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1. Karpf AR, Bai S, James SR, Mohler JL, Wilson EM: Increased expression of androgen receptor coregulator MAGE-11 in prostate cancer by DNA hypomethylation and cyclic AMP. Mol Cancer Res; 2009 Apr;7(4):523-35
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  • [Title] Increased expression of androgen receptor coregulator MAGE-11 in prostate cancer by DNA hypomethylation and cyclic AMP.
  • The present study investigated the regulatory mechanisms that control MAGE-11 expression during androgen deprivation therapy and prostate cancer progression.
  • Studies include the CWR22 xenograft model of human prostate cancer, clinical specimens of benign and malignant prostate, and prostate cancer cell lines.
  • MAGE-11 mRNA levels increased 100- to 1,500-fold during androgen deprivation therapy and prostate cancer progression, with highest levels in the castration-recurrent CWR22 xenograft and clinical specimens of castration-recurrent prostate cancer.
  • Pyrosequencing of genomic DNA from prostate cancer specimens and cell lines indicated the increase in MAGE-11 resulted from DNA hypomethylation of a CpG island in the 5' promoter of the MAGE-11 gene.
  • Sodium bisulfite sequencing of genomic DNA from benign and malignant prostate tumors and prostate cancer cell lines revealed DNA hypomethylation at individual CpG sites at the transcription start site were most critical for MAGE-11 expression.
  • Cyclic AMP (cAMP) also increased MAGE-11 expression and AR transcriptional activity in prostate cancer cell lines.
  • Increased expression of the AR coregulator MAGE-11 through promoter DNA hypomethylation and cAMP provides a novel mechanism for increased AR signaling in castration-recurrent prostate cancer.

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  • (PMID = 19372581.001).
  • [ISSN] 1541-7786
  • [Journal-full-title] Molecular cancer research : MCR
  • [ISO-abbreviation] Mol. Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA116674; United States / NCI NIH HHS / CA / P01-CA77739; United States / NCI NIH HHS / CA / R21 CA128062; United States / NICHD NIH HHS / HD / R01 HD016910-26; United States / NCI NIH HHS / CA / P01 CA077739; United States / NICHD NIH HHS / HD / R01-HD16910; United States / NCI NIH HHS / CA / R21-CA128062; United States / NCI NIH HHS / CA / P01 CA077739-090007; United States / NCI NIH HHS / CA / R01 CA116674-03; United States / NCI NIH HHS / CA / R01-CA11674; United States / NICHD NIH HHS / HD / R01 HD016910; United States / NCI NIH HHS / CA / CA077739-090007; United States / NICHD NIH HHS / HD / HD016910-26; United States / NCI NIH HHS / CA / CA116674-03
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AR protein, human; 0 / Androgens; 0 / Antigens, Neoplasm; 0 / MAGEA11 protein, human; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / Receptors, Androgen; E0399OZS9N / Cyclic AMP
  • [Other-IDs] NLM/ NIHMS94772; NLM/ PMC2670465
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2. Barnard RJ: Prostate cancer prevention by nutritional means to alleviate metabolic syndrome. Am J Clin Nutr; 2007 Sep;86(3):s889-93
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  • [Title] Prostate cancer prevention by nutritional means to alleviate metabolic syndrome.
  • When subjects were placed on the Pritikin Program, insulin fell and SHBG rose and it was suggested that prostate cancer might also be an aspect of MS.
  • A bioassay was developed with tumor cell lines grown in culture and stimulated with serum before and after a diet and exercise intervention.
  • Diet and exercise altered serum factors that slowed the growth rate and induced apoptosis in androgen-dependent prostate cancer cells.
  • Hyperinsulinemia stimulates liver production of IGF-I, plays a role in the promotion of prostate cancer, and thus is the cornerstone for both MS and prostate cancer.
  • Adopting a low-fat starch diet with daily exercise controls MS and should reduce the risk of prostate cancer.
  • [MeSH-major] Diet, Fat-Restricted. Exercise / physiology. Metabolic Syndrome X / diet therapy. Nutritional Physiological Phenomena / physiology. Prostatic Neoplasms / prevention & control
  • [MeSH-minor] Diet, Reducing. Humans. Insulin-Like Growth Factor Binding Protein 3 / metabolism. Insulin-Like Growth Factor Binding Protein 3 / physiology. Insulin-Like Growth Factor I / metabolism. Insulin-Like Growth Factor I / physiology. Male. Risk Factors. Tumor Cells, Cultured


3. Berry LJ, Au GG, Barry RD, Shafren DR: Potent oncolytic activity of human enteroviruses against human prostate cancer. Prostate; 2008 May 1;68(6):577-87
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  • [Title] Potent oncolytic activity of human enteroviruses against human prostate cancer.
  • BACKGROUND: Oncolytic virotherapy offers a unique treatment modality for prostate cancer, especially stages that are resistant to current therapies, with the additional benefit of preferentially targeting tumor cells amongst an environment of healthy tissue.
  • Herein, the low pathogenic enteroviruses; Coxsackievirus A21 (CVA21), as well as a bio-selected variant of Coxsackievirus A21 (CVA21-DAFv) and Echovirus 1 (EV1) are evaluated as novel oncolytic agents against human prostate cancer.
  • METHODS: The surface expression of viral receptors required for enterovirus cell attachment/entry, including intercellular adhesion molecule-1 (ICAM-1), decay-accelerating factor (DAF) and integrin alpha(2)beta(1) on a number of human prostate cancer lines was assessed by flow cytometry.
  • RESULTS: The majority of prostate cancer lines tested expressed surface ICAM-1 and/or DAF, or alpha(2)beta(1), facilitating significant degrees of oncolysis following in vitro viral challenge.
  • Systemic delivery of each of the three viruses induced reduction of xenograft tumor burdens in vivo, and a therapeutic dose-response was demonstrated for escalating doses of EV1 in the LNCaP animal model.
  • CONCLUSION: Enteroviruses CVA21, CVA21-DAFv, and EV1 are potentially potent oncolytic agents against human prostate cancer.
  • [MeSH-major] Enterovirus A, Human / physiology. Enterovirus B, Human / physiology. Membrane Glycoproteins / metabolism. Oncolytic Virotherapy. Oncolytic Viruses / physiology. Prostatic Neoplasms / virology
  • [MeSH-minor] Animals. Antigens, CD55 / metabolism. Cell Line, Tumor. Flow Cytometry. Humans. Integrin alpha2beta1 / metabolism. Intercellular Adhesion Molecule-1 / metabolism. Male. Mice. Mice, Inbred BALB C. Mice, SCID. Specific Pathogen-Free Organisms. Virus Replication. Xenograft Model Antitumor Assays

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  • (PMID = 18288643.001).
  • [ISSN] 0270-4137
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD55; 0 / Integrin alpha2beta1; 0 / Membrane Glycoproteins; 126547-89-5 / Intercellular Adhesion Molecule-1
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4. Moretti RM, Montagnani Marelli M, Mai S, Cariboni A, Scaltriti M, Bettuzzi S, Limonta P: Clusterin isoforms differentially affect growth and motility of prostate cells: possible implications in prostate tumorigenesis. Cancer Res; 2007 Nov 1;67(21):10325-33
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  • [Title] Clusterin isoforms differentially affect growth and motility of prostate cells: possible implications in prostate tumorigenesis.
  • The possible differential roles played by the two clusterin forms in growth and motility of nonmalignant and malignant prostate cells are investigated here. sCLU or nCLU was transiently transfected in both androgen-independent prostate cancer cells (PC3 and DU 145) and immortalized prostate epithelial cells (PNT1A, a nontumoral control).
  • Thus, CLU gene expression might play a crucial role in prostate tumorigenesis by exerting differential biological effects on normal versus tumor cells through differential processing of CLU isoforms in the two cell systems.
  • [MeSH-major] Clusterin / physiology. Prostatic Neoplasms / etiology
  • [MeSH-minor] Actinin / analysis. Actins / analysis. Cell Line, Tumor. Cell Movement. Cell Proliferation. Fluorescent Antibody Technique. Humans. Male. Protein Isoforms

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  • (PMID = 17974975.001).
  • [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 / Actins; 0 / CLU protein, human; 0 / Clusterin; 0 / Protein Isoforms; 11003-00-2 / Actinin
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5. Mottet N, Bourmaud A, Droz JP: [Prostate cancer screening and early diagnosis]. Rev Prat; 2010 Feb 20;60(2):205-11
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  • [Title] [Prostate cancer screening and early diagnosis].
  • [Transliterated title] Dépistage et diagnostic précoce du cancer de la prostate.
  • Prostate cancer is the first cancer by incidence in men.
  • This decision making strategy is also true for screening and early diagnosis.
  • The current recommendation is an individual early diagnosis procedure based on the measure of serum PSA level and Digital Rectal Examination.
  • [MeSH-major] Early Detection of Cancer. Mass Screening. Prostatic Neoplasms / diagnosis


