischer AM, Oudard S: Platelet microparticles: a potential predictive factor of survival in hormone-refractory prostate cancer patients treated with docetaxel-based chemotherapy. Eur Urol; 2009 Sep;56(3):479-84
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  • [Title] Platelet microparticles: a potential predictive factor of survival in hormone-refractory prostate cancer patients treated with docetaxel-based chemotherapy.
  • BACKGROUND: Several studies suggest a causal relationship between platelet activation and cancer metastasis.
  • OBJECTIVE: We conducted a prospective, nonrandomised, single-centre study in hormone-refractory prostate cancer (HRPC) patients to determine the impact of PMPs on the outcome.
  • In the multivariate analysis, only baseline prostate-specific antigen (PSA) and ECOG PS remained significantly predictive of risk of death.
  • A biologic association between PMPs and the OS of HRPC patients, independent of chemotherapy regimen, should be demonstrated by confirmatory prospective studies.
  • [MeSH-minor] Aged. Aged, 80 and over. Androgen Antagonists / therapeutic use. Humans. Male. Middle Aged. Orchiectomy. Prognosis. Prospective Studies. Survival Rate. Treatment Failure


63. Gonzalez-Moreno O, Segura V, Serrano D, Nguewa P, de las Rivas J, Calvo A: Methylseleninic acid enhances the effect of etoposide to inhibit prostate cancer growth in vivo. Int J Cancer; 2007 Sep 15;121(6):1197-204
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  • [Title] Methylseleninic acid enhances the effect of etoposide to inhibit prostate cancer growth in vivo.
  • New therapeutic agents are needed for the treatment of androgen-independent prostate cancer (PrCa).
  • We have investigated the effect of methylseleninic acid (MSA) on tumor stage-specific prostate cells derived from the C3 (1)/Tag model for PrCa: Pr111, a slow-growing and nontumorigenic cell line isolated from a prostate intraepithelial neoplasia lesion; Pr14, a tumorigenic line derived from a primary tumor; and Pr14C1, a sub-clone of Pr14 explanted from a lung metastasis.


64. Huss WJ, Gray DR, Tavakoli K, Marmillion ME, Durham LE, Johnson MA, Greenberg NM, Smith GJ: Origin of androgen-insensitive poorly differentiated tumors in the transgenic adenocarcinoma of mouse prostate model. Neoplasia; 2007 Nov;9(11):938-50
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  • [Title] Origin of androgen-insensitive poorly differentiated tumors in the transgenic adenocarcinoma of mouse prostate model.
  • Following castration, the transgenic adenocarcinoma of mouse prostate (TRAMP) model demonstrates rapid development of SV40-Tag-driven poorly differentiated tumors that express neuroendocrine cell markers.
  • The cell population dynamics within the prostates of castrated TRAMP mice were characterized by analyzing the incorporation of 5-bromodeoxyuridine (BrdUrd) and the expression of SV40-Tag, synaptophysin, and androgen receptor (AR).
  • These foci expanded rapidly in the postcastration prostate environment, in contrast to the AR- and SV40-Tag-expressing adenocarcinoma cells that lost SV40-Tag expression and underwent apoptosis after castration.
  • This suggests that the foci of neuroendocrine-like cells that express SV40-Tag and synaptophysin, but lack AR, arise independent of androgen-deprivation and represent the source of the poorly differentiated tumors that are the lethal phenotype in the TRAMP model.

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  • (PMID = 18030362.001).
  • [ISSN] 1476-5586
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA064851; United States / NCI NIH HHS / CA / CA84296; United States / NCI NIH HHS / CA / U01 CA084296; United States / NCI NIH HHS / CA / P01 CA077739; United States / NCI NIH HHS / CA / CA77739; United States / NCI NIH HHS / CA / CA64851
  • [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 / Antigens, Polyomavirus Transforming; 0 / Foxa2 protein, mouse; 0 / Receptors, Androgen; 0 / Synaptophysin; 135845-92-0 / Hepatocyte Nuclear Factor 3-beta; G34N38R2N1 / Bromodeoxyuridine
  • [Other-IDs] NLM/ PMC2077885
  • [Keywords] NOTNLM ; Prostate cancer / TRAMP / androgen-insensitive / neuroendocrine / synaptophysin
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65. Gleave M, Miyake H, Chi K: Beyond simple castration: targeting the molecular basis of treatment resistance in advanced prostate cancer. Cancer Chemother Pharmacol; 2005 Nov;56 Suppl 1:47-57
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  • [Title] Beyond simple castration: targeting the molecular basis of treatment resistance in advanced prostate cancer.
  • Over the past 20 years, research on hormonal treatments for prostate cancer focused on maximizing androgen ablation through combination therapy.
  • Unfortunately, maximal androgen ablation increases treatment-related side effects and expense and has not significantly prolonged time to androgen-independent (AI) progression.
  • Intermittent androgen suppression (IAS) is based on the hypothesis that if tumor cells surviving androgen withdrawal can be forced along a normal pathway of differentiation by androgen replacement, then apoptotic potential might be restored, androgen dependence may be prolonged and progression to androgen independence may be delayed.
  • Observations from animal model studies suggest that progression to androgen independence is delayed by IAS and this strategy is now being evaluated in phase III trials.
  • Another strategy for improving therapies in advanced prostate cancer involves targeting genes that are activated by either androgen withdrawal or chemotherapy to delay or prevent the emergence of the resistant AI phenotype.
  • Targeted inhibition of stress-associated increases in gene expression precipitated by androgen withdrawal or chemotherapy may enhance treatment-induced apoptosis and delay progression to AI disease.
  • The purpose of this paper is to review the rationale and progress in using targeted gene therapies to enhance tumor cell death after androgen withdrawal or taxane chemotherapy.
  • Antisense oligonucleotides offer one approach to target genes involved in cancer progression, especially those not amenable to small molecule or antibody inhibition.
  • The current status and future direction of several antisense oligonucleotides that have potential clinical use in cancer are also reviewed.