6. Bar-Shira A, Matarasso N, Rosner S, Bercovich D, Matzkin H, Orr-Urtreger A: Mutation screening and association study of the candidate prostate cancer susceptibility genes MSR1, PTEN, and KLF6. Prostate; 2006 Jul 1;66(10):1052-60
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  • [Title] Mutation screening and association study of the candidate prostate cancer susceptibility genes MSR1, PTEN, and KLF6.
  • BACKGROUND: MSR1, PTEN, and KLF6 have been implicated as candidate susceptibility genes for prostate tumorigenesis.
  • METHODS: Three hundred Jewish prostate cancer patients were screened for alterations in these genes.
  • The KLF6 IVS1-27G>A polymorphism, recently associated with prostate cancer risk, was detected in 11.9% of the patients and 17.3% of the controls (P = 0.043).
  • IVS1-27A allele frequency was significantly lower in prostate cancer patients (P = 0.030), specifically in Ashkenazi patients (P = 0.047) compared to controls.
  • CONCLUSIONS: We found no evidence that MSR1 and PTEN germline mutations are associated with prostate cancer risk in Jews.
  • The negative association between KLF6 IVS1-27A and prostate cancer risk supports a population-specific effect of susceptibility alleles in prostate tumorigenesis.
  • [MeSH-major] Genetic Predisposition to Disease. Genetic Testing. Kruppel-Like Transcription Factors / genetics. PTEN Phosphohydrolase / genetics. Prostatic Neoplasms / genetics. Proto-Oncogene Proteins / genetics. Scavenger Receptors, Class A / genetics
  • [MeSH-minor] Adult. DNA, Neoplasm / genetics. Female. Gene Expression Regulation, Neoplastic. Gene Frequency. Genotype. Germ-Line Mutation. Humans. Israel. Male. Middle Aged. Mutation, Missense. Pedigree. Polymorphism, Genetic. Reverse Transcriptase Polymerase Chain Reaction. Risk Factors

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  • [Copyright] Copyright 2005 Wiley-Liss, Inc.
  • (PMID = 16598737.001).
  • [ISSN] 0270-4137
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / KLF6 protein, human; 0 / Kruppel-Like Transcription Factors; 0 / MSR1 protein, human; 0 / Proto-Oncogene Proteins; 0 / Scavenger Receptors, Class A; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase
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7. Garbis SD, Tyritzis SI, Roumeliotis T, Zerefos P, Giannopoulou EG, Vlahou A, Kossida S, Diaz J, Vourekas S, Tamvakopoulos C, Pavlakis K, Sanoudou D, Constantinides CA: Search for potential markers for prostate cancer diagnosis, prognosis and treatment in clinical tissue specimens using amine-specific isobaric tagging (iTRAQ) with two-dimensional liquid chromatography and tandem mass spectrometry. J Proteome Res; 2008 Aug;7(8):3146-58
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  • [Title] Search for potential markers for prostate cancer diagnosis, prognosis and treatment in clinical tissue specimens using amine-specific isobaric tagging (iTRAQ) with two-dimensional liquid chromatography and tandem mass spectrometry.
  • This study aimed to identify candidate new diagnosis and prognosis markers and medicinal targets of prostate cancer (PCa), using state of the art proteomics.
  • A total of 20 prostate tissue specimens from 10 patients with benign prostatic hyperplasia (BPH) and 10 with PCa (Tumour Node Metastasis [TNM] stage T1-T3) were analyzed by isobaric stable isotope labeling (iTRAQ) and two-dimensional liquid chromatography-tandem mass spectrometry (2DLC-MS/MS) approaches using a hybrid quadrupole time-of-flight system (QqTOF).
  • Selected findings were confirmed by immunohistochemical analysis of prostate tissue specimens.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Prostatic Hyperplasia / metabolism. Prostatic Neoplasms / metabolism. Proteome / metabolism
  • [MeSH-minor] Aged. Amino Acid Sequence. Biomarkers / metabolism. Chromatography, Liquid. Humans. Immunohistochemistry. Male. Middle Aged. Molecular Sequence Data. Prognosis. Prostate-Specific Antigen / metabolism. Reproducibility of Results. Tandem Mass Spectrometry

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  • (PMID = 18553995.001).
  • [ISSN] 1535-3893
  • [Journal-full-title] Journal of proteome research
  • [ISO-abbreviation] J. Proteome Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Biomarkers, Tumor; 0 / Proteome; EC 3.4.21.77 / Prostate-Specific Antigen
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8. Holyoak JD, Crawford ED, Meacham RB: Testosterone and the prostate: implications for the treatment of hypogonadal men. Curr Urol Rep; 2008 Nov;9(6):500-5
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  • [Title] Testosterone and the prostate: implications for the treatment of hypogonadal men.
  • Because aging men are at risk for benign prostatic hyperplasia (BPH) and prostate cancer, elucidating the relationship between testosterone and these diseases is crucial to ensure its safe administration.
  • It is known that testosterone supplementation may worsen active prostate cancer and that its blockade or removal slows the disease's progression.
  • However, recent studies have attempted to show that, in individuals in whom prostate cancer has been ruled out, TRT may simply restore serum testosterone levels to within normal limits without significant adverse affects on the prostate.
  • Patients undergoing TRT should be monitored carefully for any evidence of prostatic disease.
  • [MeSH-major] Hypogonadism / drug therapy. Prostate / physiology. Testosterone / therapeutic use
  • [MeSH-minor] Humans. Male. Prostatic Hyperplasia / etiology. Prostatic Neoplasms / etiology

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  • (PMID = 18947516.001).
  • [ISSN] 1534-6285
  • [Journal-full-title] Current urology reports
  • [ISO-abbreviation] Curr Urol Rep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 3XMK78S47O / Testosterone
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9. Stachon A: [Significance of the PSA-concentration for the detection of prostate cancer]. Pathologe; 2005 Nov;26(6):469-72
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  • [Title] [Significance of the PSA-concentration for the detection of prostate cancer].
  • Prostate cancer among adult males is the most common neoplasm in western countries.
  • Prostate specific antigen (PSA) is now a well established tumor marker that aids in the early detection of localized prostate cancer.
  • Increased PSA concentrations are found in the serum of patients with benign prostatic hyperplasia or patients with prostate cancer, respectively.
  • [MeSH-major] Biomarkers, Tumor / blood. Prostate-Specific Antigen / blood. Prostatic Neoplasms / pathology
  • [MeSH-minor] Aged. Cell Transformation, Neoplastic / pathology. Diagnosis, Differential. Humans. Male. Middle Aged. Predictive Value of Tests. Prostate / pathology. Prostatic Hyperplasia / blood. Prostatic Hyperplasia / diagnosis. Prostatic Hyperplasia / pathology. Prostatic Hyperplasia / surgery. Reference Values


10. Sun T, Lee GS, Oh WK, Pomerantz M, Yang M, Xie W, Freedman ML, Kantoff PW: Single-nucleotide polymorphisms in p53 pathway and aggressiveness of prostate cancer in a Caucasian population. Clin Cancer Res; 2010 Nov 1;16(21):5244-51
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  • [Title] Single-nucleotide polymorphisms in p53 pathway and aggressiveness of prostate cancer in a Caucasian population.
  • PURPOSE: The tumor suppressor p53 plays a crucial role in maintaining genomic stability and tumor prevention.
  • Despite the importance of the p53 pathway in prostate cancer development and progression, little is known about the association of functional single-nucleotide polymorphisms (SNP) in the p53 pathway genes and prostate cancer aggressiveness.
  • EXPERIMENTAL DESIGN: In this study, we analyze the association of SNPs in p53, Mdm2, Mdm4, and Hausp genes with prostate cancer clinicopathologic variables in a large hospital-based Caucasian prostate cancer cohort (N = 4,073).
  • RESULTS: We found that the Mdm2 SNP309 T allele was associated with earlier onset prostate cancer (P = 0.004), higher Gleason scores (P = 0.004), and higher stages in men undergoing a radical prostatectomy (P = 0.011).
  • Both the Mdm4 and Hausp SNPs (rs1380576 and rs1529916) were found to be associated with higher D'Amico risk prostate cancer category at the time of diagnosis (P = 0.023 and P = 0.046, respectively).
  • We did not observe any statistically significant association between the p53 Arg72Pro polymorphism and prostate cancer aggressiveness or pathologic variables.
  • CONCLUSIONS: These results suggested the importance of these p53 regulators in prostate cancer development and progression.

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  • (PMID = 20855462.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA090381; United States / NCI NIH HHS / CA / 2 P50 CA090381-06
  • [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 / Biomarkers, Tumor; 0 / MDM4 protein, human; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins; 0 / Tumor Suppressor Protein p53; EC 3.1.2.15 / USP7 protein, human; EC 3.1.2.15 / Ubiquitin Thiolesterase; EC 6.3.2.19 / MDM2 protein, human; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2
  • [Other-IDs] NLM/ NIHMS225371; NLM/ PMC2970725
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11. Brasky TM, Velicer CM, Kristal AR, Peters U, Potter JD, White E: Nonsteroidal anti-inflammatory drugs and prostate cancer risk in the VITamins And Lifestyle (VITAL) cohort. Cancer Epidemiol Biomarkers Prev; 2010 Dec;19(12):3185-8
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  • [Title] Nonsteroidal anti-inflammatory drugs and prostate cancer risk in the VITamins And Lifestyle (VITAL) cohort.
  • INTRODUCTION: Chronic inflammation may be important in prostate carcinogenesis.
  • Several epidemiologic studies have reported inverse associations between nonsteroidal anti-inflammatory drugs (NSAIDs) and prostate cancer risk, although many studies are limited by assessment of short-term use only.
  • Cox proportional hazards models were used to estimate adjusted hazard ratios (HR) and 95% confidence intervals (95% CI) of 10-year average use of individual NSAIDs with total prostate cancer (n = 1,550) and prostate cancer by grade.
  • RESULTS: Low-dose aspirin, regular-strength aspirin, ibuprofen, and any nonaspirin NSAID (ibuprofen, naproxen, and COX-2 inhibitors) were not associated with prostate cancer risk.
  • CONCLUSION: NSAID use was not associated with prostate cancer risk in the VITAL cohort.
  • IMPACT: Our findings do not support the use of NSAIDs for chemoprevention of prostate cancer.

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  • [Copyright] ©2010 AACR.
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  • (PMID = 20935064.001).
  • [ISSN] 1538-7755
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R25 CA094880-10; United States / NCI NIH HHS / CA / K05 CA154337; United States / NCI NIH HHS / CA / R25 CA094880; United States / NCI NIH HHS / CA / K05-CA154337; United States / NCI NIH HHS / CA / R25-CA94880
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal
  • [Other-IDs] NLM/ NIHMS243668; NLM/ PMC3005534
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12. Macura KJ, Stoianovici D: Advancements in magnetic resonance-guided robotic interventions in the prostate. Top Magn Reson Imaging; 2008 Dec;19(6):297-304
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  • [Title] Advancements in magnetic resonance-guided robotic interventions in the prostate.
  • Magnetic resonance imaging (MRI) provides more detailed anatomical images of the prostate compared with the transrectal ultrasound imaging.
  • Therefore, for the purpose of intervention in the prostate gland, diagnostic or therapeutic, MRI guidance offers a possibility of more precise targeting that may be crucial to the success of prostate interventions.
  • Several systems have been already tested clinically for prostate biopsy and brachytherapy.
  • As technology matures, precise image guidance for prostate interventions performed or assisted by specialized MR-compatible robotic devices may provide a uniquely accurate solution for guiding the intervention directly based on MR findings and feedback.
  • Such an instrument would become a valuable clinical tool for biopsies directly targeting imaged tumor foci and delivering tumor-centered focal therapy.

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  • (PMID = 19512852.001).
  • [ISSN] 1536-1004
  • [Journal-full-title] Topics in magnetic resonance imaging : TMRI
  • [ISO-abbreviation] Top Magn Reson Imaging
  • [Language] ENG
  • [Grant] United States / NIBIB NIH HHS / EB / RC1 EB010936-01; United States / CCR NIH HHS / RC / EB010936-02; United States / NIBIB NIH HHS / EB / RC1 EB010936; United States / NIBIB NIH HHS / EB / RC1 EB010936-02; United States / CCR NIH HHS / RC / EB010936-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 57
  • [Other-IDs] NLM/ NIHMS284671; NLM/ PMC3099454
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13. Raffoul JJ, Banerjee S, Che M, Knoll ZE, Doerge DR, Abrams J, Kucuk O, Sarkar FH, Hillman GG: Soy isoflavones enhance radiotherapy in a metastatic prostate cancer model. Int J Cancer; 2007 Jun 1;120(11):2491-8
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  • [Title] Soy isoflavones enhance radiotherapy in a metastatic prostate cancer model.
  • We previously reported that genistein, the bioactive isoflavone of soybeans, acts as a radiosensitizer for prostate cancer.
  • Pretreatment of tumor cells with genistein potentiated radiation-induced killing in vitro and in orthotopic models in vivo.
  • Soy isoflavones inhibited cell survival and potentiated radiation cell killing in PC-3 tumor cells, in vitro.
  • In vivo, using the PC-3 orthotopic metastatic mouse model, soy isoflavones and prostate tumor irradiation led to enhanced control of primary tumor growth and metastasis, as observed with pure genistein and radiation.
  • Histologically prostate tumors, treated with soy isoflavones and radiation, showed tumor destruction and in situ tissue alterations, comparable with genistein and radiation effects.
  • However, genistein, but not soy isoflavones, caused induction of HIF1-alpha in prostate tumors, suggesting that induction of hypoxia by pure genistein could contribute to increased metastasis.
  • Our studies demonstrate the safety and potential role of soy isoflavones for enhancing the therapeutic effect of radiotherapy in prostate cancer.
  • [MeSH-major] Genistein / pharmacology. Prostatic Neoplasms / radiotherapy. Radiotherapy. Soybeans / chemistry
  • [MeSH-minor] Animals. Blotting, Western. Cell Line, Tumor. Humans. Male. Mice. Neoplasm Metastasis. Neoplasm Transplantation


14. Shah SK, Lui PD, Baldwin DD, Ruckle HC: Urothelial carcinoma after external beam radiation therapy for prostate cancer. J Urol; 2006 Jun;175(6):2063-6
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  • [Title] Urothelial carcinoma after external beam radiation therapy for prostate cancer.
  • PURPOSE: We reviewed the clinical course of patients in whom urothelial carcinoma developed following radiation therapy for prostate cancer.
  • MATERIALS AND METHODS: A retrospective review of all patients between 1990 and 2005 with the diagnosis of bladder and prostate cancer was performed.
  • Of 125 total patients new onset urothelial carcinoma developed in 11 after undergoing external beam radiation therapy for prostate cancer.
  • RESULTS: Whole pelvis external beam radiation therapy with a proton boost to the prostate was the radiation modality in 7 of the 11 patients (64%), while the remaining 4 patients received standard external beam radiation only.
  • Average patient age at diagnosis was 72 years (range 64 to 84).
  • Of the 11 patients 10 (91%) were nonsmokers at the time of urothelial carcinoma diagnosis.
  • CONCLUSIONS: Urothelial carcinoma in patients with previous radiation therapy for prostate cancer is often high grade, and the majority of patients have cancer progression requiring cystectomy.
  • [MeSH-major] Carcinoma, Transitional Cell / etiology. Neoplasms, Radiation-Induced / etiology. Prostatic Neoplasms / radiotherapy. Urinary Bladder Neoplasms / etiology


15. Crocetti E, Ciatto S, Buzzoni C, Zappa M: Prostate cancer incidence rates have started to decrease in central Italy. J Med Screen; 2010;17(1):50-1
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  • [Title] Prostate cancer incidence rates have started to decrease in central Italy.
  • The widespread use of prostate-specific antigen (PSA) testing has dramatically changed the epidemiology of prostate cancer.
  • Similar changes have been documented also in the area of the Tuscany Cancer Registry, central Italy, where prostate cancer incidence rates doubled from the early 1990s to 2003 and afterwards decreased.
  • This is the first evidence, to our knowledge, of a decline in prostate cancer incidence in Italy following the screening-related increase.
  • [MeSH-major] Prostatic Neoplasms / epidemiology
  • [MeSH-minor] Humans. Italy / epidemiology. Male. Prostate-Specific Antigen / metabolism


16. Fritzsche FR, Jung M, Xu C, Rabien A, Schicktanz H, Stephan C, Dietel M, Jung K, Kristiansen G: ADAM8 expression in prostate cancer is associated with parameters of unfavorable prognosis. Virchows Arch; 2006 Dec;449(6):628-36
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  • [Title] ADAM8 expression in prostate cancer is associated with parameters of unfavorable prognosis.
  • Gene products of the A disintegrin and metalloprotease (ADAM) family are critically involved in carcinogenesis and tumor progression of various solid tumors.
  • Little is known about ADAM8 in prostate cancer.
  • In our quest for novel diagnostic tissue markers of prostate cancer, we aimed to evaluate the expression of ADAM8 in prostate cancer and to correlate it with clinicopathological parameters.
  • One hundred twenty-eight clinicopathologically characterized prostate cancer patients, with available follow-up data, were immunostained for ADAM8.
  • Still, a significant prognostic value for the prostate-specific antigen relapse-free survival of ADAM8 could not be demonstrated.
  • Therefore, despite of its significant association with conventional parameters of an unfavorable prognosis, ADAM8 adds only limited information to the conventional histopathological assessment of prostate cancer.
  • [MeSH-major] ADAM Proteins / analysis. Membrane Proteins / analysis. Prostatic Neoplasms / chemistry
  • [MeSH-minor] Aged. Humans. Immunohistochemistry. Male. Middle Aged. Prognosis. Prostate / chemistry. RNA, Messenger / analysis

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  • (PMID = 17106710.001).
  • [ISSN] 0945-6317
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Membrane Proteins; 0 / RNA, Messenger; EC 3.4.24.- / ADAM Proteins; EC 3.4.24.- / ADAM8 protein, human
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17. Flitsch J, Bernreuther C, Hagel C, Lüdecke DK: Hypophysectomy for prostate cancer: a revival of old knowledge? J Neurosurg; 2008 Oct;109(4):760-4
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  • [Title] Hypophysectomy for prostate cancer: a revival of old knowledge?
  • The growth of prostate cancer is controlled by several hormones and growth factors.
  • In cases of metastasized prostate cancer, antigonadotropic therapy is currently considered state-of-the-art treatment.
  • The authors present the case of a 63-year-old man with metastatic prostate cancer who presented with high serum prostate-specific antigen levels (1216 microg/L) and cavernous sinus syndrome.
  • Because of the elevated prolactin and high-normal IGF-I levels he was offered a hypophysectomy in addition to pituitary tumor removal.
  • Histological examination of the resected lesion confirmed a nonsecreting pituitary adenoma with infiltration of prostate cancer cells.
  • Postoperatively the patient's prostate-specific antigen levels dropped to 876 microg/L, his bone pain resolved, and the cavernous sinus syndrome improved.
  • A reduction of IGF-I levels even in the final stage metastasized prostate cancer may play a major role.
  • [MeSH-major] Hypophysectomy. Pituitary Neoplasms / secondary. Pituitary Neoplasms / surgery. Prostatic Neoplasms / pathology