66. Small EJ, Ryan CJ: The case for secondary hormonal therapies in the chemotherapy age. J Urol; 2006 Dec;176(6 Pt 2):S66-71
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  • PURPOSE: Virtually all patients with high risk localized and metastatic prostate cancer who are treated with androgen deprivation therapy eventually have progressive clinical or biochemical disease despite this therapy.
  • Despite this fact numerous therapies are available that target the interaction of androgen and androgen receptor in the castrate testosterone milieu and many clinical investigations are under way in this area.
  • RESULTS: Despite low androgen levels the androgen receptor remains active through the amplification, mutation or alteration of coactivator function.
  • Furthermore, in the context of androgen independent tumor growth in patients with metastatic disease clinicians are now faced with the choice of using chemotherapy or secondary hormonal manipulations.
  • CONCLUSIONS: The modest activity of these secondary therapies challenges the notion that advancing prostate cancer uniformly becomes hormone refractory.
  • It offers an alternative to the early use of chemotherapy in patients with androgen independent disease.
  • [MeSH-major] Androgen Antagonists / therapeutic use. Antineoplastic Agents / therapeutic use. Prostatic Neoplasms / drug therapy

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  • (PMID = 17084172.001).
  • [ISSN] 0022-5347
  • [Journal-full-title] The Journal of urology
  • [ISO-abbreviation] J. Urol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Antineoplastic Agents
  • [Number-of-references] 39
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67. Chowdhury SK, Raha S, Tarnopolsky MA, Singh G: Increased expression of mitochondrial glycerophosphate dehydrogenase and antioxidant enzymes in prostate cancer cell lines/cancer. Free Radic Res; 2007 Oct;41(10):1116-24
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  • [Title] Increased expression of mitochondrial glycerophosphate dehydrogenase and antioxidant enzymes in prostate cancer cell lines/cancer.
  • The involvement of mitochondrial glycerophosphate dehydrogenase (mGPDH) has previously been established in the production of ROS in prostate cancer cell lines (LNCaP, DU145, PC3 and CL1).
  • The current study demonstrates that the mRNA level of mGPDH in prostate cancer cells is 3.3-8.9-fold higher compared to the normal prostate epithelial cell line, PNT1A.
  • However, cytochrome c oxidase (COX) activity is 2.9-3.2-fold down-regulated in androgen-independent prostate cancer cell lines.
  • The level of antioxidant enzymes, catalase, MnSOD and CuZnSOD are up-regulated in prostate cancer cell lines.
  • Furthermore, it was observed that the activity of mGPDH is significantly higher in liver tissues from all mice with cancer compared to liver tissues from control mice.
  • These data suggest that the up-regulation of mGPDH, due to a highly glycolytic environment, contributes to the overall increase in ROS generation and may result in the progression of the cancer.

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  • (PMID = 17886033.001).
  • [ISSN] 1071-5762
  • [Journal-full-title] Free radical research
  • [ISO-abbreviation] Free Radic. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antioxidants; EC 1.1.- / Glycerolphosphate Dehydrogenase
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68. Tan W: [Promising new treatment options for metastatic androgen-independent prostate cancer]. Actas Urol Esp; 2007 Jun;31(6):680-5
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  • [Title] [Promising new treatment options for metastatic androgen-independent prostate cancer].
  • OBJECTIVE: Review the recent advances in the treatment of androgen independent prostate cancer (AIPC).
  • METHODS: Review recent abstracts and literature utilizing Medline/PubMed using key words: androgen independent/hormone refractory prostate cancer, novel treatment options, Phase II, III trials and meeting abstracts/presentations.
  • Despite this, there is a need to improve on this survival benefit because the relapse free survival among responders is often short (6 months) and patients often would have progression of their cancer leading to death.
  • [MeSH-minor] Animals. Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Humanized. Antineoplastic Agents, Phytogenic / administration & dosage. Antineoplastic Agents, Phytogenic / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Benzamides. Benzenesulfonates / therapeutic use. Bevacizumab. Calcitriol / administration & dosage. Cancer Vaccines / therapeutic use. Drug Screening Assays, Antitumor. Epothilones / therapeutic use. Forecasting. Humans. Imatinib Mesylate. Male. Niacinamide / analogs & derivatives. Phenylurea Compounds. Piperazines / administration & dosage. Pyridines / therapeutic use. Pyrimidines / administration & dosage. Pyrrolidines / therapeutic use. Randomized Controlled Trials as Topic. Salvage Therapy. Taxoids / administration & dosage. Taxoids / therapeutic use. Thionucleotides / therapeutic use

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  • (PMID = 17896565.001).
  • [ISSN] 0210-4806
  • [Journal-full-title] Actas urologicas españolas
  • [ISO-abbreviation] Actas Urol Esp
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents, Phytogenic; 0 / Benzamides; 0 / Benzenesulfonates; 0 / Cancer Vaccines; 0 / Epothilones; 0 / Phenylurea Compounds; 0 / Piperazines; 0 / Pyridines; 0 / Pyrimidines; 0 / Pyrrolidines; 0 / Taxoids; 0 / Thionucleotides; 15H5577CQD / docetaxel; 25X51I8RD4 / Niacinamide; 2S9ZZM9Q9V / Bevacizumab; 85J5ZP6YSL / oblimersen; 8A1O1M485B / Imatinib Mesylate; 9ZOQ3TZI87 / sorafenib; FXC9231JVH / Calcitriol; K27005NP0A / ixabepilone; V6D7VK2215 / atrasentan
  • [Number-of-references] 28
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69. Chen S, Gao J, Halicka HD, Traganos F, Darzynkiewicz Z: Down-regulation of androgen-receptor and PSA by phytochemicals. Int J Oncol; 2008 Feb;32(2):405-11
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  • [Title] Down-regulation of androgen-receptor and PSA by phytochemicals.
  • The androgen receptor (AR) signaling pathway continues to be active in hormone resistant prostate cancer (HRPC) and can inappropriately activate transcription.
  • In each case, these compounds have independent activities which may partly contribute to the biological activity of PC-SPES.

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  • (PMID = 18202763.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA028704; United States / NCI NIH HHS / CA / CA028704-29; None / None / / R01 CA028704-28; United States / NCI NIH HHS / CA / R01 CA028704-28; United States / NCI NIH HHS / CA / R01 CA028704-29
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Chalcones; 0 / Diterpenes; 0 / Diterpenes, Kaurane; 0 / Flavanones; 0 / Plant Extracts; 0 / Receptors, Androgen; 0APJ98UCLQ / oridonin; 632-85-9 / wogonin; B9CTI9GB8F / isoliquiritigenin; EC 3.4.21.77 / Prostate-Specific Antigen
  • [Other-IDs] NLM/ NIHMS75220; NLM/ PMC2586941
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70. Salah Z, Maoz M, Cohen I, Pizov G, Pode D, Runge MS, Bar-Shavit R: Identification of a novel functional androgen response element within hPar1 promoter: implications to prostate cancer progression. FASEB J; 2005 Jan;19(1):62-72
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  • [Title] Identification of a novel functional androgen response element within hPar1 promoter: implications to prostate cancer progression.
  • We have identified a functional androgen response element (ARE) located in the hPar1 promoter upstream of the transcription start site at -1791 to -1777.
  • Dihydrotestosterone treatment of the prostate cancer cell line LNCaP increased endogenous hPar1 mRNA levels, consistent with the threefold increase in promoter activity of hPar1-luciferase reporter construct.
  • In parallel, we show that hormone ablation therapy markedly reduces the otherwise high hPar1 expression levels in prostate cancer biopsy specimens.
  • A major limitation of hormonal deprivation is that it causes only a temporary remission, and the cancer eventually reappears in a more malignant, androgen-independent form. hPar1 is also overexpressed in CL1 cells, an aggressively metastasizing, hormone-independent subclone of LNCaP, and in PC3 prostate adenocarcinoma lacking AR in a mechanism yet to be fully elucidated.
  • These data may imply that hPar1 expression correlates with prostate cancer progression in androgen-dependent and -independent phases and therefore, provides an instrumental, therapeutic target for treatment in prostate cancer.
  • [MeSH-minor] Androgen Antagonists / pharmacology. Androgen Antagonists / therapeutic use. Antineoplastic Agents, Hormonal / pharmacology. Antineoplastic Agents, Hormonal / therapeutic use. Base Composition / genetics. Base Sequence. Cell Line, Tumor. Chromatin Immunoprecipitation / methods. DNA / metabolism. Disease Progression. Gene Expression Regulation, Neoplastic / drug effects. Gene Expression Regulation, Neoplastic / physiology. Humans. Male. Molecular Sequence Data. Protein Binding / drug effects

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  • (PMID = 15629896.001).
  • [ISSN] 1530-6860
  • [Journal-full-title] FASEB journal : official publication of the Federation of American Societies for Experimental Biology
  • [ISO-abbreviation] FASEB J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Androgens; 0 / Antineoplastic Agents, Hormonal; 0 / Receptor, PAR-1; 9007-49-2 / DNA
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71. Le Page C, Karakiewicz PI, Mes-Masson AM, Saad F: Ebp1 expression in benign and malignant prostate. Cancer Cell Int; 2008 Nov 24;8:18
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  • [Title] Ebp1 expression in benign and malignant prostate.
  • ErbB3 and other members of the EGFR family have been implicated in cancer progression, it however remains unknown whether Ebp1 participate in prostate cancer progression in vivo.
  • Ebp1 expression was also correlated to known Ebp1 regulated proteins (Androgen receptor (AR), Cyclin D1 & ErbB3) and the proliferation marker Ki67.
  • METHODS: The expression of Ebp1, AR, Cyclin D1, ErbB3 and Ki67 were evaluated by immunohistochemistry using three separate tissue micro-arrays containing normal prostate tissues, non-cancerous tissue adjacent to the primary tumor, hormone-sensitive and hormone-refractory cancerous tissues.
  • Furthermore, we observed strong correlation between Ebp1 expression and the nuclear expression of AR, Cyclin D1 and ErbB3 in both normal adjacent and cancer tissues.
  • Finally, in a multivariate analysis with a base clinical model (Gleason, Pre-op PSA, surgical margins and P-stage) we identified the multi-marker combination of Ebp1+/Cyclin D1- as an independent predictor of PSA relapse with a hazard ratio of 4.79.