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  • (PMID = 18826367.001).
  • [ISSN] 0022-3085
  • [Journal-full-title] Journal of neurosurgery
  • [ISO-abbreviation] J. Neurosurg.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 67763-96-6 / Insulin-Like Growth Factor I
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18. Rodriguez C, Patel AV, Mondul AM, Jacobs EJ, Thun MJ, Calle EE: Diabetes and risk of prostate cancer in a prospective cohort of US men. Am J Epidemiol; 2005 Jan 15;161(2):147-52
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  • [Title] Diabetes and risk of prostate cancer in a prospective cohort of US men.
  • One previous study has suggested that diabetes may decrease risk of prostate cancer but only several years after diagnosis of diabetes.
  • The authors examined the role of timing of diabetes diagnosis in relation to risk of prostate cancer among men in the Cancer Prevention Study II Nutrition Cohort.
  • The authors documented 5,318 cases of incident prostate cancer through August 31, 2001, among 72,670 men.
  • Results from Cox proportional hazards models showed that diabetes was associated with a lower incidence of prostate cancer (rate ratio (RR) = 0.67, 95% confidence interval (CI): 0.60, 0.75).
  • This association differed significantly by time since diagnosis of diabetes (p < 0.0002); risk of prostate cancer was slightly increased during the first 3 years after diagnosis of diabetes (RR = 1.23, 95% CI: 0.92, 1.65) but was reduced among men diagnosed 4 or more years before (RR = 0.63, 95% CI: 0.56, 0.71).
  • Study results are consistent with the hypothesis that diabetes is associated with reduced risk of prostate cancer but only several years after diagnosis of diabetes.
  • [MeSH-major] Diabetes Mellitus, Type 2 / complications. Prostatic Neoplasms / etiology


19. Chuu CP, Kokontis JM, Hiipakka RA, Liao S: Modulation of liver X receptor signaling as novel therapy for prostate cancer. J Biomed Sci; 2007 Sep;14(5):543-53
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  • [Title] Modulation of liver X receptor signaling as novel therapy for prostate cancer.
  • Recently we observed that LXR agonists suppressed proliferation of prostate and breast cancer cells in vitro and treatment of mice with the LXR agonist T0901317 suppressed the growth of prostate tumor xenografts.
  • T0901317 induced expression of ATP-binding cassette transporter A1 (ABCA1) and delayed the progression of androgen-dependent human prostate tumor xenografts towards androgen-independency in mice.
  • Phytosterols, the plant equivalent of mammalian cholesterol, have recently been shown to be agonists for LXRs. beta-Sitosterol and campesterol, the two most common phytosterols, suppressed proliferation of prostate and breast cancer cells.
  • This review examines the potential use of LXR signaling as a therapeutic target in prostate and other cancers.

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  • (PMID = 17372849.001).
  • [ISSN] 1021-7770
  • [Journal-full-title] Journal of biomedical science
  • [ISO-abbreviation] J. Biomed. Sci.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA058073; United States / NCI NIH HHS / CA / CA58073
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / DNA-Binding Proteins; 0 / Orphan Nuclear Receptors; 0 / Receptors, Cytoplasmic and Nuclear; 0 / liver X receptor
  • [Number-of-references] 88
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20. Guo CC, Pisters LL, Troncoso P: Prostate cancer invading the rectum: a clinicopathological study of 18 cases. Pathology; 2009;41(6):539-43
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  • [Title] Prostate cancer invading the rectum: a clinicopathological study of 18 cases.
  • AIMS: Prostate cancer may involve the rectum and cause severe perineal pain.
  • The aim of this study was to understand the rectal involvement by prostate cancer and its clinical significance.
  • METHODS: We evaluated pathological and clinical features of 18 cases of prostate cancer with rectal involvement.
  • Twelve patients received rectal biopsies, which revealed poorly differentiated prostatic adenocarcinoma (n = 6), squamous cell carcinoma (n = 3), angiosarcoma (n = 1), or no tumour (n = 2).
  • All patients received palliative total pelvic exenteration, which demonstrated prostate cancer invading the rectal wall.
  • In these resection specimens, the tumour consisted of poorly differentiated prostatic adenocarcinoma (n = 16), squamous cell carcinoma (n = 1), or angiosarcoma (n = 1).
  • In addition, six cases of prostatic adenocarcinomas also showed focal squamous (n = 3) or high-grade neuroendocrine (n = 3) differentiation.
  • CONCLUSIONS: Prostate cancer with rectal involvement often develops heterogeneous differentiation and carries a dismal prognosis.
  • [MeSH-major] Adenocarcinoma / pathology. Carcinoma, Squamous Cell / pathology. Hemangiosarcoma / pathology. Prostatic Neoplasms / pathology. Rectal Neoplasms / pathology
  • [MeSH-minor] Aged. Biopsy. Combined Modality Therapy. Fatal Outcome. Humans. Male. Middle Aged. Neoplasm Invasiveness. Prognosis

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  • (PMID = 19900102.001).
  • [ISSN] 1465-3931
  • [Journal-full-title] Pathology
  • [ISO-abbreviation] Pathology
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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21. de Muga S, Hernández S, Agell L, Salido M, Juanpere N, Lorenzo M, Lorente JA, Serrano S, Lloreta J: Molecular alterations of EGFR and PTEN in prostate cancer: association with high-grade and advanced-stage carcinomas. Mod Pathol; 2010 May;23(5):703-12
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  • [Title] Molecular alterations of EGFR and PTEN in prostate cancer: association with high-grade and advanced-stage carcinomas.
  • Prostate cancer is the second cause of cancer-related death in men of the Western world.
  • The potential prognostic role of the combined alterations in EGFR and PTEN in prostate cancer is not well established.
  • Prevalence of EGFR and PTEN somatic mutations, EGFR amplification and EGFR protein expression were investigated in a series of prostate adenocarcinomas, classified according to the current Gleason grading system.
  • Mutational analysis revealed eight EGFR and three PTEN mutations in 98 (8%) and 92 (3%) prostate adenocarcinomas, respectively.
  • In 35% of adenocarcinomas we found some type of EGFR-PTEN alteration, with a tendency to be associated with advanced-stage prostate adenocarcinomas (P=0.04).
  • The IVS18+19 polymorphism was also associated with more advanced prostate adenocarcinomas.
  • This is the first study reporting mutations of EGFR and PTEN in the same series of prostate adenocarcinomas.
  • Mutations in EGFR and PTEN genes are a minor event, although prostate cancer represents the third neoplasm in which the EGFR gene mutations are more prevalent.
  • Alterations in the EGFR-PTEN signaling pathway are present in a third of prostate adenocarcinomas, particularly affecting the more advanced cases.
  • [MeSH-major] Adenocarcinoma / genetics. PTEN Phosphohydrolase / genetics. Prostatic Neoplasms / genetics. Receptor, Epidermal Growth Factor / genetics
  • [MeSH-minor] DNA Mutational Analysis. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Male. Mutation. Neoplasm Staging. Polymerase Chain Reaction. Polymorphism, Genetic. Severity of Illness Index. Signal Transduction / genetics


22. Hoffman RM, Barry MJ, Stanford JL, Hamilton AS, Hunt WC, Collins MM: Health outcomes in older men with localized prostate cancer: results from the Prostate Cancer Outcomes Study. Am J Med; 2006 May;119(5):418-25
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  • [Title] Health outcomes in older men with localized prostate cancer: results from the Prostate Cancer Outcomes Study.
  • PURPOSE: We compared health-related quality-of-life (HRQOL) outcomes and survival of men with localized prostate cancer who received aggressive treatment with those receiving conservative management.
  • We used medical record abstractions and patient surveys to obtain clinical and HRQOL data at diagnosis and 24-month follow-up.
  • RESULTS: At 24 months following diagnosis, aggressively treated men were more likely to report daily urinary leakage (odds ratio [OR] = 2.9, 95% confidence interval [CI] 1.2-7.0) and to be bothered by urinary problems (OR = 5.1, 95% CI, 1.3-9.1) and sexual problems (OR = 2.8, 95% CI, 1.2-6.3).
  • However, men who were aggressively treated for localized cancer had a minimally reduced absolute risk of dying from prostate cancer.
  • [MeSH-major] Prostatic Neoplasms / pathology. Prostatic Neoplasms / therapy. Quality of Life