72. Vijayababu MR, Kanagaraj P, Arunkumar A, Ilangovan R, Aruldhas MM, Arunakaran J: Quercetin-induced growth inhibition and cell death in prostatic carcinoma cells (PC-3) are associated with increase in p21 and hypophosphorylated retinoblastoma proteins expression. J Cancer Res Clin Oncol; 2005 Nov;131(11):765-71
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  • Prostate cancer is the major health problem and the leading cause of male cancer death.
  • Quercetin is a novel antitumor and antioxidant, whose molecular mechanism involved in cell cycle arrest in androgen independent prostate cancer cells remains unclear.
  • In this study, we investigated the effects of quercetin on proliferation and cell cycle arrest by modulation of Cdc2/Cdk-1 protein in prostate cancer cells (PC-3).
  • PC- 3 cells are human androgen independent cancer cells and were cultured with quercetin at concentrations of 50 and 100 microM for 24 h.
  • From this study, it was concluded that quercetin inhibits prostate cancer cell proliferation by altering the expression of cell cycle regulators and apoptotic proteins.

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  • (PMID = 16049707.001).
  • [ISSN] 0171-5216
  • [Journal-full-title] Journal of cancer research and clinical oncology
  • [ISO-abbreviation] J. Cancer Res. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / CDKN1A protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Retinoblastoma Protein; 9IKM0I5T1E / Quercetin
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73. Istfan NW, Person KS, Holick MF, Chen TC: 1alpha,25-Dihydroxyvitamin D and fish oil synergistically inhibit G1/S-phase transition in prostate cancer cells. J Steroid Biochem Mol Biol; 2007 Mar;103(3-5):726-30
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  • [Title] 1alpha,25-Dihydroxyvitamin D and fish oil synergistically inhibit G1/S-phase transition in prostate cancer cells.
  • Laboratory and epidemiological studies have indicated that 1alpha,25-dihydroxyvitamin D(3) [1alpha,25(OH)(2)D(3)] and dietary omega3-polyunsaturated fatty acids (PUFAs) are capable of inhibiting prostate cancer at the initiation and progression stages.
  • The objective of this study is to investigate the influence of 1alpha,25(OH)(2)D(3) and PUFAs in the form of fish oil applied alone or in combination on cell cycle kinetics in the exponentially growing androgen-dependent and -independent prostate cancer cells.
  • Our data indicate that the high passage androgen-independent cell line, LNCaP-c115 had a much greater inhibitory response at the level of the G(1)/S-phase transition in response to fish oil treatment than androgen-dependent low passage LNCaP-c38 cells.
  • This interaction appears to be specific for androgen-independent prostate cancer cell lines.
  • Based on these results, we hypothesize that dietary components, such as omega3PUFAs and Vitamin D, have the potential to delay the progression of prostate cancer cells to an aggressive and un-treatable state.

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  • (PMID = 17223546.001).
  • [ISSN] 0960-0760
  • [Journal-full-title] The Journal of steroid biochemistry and molecular biology
  • [ISO-abbreviation] J. Steroid Biochem. Mol. Biol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA 103065; United States / NIDDK NIH HHS / DK / P30 DK040561; None / None / / P30 DK040561-11; United States / NIDDK NIH HHS / DK / P30 DK040561-11; United States / NCI NIH HHS / CA / R03 CA103065
  • [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 / Fish Oils; 1406-16-2 / Vitamin D; 66772-14-3 / 1,25-dihydroxyvitamin D
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74. Ratliff TL: High molecular mass proteome of androgen-independent prostate cancer. J Urol; 2005 Aug;174(2):787
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  • [Title] High molecular mass proteome of androgen-independent prostate cancer.

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  • [CommentOn] Proteomics. 2005 Mar;5(4):1097-112 [15712236.001]
  • (PMID = 16006978.001).
  • [ISSN] 0022-5347
  • [Journal-full-title] The Journal of urology
  • [ISO-abbreviation] J. Urol.
  • [Language] eng
  • [Publication-type] Comment; Journal Article
  • [Publication-country] United States
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75. Richards A, McGeechan K, Niknam M, Salomon R, Kurek C, Dong Q, Patel MI: Prolonging androgen sensitivity in prostate cancer - a role for COX inhibitors? ANZ J Surg; 2009 Sep;79(9):641-7
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  • [Title] Prolonging androgen sensitivity in prostate cancer - a role for COX inhibitors?
  • BACKGROUND: Advanced prostate cancer has long been known to respond to androgen deprivation, but disease inevitably progresses to become androgen independent.
  • This study aims to determine whether cyclooxygenase-2 (COX-2) inhibitors are potentially useful agents in prolonging androgen sensitivity.
  • METHODS: The expression of COX-2 in human prostate surgical specimens, both benign and malignant, androgen dependent and independent, was determined by immunohistochemistry.
  • Nude mice, in which prostate cancer xenografts had been established, were castrated and randomized to receive either COX-2 inhibitor or vehicle for 8 weeks.
  • Time to androgen independence (AIPC), growth rate and rate of PSA rise were compared between groups.
  • COX-2 expression, at the mRNA and protein level, was determined in the native xenograft cell line and in tissues of varying androgen sensitivity derived from the xenografts.
  • RESULTS: In human tissues, COX-2 protein was expressed in prostate epithelium and was upregulated in prostate cancer and remained upregulated after androgen ablation and in the androgen-independent state.
  • CONCLUSION: This study does not support a role for COX-2 inhibitors in prolonging androgen responsiveness in prostate cancer.

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  • (PMID = 19895521.001).
  • [ISSN] 1445-2197
  • [Journal-full-title] ANZ journal of surgery
  • [ISO-abbreviation] ANZ J Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Androgens; 0 / Cyclooxygenase 2 Inhibitors; EC 1.14.99.1 / Cyclooxygenase 2
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76. 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.

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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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77. Tokar EJ, Webber MM: Cholecalciferol (vitamin D3) inhibits growth and invasion by up-regulating nuclear receptors and 25-hydroxylase (CYP27A1) in human prostate cancer cells. Clin Exp Metastasis; 2005;22(3):275-84
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  • [Title] Cholecalciferol (vitamin D3) inhibits growth and invasion by up-regulating nuclear receptors and 25-hydroxylase (CYP27A1) in human prostate cancer cells.
  • Epidemiological evidence suggests an inverse relationship between prostate cancer and serum vitamin D levels.
  • The RWPE2-W99 human prostate epithelial cell line, which forms slow-growing tumors in nude mice, was used because it mimics the behavior of the majority of primary human prostate cancers.
  • Cholecalciferol, at physiological levels: (i) inhibited anchorage-dependent and -independent growth;.
  • (iii) decreased MMP-9 and MMP-2 activity with concomitant decrease in invasion; and (iv) exerted its effects by up-regulating vitamin D receptor (VDR), retinoid-X receptor-alpha (RXR-alpha), and androgen receptor (AR) in a dose-dependent manner.
  • Furthermore, we found that RWPE2-W99 prostate cancer cells, similar to RWPE-1 cells (Tokar and Webber.
  • Because it can inhibit cellular changes associated with malignant transformation and invasion, we propose that cholecalciferol may be an effective agent for the treatment of prostate cancer.
  • [MeSH-minor] Calcitriol / pharmacology. Cell Line, Tumor. Cell Movement / drug effects. Cell Proliferation / drug effects. Chemotaxis / drug effects. Cholestanetriol 26-Monooxygenase. Colony-Forming Units Assay / methods. Dose-Response Relationship, Drug. Humans. Male. Matrix Metalloproteinase 2 / drug effects. Matrix Metalloproteinase 2 / metabolism. Matrix Metalloproteinase 9 / drug effects. Matrix Metalloproteinase 9 / metabolism. Receptors, Androgen / biosynthesis. Receptors, Androgen / drug effects. Receptors, Calcitriol / biosynthesis. Receptors, Calcitriol / drug effects. Retinoid X Receptors / biosynthesis. Retinoid X Receptors / drug effects. Vimentin / biosynthesis. Vimentin / drug effects

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  • (PMID = 16158255.001).
  • [ISSN] 0262-0898
  • [Journal-full-title] Clinical & experimental metastasis
  • [ISO-abbreviation] Clin. Exp. Metastasis
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Receptors, Androgen; 0 / Receptors, Calcitriol; 0 / Receptors, Cytoplasmic and Nuclear; 0 / Retinoid X Receptors; 0 / Vimentin; 1C6V77QF41 / Cholecalciferol; EC 1.14.- / Steroid Hydroxylases; EC 1.14.15.15 / CYP27A1 protein, human; EC 1.14.15.15 / Cholestanetriol 26-Monooxygenase; EC 3.4.24.24 / Matrix Metalloproteinase 2; EC 3.4.24.35 / Matrix Metalloproteinase 9; FXC9231JVH / Calcitriol
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78. Shi GH, Ye DW, Yao XD, Zhang SL, Dai B, Zhang HL, Shen YJ, Zhu Y, Zhu YP, Xiao WJ, Ma CG: Involvement of microRNA-21 in mediating chemo-resistance to docetaxel in androgen-independent prostate cancer PC3 cells. Acta Pharmacol Sin; 2010 Jul;31(7):867-73
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  • [Title] Involvement of microRNA-21 in mediating chemo-resistance to docetaxel in androgen-independent prostate cancer PC3 cells.
  • AIM: To investigate whether microRNA-21 was involved in mediating the chemoresistance of prostate cancer cells to docetaxel.
  • RESULTS: A docetaxel-resistant prostate cancer PC3 cell line (PC3R) was established .
  • CONCLUSION: Our findings suggest that miR-21 contributed to the resistance of PC3 cells to docetaxel, and that targeting miR-21 may offer a promising therapeutic approach in sensitizing prostate cancer to docetaxel treatment.