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  • (PMID = 16651054.001).
  • [ISSN] 1555-7162
  • [Journal-full-title] The American journal of medicine
  • [ISO-abbreviation] Am. J. Med.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / PC / N01-PC-67000; United States / NCI NIH HHS / PC / N01-PC-67005; United States / NCI NIH HHS / PC / N01-PC-67006; United States / NCI NIH HHS / PC / N01-PC-67007; United States / NCI NIH HHS / PC / N01-PC-67010; United States / PHS HHS / / N01-PCN-67009
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
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23. Stamatiou K, Skolarikos A, Heretis I, Papadimitriou V, Alevizos A, Ilias G, Karanasiou V, Mariolis A, Sofras F: Does educational printed material manage to change compliance with prostate cancer screening? World J Urol; 2008 Aug;26(4):365-73
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  • [Title] Does educational printed material manage to change compliance with prostate cancer screening?
  • The aim of our study was to evaluate the impact of similar printed educational material on prostate cancer screening by PSA and DRE.
  • MATERIAL AND METHODS: Thousand five hundred men aged between 50 and 86 years of age, who attended our institutions for various medical conditions except prostate-related conditions, were randomly assigned to two study groups.
  • Men in the informed group, received an educational leaflet with simple, general information on prostate cancer screening methods given by their physician along with treatment and other regular recommendations, while men in the non-informed group, were only informed by their physician in the examination room during an interview.
  • CONCLUSIONS: A single, one-shift distribution of printed educational material on prostate cancer screening, changed their attitude regarding prostate cancer screening only in favour of PSA testing, while did not manage to change the DRE acceptance behavior.
  • However, since the combination of the two tests is more sensitive for diagnosis than either one alone, there is a need of introducing intervention strategies, in the efforts of ameliorating the prostate cancer screening behavior.
  • [MeSH-major] Mass Screening / methods. Pamphlets. Patient Compliance. Patient Education as Topic / methods. Prostatic Neoplasms / diagnosis
  • [MeSH-minor] Aged. Aged, 80 and over. Digital Rectal Examination. Health Behavior. Humans. Male. Middle Aged. Prostate-Specific Antigen / blood. Surveys and Questionnaires

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  • (PMID = 18421460.001).
  • [ISSN] 0724-4983
  • [Journal-full-title] World journal of urology
  • [ISO-abbreviation] World J Urol
  • [Language] eng
  • [Publication-type] Journal Article; Randomized Controlled Trial
  • [Publication-country] Germany
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24. Pal P, Xi H, Kaushal R, Sun G, Jin CH, Jin L, Suarez BK, Catalona WJ, Deka R: Variants in the HEPSIN gene are associated with prostate cancer in men of European origin. Hum Genet; 2006 Sep;120(2):187-92
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  • [Title] Variants in the HEPSIN gene are associated with prostate cancer in men of European origin.
  • There is considerable evidence that genetic factors are involved in prostate cancer susceptibility.
  • We have studied the association of 11 single nucleotide polymorphisms (SNPs) in the HEPSIN gene (HPN) with prostate cancer in men of European ancestry.
  • HPN is a likely candidate in prostate cancer susceptibility, as it encodes a transmembrane cell surface serum protease, which is overexpressed in prostate cancer; HPN is also located on 19q11-q13.2, where linkage is found with prostate cancer susceptibility.
  • In this case-control association study (590 men with histologically verified prostate cancer and 576 unrelated controls, all of European descent), we find significant allele frequency differences between cases and controls at five SNPs that are located contiguously within the gene.
  • A major 11-locus haplotype is significantly associated, which provides further support that HPN is a potentially important candidate gene involved in prostate cancer susceptibility.
  • Association of one of the SNPs with Gleason score is also suggestive of a plausible role of HPN in tumor aggressiveness.
  • [MeSH-major] European Continental Ancestry Group / genetics. Genetic Predisposition to Disease. Polymorphism, Single Nucleotide. Prostatic Neoplasms / genetics. Serine Endopeptidases / genetics

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  • (PMID = 16783571.001).
  • [ISSN] 0340-6717
  • [Journal-full-title] Human genetics
  • [ISO-abbreviation] Hum. Genet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.- / hepsin
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25. Liu P, Ramachandran S, Ali Seyed M, Scharer CD, Laycock N, Dalton WB, Williams H, Karanam S, Datta MW, Jaye DL, Moreno CS: Sex-determining region Y box 4 is a transforming oncogene in human prostate cancer cells. Cancer Res; 2006 Apr 15;66(8):4011-9
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  • [Title] Sex-determining region Y box 4 is a transforming oncogene in human prostate cancer cells.
  • Prostate cancer is the most commonly diagnosed noncutaneous neoplasm and second most common cause of cancer-related mortality in western men.
  • To investigate the mechanisms of prostate cancer development and progression, we did expression profiling of human prostate cancer and benign tissues.
  • We show that the SOX4 is overexpressed in prostate tumor samples compared with benign tissues by microarray analysis, real-time PCR, and immunohistochemistry.
  • Silencing of SOX4 by small interfering RNA transfection induced apoptosis of prostate cancer cells, suggesting that SOX4 could be a therapeutic target for prostate cancer.
  • Stable transfection of SOX4 into nontransformed prostate cells enabled colony formation in soft agar, suggesting that, in the proper cellular context, SOX4 can be a transforming oncogene.
  • [MeSH-major] Cell Transformation, Neoplastic / genetics. High Mobility Group Proteins / genetics. Oncogenes. Prostatic Neoplasms / genetics. Trans-Activators / genetics
  • [MeSH-minor] Apoptosis / genetics. Cell Growth Processes / physiology. Cell Line, Transformed. Cell Line, Tumor. Gene Expression Profiling. Humans. Male. RNA, Small Interfering / genetics. Reverse Transcriptase Polymerase Chain Reaction. SOXC Transcription Factors. Transfection

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  • (PMID = 16618720.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NIGMS NIH HHS / GM / T32 GM008169; United States / NCI NIH HHS / CA / CA91435; United States / NCI NIH HHS / CA / K22-CA96560; United States / NIDDK NIH HHS / DK / DK60647; United States / NIGMS NIH HHS / GM / T32 GM008490; United States / NCI NIH HHS / CA / R01-CA106826
  • [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 / High Mobility Group Proteins; 0 / RNA, Small Interfering; 0 / SOX4 protein, human; 0 / SOXC Transcription Factors; 0 / Trans-Activators
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26. Krejcarek SC, Chen MH, Renshaw AA, Loffredo M, Sussman B, D'Amico AV: Prediagnostic prostate-specific antigen velocity and probability of detecting high-grade prostate cancer. Urology; 2007 Mar;69(3):515-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prediagnostic prostate-specific antigen velocity and probability of detecting high-grade prostate cancer.
  • OBJECTIVES: Men with high-grade prostate cancer experience a survival benefit when androgen suppression therapy is combined with radiotherapy (RT) compared with RT alone.
  • We evaluated whether an association exists between the pretreatment prostate-specific antigen (PSA) velocity and high-grade prostate cancer at diagnosis, controlling for known predictors of high-grade disease.
  • METHODS: The study cohort consisted of 358 men with Stage T1c-T4 prostate cancer treated with external beam RT from 1989 to 2002.
  • Univariate and multivariate logistic regression analyses were used to assess whether an association exists between the pretreatment PSA velocity, PSA level, age, clinical T stage, and Gleason score 4+3 or greater compared with Gleason score 3+4 or less prostate cancer.
  • On multivariate analysis, the PSA velocity (odds ratio 1.06, 95% confidence interval 1.02 to 1.10, P = 0.004), age (odds ratio 1.07, 95% confidence interval 1.02 to 1.13, P = 0.008), and clinical T stage (odds ratio 2.17, 95% confidence interval 1.21 to 3.92, P = 0.01) were significantly associated with the detection of Gleason score 4+3 or greater prostate cancer.
  • CONCLUSIONS: The prediagnostic PSA velocity, patient age, and clinical T stage were significantly associated with high-grade prostate cancer at diagnosis.
  • Because a biopsy Gleason score of 4+3 or greater is associated with a prostatectomy Gleason score of 7 or greater in the vast majority of cases, these parameters can identify men at high risk of harboring occult high-grade prostate cancer, permitting improved selection of RT fields and the use of androgen suppression therapy.
  • [MeSH-major] Prostate-Specific Antigen / blood. Prostatic Neoplasms / diagnosis. Prostatic Neoplasms / pathology


27. Xu RS, Michailovich O, Salama M: Information tracking approach to segmentation of ultrasound imagery of the prostate. IEEE Trans Ultrason Ferroelectr Freq Control; 2010 Aug;57(8):1748-61
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  • [Title] Information tracking approach to segmentation of ultrasound imagery of the prostate.
  • The volume of the prostate is known to be a pivotal quantity used by clinicians to assess the condition of the gland during prostate cancer screening.
  • As an alternative to palpation, an increasing number of methods for estimation of the volume of the prostate are based on using imagery data.
  • In particular, the use of transrectal ultrasound (TRUS) imaging in prostate cancer screening seems to be becoming a standard clinical practice because of the high benefit-to-cost ratio of this imaging modality.
  • Unfortunately, the segmentation of TRUS images is still hampered by relatively low contrast and reduced SNR of the images, thereby requiring the segmentation algorithms to incorporate prior knowledge about the geometry of the gland.
  • The proposed approach is based on the concept of distribution tracking, which provides a unified framework for modeling and fusing image-related and morphological features of the prostate.
  • [MeSH-major] Prostate / ultrasonography. Signal Processing, Computer-Assisted. Ultrasonography / methods

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  • (PMID = 20679005.001).
  • [ISSN] 1525-8955
  • [Journal-full-title] IEEE transactions on ultrasonics, ferroelectrics, and frequency control
  • [ISO-abbreviation] IEEE Trans Ultrason Ferroelectr Freq Control
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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28. Koga N, Noguchi M, Moriya F, Ohshima K, Yoshitake N, Matsuoka K: A case of primary mucosa-associated lymphoid tissue lymphoma of the prostate. Rare Tumors; 2009;1(2):e55
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  • [Title] A case of primary mucosa-associated lymphoid tissue lymphoma of the prostate.
  • We report a case of primary mucosa-associated lymphoid tissue (MALT) lymphoma of the prostate.
  • A 67-year-old man presented with urinary obstruction and an elevated prostate-specific antigen (PSA) level.
  • A physical examination revealed mild prostate enlargement and no lymphadenopathy.
  • A needle biopsy and immunohistochemical studies of the prostate were performed, which revealed marginal zone B-cell MALT-type lymphoma.
  • The patient was diagnosed and staged as extranodal marginal zone B-cell MALT-type lymphoma of the prostate, low grade and stage I.
  • The patient received external beam radiation therapy to the prostate with a total dose of 3600cGy in 22 fractions, and became free of disease within the following 15 months.

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  • (PMID = 21139934.001).
  • [ISSN] 2036-3613
  • [Journal-full-title] Rare tumors
  • [ISO-abbreviation] Rare Tumors
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Other-IDs] NLM/ PMC2994450
  • [Keywords] NOTNLM ; mucosa-associated lymphoid tissue lymphoma / prostate / prostate-specific antigen / radiation therapy.
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29. Petrovics G, Liu A, Shaheduzzaman S, Furusato B, Sun C, Chen Y, Nau M, Ravindranath L, Chen Y, Dobi A, Srikantan V, Sesterhenn IA, McLeod DG, Vahey M, Moul JW, Srivastava S: Frequent overexpression of ETS-related gene-1 (ERG1) in prostate cancer transcriptome. Oncogene; 2005 May 26;24(23):3847-52
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  • [Title] Frequent overexpression of ETS-related gene-1 (ERG1) in prostate cancer transcriptome.
  • This study, analysing laser microdissected paired benign and malignant prostate epithelial cells from prostate cancer (CaP) patients (n=114; 228 specimen) by GeneChip and quantitative real-time RT-PCR, identifies ETS-related gene (ERG), a member of the ETS transcription factor family, as the most frequently overexpressed proto-oncogene in the transcriptome of malignant prostate epithelial cells.
  • Comprehensive evaluation of quantitative ERG1 expression with clinicopathological features also suggested that ERG1 expression level in prostate tumor cells relative to benign epithelial cells is indicator of disease-free survival after radical prostatectomy.
  • [MeSH-major] DNA-Binding Proteins / genetics. Prostatic Neoplasms / genetics. Trans-Activators / genetics
  • [MeSH-minor] Antigens, Neoplasm / genetics. Glutathione S-Transferase pi. Glutathione Transferase / genetics. Humans. Isoenzymes / genetics. Male. Racemases and Epimerases / genetics. Reverse Transcriptase Polymerase Chain Reaction. Transcription, Genetic

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  • [ErratumIn] Oncogene. 2007 Oct 11;26(46):6684. Furasato, Bungo [corrected to Furusato, Bungo]
  • (PMID = 15750627.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK065977
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / DNA-Binding Proteins; 0 / ERG protein, human; 0 / Isoenzymes; 0 / Trans-Activators; 0 / prostate cancer antigen 3, human; EC 2.5.1.18 / GSTP1 protein, human; EC 2.5.1.18 / Glutathione S-Transferase pi; EC 2.5.1.18 / Glutathione Transferase; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
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30. Tang J, Yang JC, Li Y, Li J, Shi H: Peripheral zone hypoechoic lesions of the prostate: evaluation with contrast-enhanced gray scale transrectal ultrasonography. J Ultrasound Med; 2007 Dec;26(12):1671-9
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  • [Title] Peripheral zone hypoechoic lesions of the prostate: evaluation with contrast-enhanced gray scale transrectal ultrasonography.
  • OBJECTIVE: The purpose of this study was to evaluate the efficacy of contrast-enhanced gray scale transrectal ultrasonography (TRUS) for detection of prostate cancer in peripheral zone hypoechoic lesions of the prostate.
  • The lesions were evaluated with contrast-enhanced TRUS to differentiate prostate cancer from benign lesions, and the results were compared with color Doppler ultrasonographic findings.
  • RESULTS: Transrectal ultrasonographically guided biopsy of the hypoechoic lesions revealed prostate cancer in 30 patients and benign prostatic diseases in 36.
  • Flow signals within the lesions were classified as no, increased, equal, and decreased flow compared with surrounding peripheral zone tissue as follows: 1, 16, 12, and 1, respectively, in the prostate cancer group and 10, 12, 10, and 4 in the benign disease group.
  • If we considered an increased flow signal within a peripheral hypoechoic lesion as a sign of prostate cancer, color Doppler ultrasonography had low sensitivity and specificity (55.2% and 53.8%, respectively).
  • The enhancement intensity within the lesions was classified as no, increased, equal, and decreased enhancement compared with surrounding peripheral zone tissue as follows: 2, 20, 3, and 5 in the prostate cancer group and 14, 8, 4, and 10 in the benign disease group.
  • CONCLUSIONS: Contrast-enhanced TRUS could reveal the presence of vasculature within peripheral zone hypoechoic lesions more objectively than color Doppler ultrasonography and could be promising in guidance of prostate biopsy.
  • [MeSH-major] Phospholipids. Prostate / ultrasonography. Prostatic Neoplasms / ultrasonography. Rectum / ultrasonography. Sulfur Hexafluoride. Ultrasonography / methods

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  • (PMID = 18029918.001).
  • [ISSN] 0278-4297
  • [Journal-full-title] Journal of ultrasound in medicine : official journal of the American Institute of Ultrasound in Medicine
  • [ISO-abbreviation] J Ultrasound Med
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Contrast Media; 0 / Phospholipids; 0 / contrast agent BR1; WS7LR3I1D6 / Sulfur Hexafluoride
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31. Marks LS, Fradet Y, Deras IL, Blase A, Mathis J, Aubin SM, Cancio AT, Desaulniers M, Ellis WJ, Rittenhouse H, Groskopf J: PCA3 molecular urine assay for prostate cancer in men undergoing repeat biopsy. Urology; 2007 Mar;69(3):532-5
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  • [Title] PCA3 molecular urine assay for prostate cancer in men undergoing repeat biopsy.
  • OBJECTIVES: Men with elevated serum prostate-specific antigen (PSA) levels and negative prostate biopsy findings present a dilemma because of the lack of an accurate diagnostic test.
  • We evaluated the potential utility of the investigational prostate cancer gene 3 (PCA3) urine assay to predict the repeat biopsy outcome.
  • Repeat biopsy revealed prostate cancer in 60 (27%) of the of 226 remaining subjects.
  • At PCA3 scores of less than 5, only 12% of men had prostate cancer on repeat biopsy; at PCA3 scores greater than 100, the risk of positive biopsy was 50%.
  • CONCLUSIONS: In men undergoing repeat prostate biopsy to rule out cancer, the urinary PCA3 score was superior to serum PSA determination for predicting the biopsy outcome.
  • The high specificity and informative rate suggest that the PCA3 assay could have an important role in prostate cancer diagnosis.
  • [MeSH-major] Antigens, Neoplasm / urine. Prostatic Neoplasms / diagnosis
  • [MeSH-minor] Aged. Aged, 80 and over. Biopsy, Needle. Gene Expression. Humans. Immunoassay / methods. Male. Middle Aged. Prostate-Specific Antigen / genetics. RNA, Messenger / analysis. ROC Curve. Sensitivity and Specificity


32. Chang CH, Chiu CF, Wu HC, Tseng HC, Wang CH, Lin CC, Tsai CW, Liang SY, Wang CL, Bau DT: Significant association of XRCC4 single nucleotide polymorphisms with prostate cancer susceptibility in Taiwanese males. Mol Med Rep; 2008 Jul-Aug;1(4):525-30
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  • [Title] Significant association of XRCC4 single nucleotide polymorphisms with prostate cancer susceptibility in Taiwanese males.
  • In this case-control study, several novel polymorphic variants of XRCC4, including C-1622T (rs7727691), G-1394T (rs6869366), C-571T (rs2075686) and intron3 DIP (rs28360071), were investigated, and the correlation of these variants to prostate cancer susceptibility in a Taiwanese population was observed.
  • A total of 134 prostate cancer patients were recruited along with 134 age-matched healthy controls, and the association of their selected genotypes with susceptibility to prostate cancer was determined.
  • The G-1394T variant of XRCC4 proved, after analysis of the frequencies of each variant in the prostate cancer and control groups, to be a significant single nucleotide polymorphism (SNP) in prostate carcinogenesis.
  • Our data clearly indicate that the heterogeneous G of G-1394T increases the risk of suceptibility to prostate cancer (P=0.0106), while no difference in distribution of XRCC4 C-1622T (rs7727691), C-571T (rs2075686) or intron3 DIP (rs28360071) between the prostate cancer and control groups was found.
  • In conclusion, our findings suggest that the G allele of XRCC4 G-1394T may be responsible for prostate carcinogenesis, and could be useful in the early detection and prevention of the disease.