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  • (PMID = 20581857.001).
  • [ISSN] 1745-7254
  • [Journal-full-title] Acta pharmacologica Sinica
  • [ISO-abbreviation] Acta Pharmacol. Sin.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Apoptosis Regulatory Proteins; 0 / Lipids; 0 / Lipofectamine; 0 / MIRN21 microRNA, human; 0 / MicroRNAs; 0 / PDCD4 protein, human; 0 / RNA-Binding Proteins; 0 / Taxoids; 15H5577CQD / docetaxel
  • [Other-IDs] NLM/ PMC4007720
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79. 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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  • [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.

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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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80. Zhigang Z, Wenlu S: Complete androgen ablation suppresses prostate stem cell antigen (PSCA) mRNA expression in human prostate carcinoma. Prostate; 2005 Dec 1;65(4):299-305
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  • [Title] Complete androgen ablation suppresses prostate stem cell antigen (PSCA) mRNA expression in human prostate carcinoma.
  • BACKGROUND: Prostate stem cell antigen (PSCA) is a recently identified glycosylphosphatidylinositol (GPI)-anchored cell surface protein belonging to the Thy-1/Ly-6 family of cell surface antigens.
  • Prior data in prostate cancers indicated that PSCA is directly regulated by androgens and PSCA expression increases with high-tumor grade, advanced stage, extracapsular invasion, and androgen-independent progression.
  • The effect of complete androgen ablation (CAA) on tumor PSCA mRNA expression has not been elucidated.
  • The purpose of the present study was to investigate the variations in the expression levels of PSCA mRNA before and after CAA, and further evaluate the clinically prognostic value of PSCA in human prostate carcinoma.
  • MATERIALS AND METHODS: PSCA in situ hybridization (ISH) was performed on the cancerous pretreatment biopsy or transurethral resection of prostate (TURP) tissue of 42 men with primarily organ-confined prostate cancer before CAA, and on their tumor tissue from radical retropubic prostatectomy after CAA with bicalutamide and goserelin acetate for 3 months prior to undergoing radical prostatectomy.
  • Tumor cytoplasmic staining of PSCA mRNA was evaluated by two independent pathologists and the differences of PSCA mRNA expression levels between the samples before and after CAA were analyzed using the Student's t-test.
  • Thirty-six to forty months follow-up studies after radical retropubic prostatectomy were performed and aimed at assessing the correlation of PSCA mRNA expression level with local recurrences or metastases from the cancer.
  • CONCLUSIONS: Our data demonstrate that CAA for prostate cancer can suppress PSCA mRNA expression with a tumor grade dependence and the increased expression of PSCA mRNA after CAA may be a clinically adverse predictor for tumor recurrences or distant metastases.
  • [MeSH-major] Androgen Antagonists / therapeutic use. Anilides / therapeutic use. Membrane Glycoproteins / biosynthesis. Neoplasm Proteins / biosynthesis. Neoplasms, Hormone-Dependent / drug therapy. Neoplasms, Hormone-Dependent / metabolism. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / metabolism

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  • [Copyright] Copyright (c) 2005 Wiley-Liss, Inc.
  • (PMID = 16015594.001).
  • [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 / Androgen Antagonists; 0 / Anilides; 0 / Antigens, Neoplasm; 0 / GPI-Linked Proteins; 0 / Membrane Glycoproteins; 0 / Neoplasm Proteins; 0 / Nitriles; 0 / PSCA protein, human; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Tosyl Compounds; A0Z3NAU9DP / bicalutamide
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81. Kokontis JM, Hsu S, Chuu CP, Dang M, Fukuchi J, Hiipakka RA, Liao S: Role of androgen receptor in the progression of human prostate tumor cells to androgen independence and insensitivity. Prostate; 2005 Dec 1;65(4):287-98
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  • [Title] Role of androgen receptor in the progression of human prostate tumor cells to androgen independence and insensitivity.
  • BACKGROUND: Various studies have implicated the androgen receptor (AR) in the progression of androgen-dependent human prostate cancer cells to androgen-independent and androgen-insensitive phenotypes, but the exact role of AR in progression is unclear.
  • METHODS: To mimic the clinical situation and test the role of AR in progression, we cultured androgen-dependent LNCaP 104-S prostate tumor cells in the presence of the antiandrogen Casodex (bicalutamide) to derive resistant (CDXR) clones.
  • In a second step, we cultured CDXR cells in the presence of the androgen R1881, which generated androgen- and Casodex-insensitive (IS) cells.
  • These cells were then characterized with regard to AR function and the effect of ectopic AR expression or AR knockdown on androgen sensitivity.
  • CDXR cell proliferation was unaffected by Casodex but was repressed by androgen in vitro and in vivo.
  • Knockdown of AR expression in CDXR cells produced cells that were insensitive to androgen.
  • Conversely, re-expression of AR in IS cells regenerated cells that were repressed by androgen.
  • Knockdown of AR expression in 104-S cells produced cells that remained stimulated by androgen, while overexpression of AR in 104-S cells generated an androgen-repressed phenotype but did not confer androgen-independent growth.
  • CONCLUSIONS: Increased AR expression determines whether prostate cancer cells are repressed by androgen, but is not required for androgen independence.
  • These results may have implications for anti-AR therapy for prostate cancer.