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  • (PMID = 21479444.001).
  • [ISSN] 1791-2997
  • [Journal-full-title] Molecular medicine reports
  • [ISO-abbreviation] Mol Med Rep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
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33. Liu X, Cicek MS, Plummer SJ, Jorgenson E, Casey G, Witte JS: Association of testis derived transcript gene variants and prostate cancer risk. J Urol; 2007 Mar;177(3):894-8
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  • [Title] Association of testis derived transcript gene variants and prostate cancer risk.
  • PURPOSE: The testis derived transcript gene has been suggested as a tumor suppressor gene for prostate cancer at 7q31.
  • To investigate this concept we evaluated the effects of 7 tagging single nucleotide polymorphisms that comprehensively captured the common genetic variants in TES on aggressive prostate cancer in a case-control study.
  • MATERIALS AND METHODS: A total of 506 cases diagnosed with aggressive prostate cancer, and an equal number of age, institute and ethnicity matched controls, were recruited from the major medical institutions in Cleveland, Ohio.
  • A logistic regression model was used to evaluate the association between SNPs/multimarker haplotypes and prostate cancer.
  • CONCLUSIONS: Our findings suggest that the variants in TES, or in a nearby gene, may be associated with prostate cancer in black men.
  • [MeSH-major] African Americans / genetics. European Continental Ancestry Group / genetics. Homeodomain Proteins / genetics. Polymorphism, Single Nucleotide / genetics. Prostatic Neoplasms / ethnology. Prostatic Neoplasms / genetics. Tumor Suppressor Proteins / genetics
  • [MeSH-minor] Aged. Case-Control Studies. Cytoskeletal Proteins. Genotype. Humans. LIM Domain Proteins. Male. Middle Aged. Neoplasm Staging

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  • (PMID = 17296370.001).
  • [ISSN] 0022-5347
  • [Journal-full-title] The Journal of urology
  • [ISO-abbreviation] J. Urol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA88164; United States / NCI NIH HHS / CA / CA94211; United States / NCI NIH HHS / CA / CA98683
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytoskeletal Proteins; 0 / Homeodomain Proteins; 0 / LIM Domain Proteins; 0 / TES protein, human; 0 / Tumor Suppressor Proteins
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34. Escaff S, Fernández JM, González LO, Suárez A, González-Reyes S, González JM, Vizoso FJ: Study of matrix metalloproteinases and their inhibitors in prostate cancer. Br J Cancer; 2010 Mar 2;102(5):922-9
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  • [Title] Study of matrix metalloproteinases and their inhibitors in prostate cancer.
  • BACKGROUND: Extracellular matrix metalloproteases (MMPs) have raised an extraordinary interest in cancer research because of their potential role in basal membrane and extracellular matrix degradation, consequently facilitating tumour invasion and metastases development.
  • More than 2600 determinations on cancer specimens from 133 patients with clinically localised prostate carcinoma, 20 patients with prostatic intraepithelial neoplasia and 50 patients with benign prostate hyperplasia and controls, were performed.
  • RESULTS: When compared with benign pathologies, prostate carcinomas had higher expression of all MMPs and TIMPs.
  • CONCLUSION: The expression of MMPs and TIMPs seems to have an important role in the molecular biology of prostate carcinomas, and their expression by tumours may be of clinical interest to used as indicators of tumour aggressiveness.
  • [MeSH-major] Adenocarcinoma / metabolism. Matrix Metalloproteinases / metabolism. Prostatic Hyperplasia / metabolism. Prostatic Intraepithelial Neoplasia / metabolism. Prostatic Neoplasms / metabolism. Tissue Inhibitor of Metalloproteinases / metabolism
  • [MeSH-minor] Aged. Biomarkers, Tumor / metabolism. Follow-Up Studies. Humans. Immunoenzyme Techniques. Male. Middle Aged. Neoplasm Recurrence, Local / metabolism. Neoplasm Recurrence, Local / pathology. Prognosis. Survival Rate. Tissue Array Analysis

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  • (PMID = 20160732.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Tissue Inhibitor of Metalloproteinases; EC 3.4.24.- / Matrix Metalloproteinases
  • [Other-IDs] NLM/ PMC2833257
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35. Trock BJ, Han M, Freedland SJ, Humphreys EB, DeWeese TL, Partin AW, Walsh PC: Prostate cancer-specific survival following salvage radiotherapy vs observation in men with biochemical recurrence after radical prostatectomy. JAMA; 2008 Jun 18;299(23):2760-9
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  • [Title] Prostate cancer-specific survival following salvage radiotherapy vs observation in men with biochemical recurrence after radical prostatectomy.
  • OBJECTIVES: To quantify the relative improvement in prostate cancer-specific survival of salvage radiotherapy vs no therapy after biochemical recurrence following prostatectomy, and to identify subgroups for whom salvage treatment is most beneficial.
  • MAIN OUTCOME MEASURE: Prostate cancer-specific survival defined from time of recurrence until death from disease.
  • RESULTS: With a median follow-up of 6 years after recurrence and 9 years after prostatectomy, 116 men (18%) died from prostate cancer, including 89 (22%) who received no salvage treatment, 18 (11%) who received salvage radiotherapy alone, and 9 (12%) who received salvage radiotherapy and hormonal therapy.
  • Salvage radiotherapy alone was associated with a significant 3-fold increase in prostate cancer-specific survival relative to those who received no salvage treatment (hazard ratio [HR], 0.32 [95% confidence interval {CI}, 0.19-0.54]; P<.001).
  • Addition of hormonal therapy to salvage radiotherapy was not associated with any additional increase in prostate cancer-specific survival (HR, 0.34 [95% CI, 0.17-0.69]; P = .003).
  • The increase in prostate cancer-specific survival associated with salvage radiotherapy was limited to men with a prostate-specific antigen doubling time of less than 6 months and remained after adjustment for pathological stage and other established prognostic factors.
  • Salvage radiotherapy initiated more than 2 years after recurrence provided no significant increase in prostate cancer-specific survival.
  • Men whose prostate-specific antigen level never became undetectable after salvage radiotherapy did not experience a significant increase in prostate cancer-specific survival.
  • CONCLUSIONS: Salvage radiotherapy administered within 2 years of biochemical recurrence was associated with a significant increase in prostate cancer-specific survival among men with a prostate-specific antigen doubling time of less than 6 months, independent of other prognostic features such as pathological stage or Gleason score.


36. Lindström S, Ma J, Altshuler D, Giovannucci E, Riboli E, Albanes D, Allen NE, Berndt SI, Boeing H, Bueno-de-Mesquita HB, Chanock SJ, Dunning AM, Feigelson HS, Gaziano JM, Haiman CA, Hayes RB, Henderson BE, Hunter DJ, Kaaks R, Kolonel LN, Le Marchand L, Martínez C, Overvad K, Siddiq A, Stampfer M, Stattin P, Stram DO, Thun MJ, Trichopoulos D, Tumino R, Virtamo J, Weinstein SJ, Yeager M, Kraft P, Freedman ML: A large study of androgen receptor germline variants and their relation to sex hormone levels and prostate cancer risk. Results from the National Cancer Institute Breast and Prostate Cancer Cohort Consortium. J Clin Endocrinol Metab; 2010 Sep;95(9):E121-7
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  • [Title] A large study of androgen receptor germline variants and their relation to sex hormone levels and prostate cancer risk. Results from the National Cancer Institute Breast and Prostate Cancer Cohort Consortium.
  • BACKGROUND: Androgens are key regulators of prostate gland maintenance and prostate cancer growth, and androgen deprivation therapy has been the mainstay of treatment for advanced prostate cancer for many years.
  • A long-standing hypothesis has been that inherited variation in the androgen receptor (AR) gene plays a role in prostate cancer initiation.
  • OBJECTIVE AND METHODS: We investigated the association of AR sequence variants with circulating sex hormone levels and prostate cancer risk in 6058 prostate cancer cases and 6725 controls of Caucasian origin within the Breast and Prostate Cancer Cohort Consortium.
  • We genotyped a highly polymorphic CAG microsatellite in exon 1 and six haplotype tagging single nucleotide polymorphisms and tested each genetic variant for association with prostate cancer risk and with sex steroid levels.
  • RESULTS: We observed no association between AR genetic variants and prostate cancer risk.
  • CONCLUSIONS: This study is the largest to date investigating AR sequence variants, sex steroid levels, and prostate cancer risk.
  • Although we observed no association between AR sequence variants and prostate cancer risk, our results support earlier findings of a relation between the number of CAG repeats and circulating levels of testosterone and estradiol.
  • [MeSH-major] Carcinoma / genetics. Gonadal Steroid Hormones / blood. Prostatic Neoplasms / genetics. Receptors, Androgen / genetics
  • [MeSH-minor] Aged. Breast Neoplasms / genetics. Case-Control Studies. Cohort Studies. Female. Genetic Association Studies. Genetic Predisposition to Disease. Germ-Line Mutation / physiology. Humans. Male. Middle Aged. National Cancer Institute (U.S.). Risk. Trinucleotide Repeats / genetics. United States