82. Wang LG, Beklemisheva A, Liu XM, Ferrari AC, Feng J, Chiao JW: Dual action on promoter demethylation and chromatin by an isothiocyanate restored GSTP1 silenced in prostate cancer. Mol Carcinog; 2007 Jan;46(1):24-31
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  • [Title] Dual action on promoter demethylation and chromatin by an isothiocyanate restored GSTP1 silenced in prostate cancer.
  • Prostate carcinoma is characterized by the silencing of pi-class glutathione S-transferase gene (GSTP1), which encodes a detoxifying enzyme.
  • The silencing of GSTP1, due to aberrant methylation at the CpG island in the promoter/5'-UTR, occurs in the vast majority of prostate tumors and precancerous lesions.
  • Several isothiocyanates, including phenethyl isothiocyanate (PEITC), found naturally in cruciferous vegetables, induced growth arrest and apoptosis in prostate cancer cells in culture and xenografts.
  • Exposure of prostate cancer LNCaP cells to PEITC inhibited the activity and level of histone deacetylases (HDACs), and induced selective histone acetylation and methylation for chromatin unfolding.
  • Concurrently PEITC demethylated the promoter and restored the unmethylated GSTP1 in both androgen-dependent and -independent LNCaP cancer cells to the level found in normal prostatic cells, as quantified by methylation-specific PCR and pyrosequencing.
  • The PEITC-mediated cross-talk between the DNA and chromatin in demethylating and reactivating GSTP1 genes, which is critically inactivated in prostate carcinogenesis, underlines a primary mechanism of cancer chemoprevention.


83. Yuan TC, Veeramani S, Lin FF, Kondrikou D, Zelivianski S, Igawa T, Karan D, Batra SK, Lin MF: Androgen deprivation induces human prostate epithelial neuroendocrine differentiation of androgen-sensitive LNCaP cells. Endocr Relat Cancer; 2006 Mar;13(1):151-67
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  • [Title] Androgen deprivation induces human prostate epithelial neuroendocrine differentiation of androgen-sensitive LNCaP cells.
  • Neuroendocrine (NE) cells are the minor cell populations in normal prostate epithelial compartments.
  • During prostate carcinogenesis, the number of NE cells in malignant lesions increases, correlating with its tumorigenicity and hormone-refractory growth.
  • It is thus proposed that cancerous NE cells promote prostate cancer (PCa) cell progression and its androgen-independent proliferation, although the origin of the cancerous NE cells is not clear.
  • To investigate the role of cancerous NE cells in prostate carcinogenesis, we characterized three NE subclone cell lines-NE-1.3, NE-1.8 and NE-1.9, which were transdifferentiated from androgen-sensitive human PCa LNCaP cells by culturing in an androgen-depleted environment, resembling clinical androgen-ablation therapy.
  • These subclone cells acquire many features of NE cells seen in clinical prostate carcinomas, for example exhibiting a neuronal morphology and expressing multiple NE markers, including neuron-specific enolase, chromogranin B, neurotensin, parathyroid hormone-related peptide, and to a lesser degree for chromogranin A, while lacking androgen receptor (AR) or prostate specific antigen (PSA) expression.
  • Furthermore, media conditioned by these NE cells exhibited a stimulatory effect on proliferation and PSA secretion by LNCaP cells in androgen-deprived conditions.
  • [MeSH-minor] Animals. Cell Differentiation / physiology. Chromogranin A. Chromogranins / metabolism. Epithelial Cells / metabolism. Epithelial Cells / pathology. Humans. Male. Mice. Mice, Inbred BALB C. Mice, Nude. Neurotensin / metabolism. Parathyroid Hormone-Related Protein / metabolism. Phosphopyruvate Hydratase / metabolism. Prostate-Specific Antigen / metabolism. Protein Tyrosine Phosphatases / metabolism. Receptor-Like Protein Tyrosine Phosphatases, Class 4. Receptors, Androgen / metabolism. Receptors, Cell Surface / metabolism. Tumor Cells, Cultured

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  • (PMID = 16601285.001).
  • [ISSN] 1351-0088
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 88184; United States / NCRR NIH HHS / RR / P20 RR 017675; United States / NCRR NIH HHS / RR / P20 RR 018759
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AR protein, human; 0 / Androgens; 0 / Chromogranin A; 0 / Chromogranins; 0 / Parathyroid Hormone-Related Protein; 0 / Receptors, Androgen; 0 / Receptors, Cell Surface; 39379-15-2 / Neurotensin; EC 3.1.3.48 / PTPRA protein, human; EC 3.1.3.48 / Protein Tyrosine Phosphatases; EC 3.1.3.48 / Ptpra protein, mouse; EC 3.1.3.48 / Receptor-Like Protein Tyrosine Phosphatases, Class 4; EC 3.4.21.77 / Prostate-Specific Antigen; EC 4.2.1.11 / Phosphopyruvate Hydratase
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84. Shamash J, Davies A, Ansell W, Mcfaul S, Wilson P, Oliver T, Powles T: A phase II study investigating the re-induction of endocrine sensitivity following chemotherapy in androgen-independent prostate cancer. Br J Cancer; 2008 Jan 15;98(1):22-4
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  • [Title] A phase II study investigating the re-induction of endocrine sensitivity following chemotherapy in androgen-independent prostate cancer.
  • When chemotherapy is used in androgen-independent prostate cancer (AIPC), androgen deprivation is continued despite its failure.
  • A phase II prospective study investigated the effects of reintroduction of endocrine therapy after oral chemotherapy in 56 patients with AIPC, which was given without concurrent androgen deprivation.
  • After chemotherapy, patients were given maximum androgen blockade until failure when treatment was switched to diethylstilbestrol and dexamethasone.
  • [MeSH-minor] Aged. Aged, 80 and over. Castration. Humans. Male. Middle Aged. Prognosis. Prospective Studies. Prostate-Specific Antigen / blood. Survival Rate


85. 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.

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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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86. Chua CW, Lee DT, Ling MT, Zhou C, Man K, Ho J, Chan FL, Wang X, Wong YC: FTY720, a fungus metabolite, inhibits in vivo growth of androgen-independent prostate cancer. Int J Cancer; 2005 Dec 20;117(6):1039-48
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  • [Title] FTY720, a fungus metabolite, inhibits in vivo growth of androgen-independent prostate cancer.
  • Our study evaluates the therapeutic potential of FTY720 in the treatment of androgen-independent prostate cancer using a human prostate cancer xenograft in nude mice.
  • CWR22R, an androgen-independent human prostate tumor xenograft was inoculated into castrated nude mice and the animals were administrated with either normal saline or FTY720 (10 mg/kg) through intraperitoneal (i.p.) injection for 20 days.
  • Body weight and tumor volume were recorded every 2 days, and serum prostate specific antigen (PSA) levels were also measured before and after the treatment.
  • In addition, the potential inhibitory effect of FTY720 on prostate cancer angiogenesis and metastasis was investigated by immunostaining of CD31, VEGF, E-cadherin and beta-catenin.
  • Our results suggest a potential novel agent in the suppression of androgen-independent prostate cancer.
  • [MeSH-minor] Animals. Antigens, CD31 / analysis. Apoptosis / drug effects. Body Weight. Cadherins / analysis. Caspase 3. Caspases / analysis. Cell Division / drug effects. Fingolimod Hydrochloride. Humans. Immunohistochemistry. In Situ Nick-End Labeling. Male. Mice. Mice, Nude. Neoplasm Metastasis / prevention & control. Neoplasm Transplantation. Neovascularization, Pathologic / prevention & control. Orchiectomy. Prostate-Specific Antigen / blood. Proto-Oncogene Proteins c-bcl-2 / analysis. Sphingosine / analogs & derivatives. Vascular Endothelial Growth Factor A / analysis. beta Catenin / analysis

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  • [Copyright] Copyright 2005 Wiley-Liss, Inc
  • (PMID = 15986440.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Antigens, CD31; 0 / Cadherins; 0 / Propylene Glycols; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Vascular Endothelial Growth Factor A; 0 / beta Catenin; EC 3.4.21.77 / Prostate-Specific Antigen; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Casp3 protein, mouse; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases; G926EC510T / Fingolimod Hydrochloride; NGZ37HRE42 / Sphingosine
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87. Descazeaud A, Rubin MA, Hofer M, Setlur S, Nikolaief N, Vacherot F, Soyeux P, Kheuang L, Abbou CC, Allory Y, de la Taille A: BPH gene expression profile associated to prostate gland volume. Diagn Mol Pathol; 2008 Dec;17(4):207-13
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  • [Title] BPH gene expression profile associated to prostate gland volume.
  • Five clinical parameters were statistically different between the 2 groups: in group 1 compared with group 2, patients had larger prostate glands, had higher prostate specific antigen levels, were more likely to be treated by alpha blockers, to be operated by prostatectomy, and to have major irritative symptoms.
  • The sole independent parameter associated with this dichotome clustering, however, was the prostate gland volume.
  • Therefore, the role of prostate volume was explored in a supervised analysis.
  • Gene expression of prostate glands <60 mL and >60 mL were compared using significance analysis of microarrays and 227 genes were found differentially expressed between the 2 groups (>2 change and false discovery rate of <5%).
  • Several specific pathways including growth factors genes, cell cycle genes, apoptose genes, inflammation genes, and androgen regulated genes, displayed major differences between small and large prostate glands.

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  • (PMID = 18936709.001).
  • [ISSN] 1533-4066
  • [Journal-full-title] Diagnostic molecular pathology : the American journal of surgical pathology, part B
  • [ISO-abbreviation] Diagn. Mol. Pathol.
  • [Language] ENG
  • [Grant] United States / PHS HHS / / 137962
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 3.4.21.77 / Prostate-Specific Antigen
  • [Other-IDs] NLM/ HALMS349851; NLM/ PMC2822796
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88. Maruyama-Takahashi K, Shimada N, Imada T, Maekawa-Tokuda Y, Ishii T, Ouchi J, Kusaka H, Miyaji H, Akinaga S, Tanaka A, Shitara K: A neutralizing anti-fibroblast growth factor (FGF) 8 monoclonal antibody shows anti-tumor activity against FGF8b-expressing LNCaP xenografts in androgen-dependent and -independent conditions. Prostate; 2008 May 1;68(6):640-50
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