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  • (PMID = 20534771.001).
  • [ISSN] 1945-7197
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / UO1-CA98758; United Kingdom / Cancer Research UK / / A10123; United States / NCI NIH HHS / CA / U01 CA098216; United States / Intramural NIH HHS / / ; United States / NCI NIH HHS / CA / UO1-CA98233; United States / NCI NIH HHS / CA / UO1-CA98216; United States / NCI NIH HHS / CA / U01 CA098233; United States / NCI NIH HHS / CA / U01 CA098758; United States / NCI NIH HHS / CA / UO1-CA98710; United States / NCI NIH HHS / CA / R01 CA097193; United States / NCI NIH HHS / CA / U01 CA098710
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AR protein, human; 0 / Gonadal Steroid Hormones; 0 / Receptors, Androgen
  • [Other-IDs] NLM/ PMC2936075
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37. Tomlins SA, Mehra R, Rhodes DR, Cao X, Wang L, Dhanasekaran SM, Kalyana-Sundaram S, Wei JT, Rubin MA, Pienta KJ, Shah RB, Chinnaiyan AM: Integrative molecular concept modeling of prostate cancer progression. Nat Genet; 2007 Jan;39(1):41-51
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Integrative molecular concept modeling of prostate cancer progression.
  • Despite efforts to profile prostate cancer, the genetic alterations and biological processes that correlate with the observed histological progression are unclear.
  • Using laser-capture microdissection to isolate 101 cell populations, we have profiled prostate cancer progression from benign epithelium to metastatic disease.
  • Of note, relative to low-grade prostate cancer (Gleason pattern 3), high-grade cancer (Gleason pattern 4) shows an attenuated androgen signaling signature, similar to metastatic prostate cancer, which may reflect dedifferentiation and explain the clinical association of grade with prognosis.
  • [MeSH-major] Gene Expression Profiling. Models, Theoretical. Prostatic Neoplasms / genetics. Prostatic Neoplasms / pathology
  • [MeSH-minor] Androgens / metabolism. Disease Progression. Humans. Male. Neoplasm Metastasis. Prostatic Hyperplasia / genetics. Prostatic Hyperplasia / pathology. Prostatic Intraepithelial Neoplasia / genetics. Prostatic Intraepithelial Neoplasia / pathology. Signal Transduction. Systems Integration

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  • (PMID = 17173048.001).
  • [ISSN] 1061-4036
  • [Journal-full-title] Nature genetics
  • [ISO-abbreviation] Nat. Genet.
  • [Language] eng
  • [Databank-accession-numbers] GEO/ GSE6099
  • [Grant] United States / NCI NIH HHS / CA / 5P30 CA46592; United States / NCI NIH HHS / CA / P50CA69568; United States / NCI NIH HHS / CA / R01 CA102872; United States / NIDA NIH HHS / DA / U54 DA021519-01A1; United States / NCI NIH HHS / CA / UO1 CA111275-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens
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38. Rayford W: Managing the low-socioeconomic-status prostate cancer patient. J Natl Med Assoc; 2006 Apr;98(4):521-30
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  • [Title] Managing the low-socioeconomic-status prostate cancer patient.
  • Management of patients with low socioeconomic status and/or low literacy who have prostate cancer presents a challenge to healthcare professionals.
  • Improving treatment outcomes for these men requires specific educational programs to provide a better understanding of prostate cancer including careful posttreatment follow-up to ensure they have recovered well, that the cancer is not progressing and that complications are not proving troublesome.
  • Education and knowledgeable advice can lead to earlier diagnosis of prostate cancer, improved patient participation in the treatment decision-making process and effective management of posttreatment complications.
  • [MeSH-major] Decision Making. Prostatic Neoplasms / therapy. Social Class

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  • (PMID = 16623064.001).
  • [ISSN] 1943-4693
  • [Journal-full-title] Journal of the National Medical Association
  • [ISO-abbreviation] J Natl Med Assoc
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 34
  • [Other-IDs] NLM/ PMC2569254
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39. Chapel-Fernandes S, Jordier F, Lauro F, Maitland N, Chiaroni J, de Micco P, Mannoni P, Bagnis C: Use of the PSA enhancer core element to modulate the expression of prostate- and non-prostate-specific basal promoters in a lentiviral vector context. Cancer Gene Ther; 2006 Oct;13(10):919-29
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  • [Title] Use of the PSA enhancer core element to modulate the expression of prostate- and non-prostate-specific basal promoters in a lentiviral vector context.
  • Composite promoters combining the prostate-specific antigen (PSA) enhancer core element with promoter elements derived from gene coding for human prostate-specific transglutaminase gene, prostate-specific membrane antigen gene, prostate-specific antigen, rat probasin or phosphoglycerate kinase were characterized for their ability to specifically express the enhanced green fluorescent protein (EGFP) gene in prostate versus non-prostate cancer cell lines when transferred with a human immunodeficiency virus-1-based lentiviral vector.
  • By themselves minimal proximal promoter elements were found to inefficiently promote relevant tissue-specific expression; in all the vectors tested, addition of the PSA enhancer core element markedly improved EGFP expression in LnCaP, a cancer prostate cell line used as a model for prostate cancer.
  • The composite promoter was inactive in HuH7, a hepatocarcinoma cell line used as a model of neighboring non-prostate cancer cells.
  • Our data suggest that composite prostate-specific promoters constructed by combining key elements from various promoters can improve and/or confer tissue specific expression in a lentiviral vector context.
  • [MeSH-major] Enhancer Elements, Genetic. Genetic Vectors. Lentivirus / genetics. Promoter Regions, Genetic. Prostate / metabolism. Prostate-Specific Antigen / genetics
  • [MeSH-minor] Cell Line, Tumor. Green Fluorescent Proteins / genetics. Humans. Male

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  • (PMID = 16741521.001).
  • [ISSN] 0929-1903
  • [Journal-full-title] Cancer gene therapy
  • [ISO-abbreviation] Cancer Gene Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / enhanced green fluorescent protein; 147336-22-9 / Green Fluorescent Proteins; EC 3.4.21.77 / Prostate-Specific Antigen
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40. Urba WJ, Nemunaitis J, Marshall F, Smith DC, Hege KM, Ma J, Nguyen M, Small EJ: Treatment of biochemical recurrence of prostate cancer with granulocyte-macrophage colony-stimulating factor secreting, allogeneic, cellular immunotherapy. J Urol; 2008 Nov;180(5):2011-7; discussion 2017-8
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  • [Title] Treatment of biochemical recurrence of prostate cancer with granulocyte-macrophage colony-stimulating factor secreting, allogeneic, cellular immunotherapy.
  • PURPOSE: This phase I-II study evaluated the safety, clinical activity and immunogenicity of an immunotherapy developed from human prostate cancer cell lines (PC-3 and LNCaP) modified to secrete granulocyte-macrophage colony-stimulating factor.
  • MATERIALS AND METHODS: Patients with noncastrate prostate cancer (19) with biochemical (prostate specific antigen) recurrence following prostatectomy or radiation therapy and no radiological evidence of metastasis were enrolled in the study.
  • The adverse event profile, prostate specific antigen response, changes in prostate specific antigen kinetics and immunogenicity were assessed.
  • A negative deflection in prostate specific antigen slope was observed in 84% of patients after treatment with a significant increase in median prostate specific antigen doubling time from 28.7 weeks before treatment to 57.1 weeks after treatment (p = 0.0095).
  • Median time to prostate specific antigen progression was 9.7 months.
  • Induction of antibody responses reactive against PC-3 in general, and to the PC-3 associated filamin-B protein specifically, were positively associated with treatment associated changes in prostate specific antigen kinetics.
  • CONCLUSIONS: Granulocyte-macrophage colony-stimulating factor secreting cellular immunotherapy has a favorable toxicity profile with signals of clinical and immunological activity against hormone naïve prostate cancer.
  • An association between immune response and prostate specific antigen changes was observed.
  • Phase 3 trials in patients with advanced, metastatic, hormone refractory prostate cancer are under way.
  • [MeSH-major] Cancer Vaccines / administration & dosage. Granulocyte-Macrophage Colony-Stimulating Factor / administration & dosage. Immunotherapy / methods. Neoplasm Recurrence, Local / therapy. Prostate-Specific Antigen / blood. Prostatic Neoplasms / therapy
  • [MeSH-minor] Aged. Aged, 80 and over. Dose-Response Relationship, Drug. Drug Administration Schedule. Humans. Injections, Subcutaneous. Male. Middle Aged. Neoplasm Staging. Probability. Prognosis. Prostatectomy / methods. Radiotherapy, Conformal / methods. Risk Assessment. Statistics, Nonparametric. Survival Rate. Treatment Outcome

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  • (PMID = 18801509.001).
  • [ISSN] 1527-3792
  • [Journal-full-title] The Journal of urology
  • [ISO-abbreviation] J. Urol.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase I; Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cancer Vaccines; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor; EC 3.4.21.77 / Prostate-Specific Antigen
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41. Wu GJ, Fu P, Chiang CF, Huss WJ, Greenberg NM, Wu MW: Increased expression of MUC18 correlates with the metastatic progression of mouse prostate adenocarcinoma in the TRAMP model. J Urol; 2005 May;173(5):1778-83
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  • [Title] Increased expression of MUC18 correlates with the metastatic progression of mouse prostate adenocarcinoma in the TRAMP model.
  • PURPOSE: The transgenic adenocarcinoma mouse prostate (TRAMP) model is a paradigm that closely mimics the progression of clinical prostate cancer.
  • We have previously reported that MUC18, a cell adhesion molecule in the Ig gene superfamily, is a marker as well as an important mediator for the metastatic potential of human prostate cancer cells.
  • In this study we investigated the possible correlation of increased MUC18 expression with the malignant progression of prostate cancer in the TRAMP model.
  • MATERIALS AND METHODS: We used immunohistochemistry, Western blot and reverse transcriptase-polymerase chain reaction analyses to determine MUC18 expression in the prostate gland of 178 to 282-day-old TRAMP positive males with a prostate tumor size of 0.4 to 12.7 gm.
  • Eight normal prostates, 10 prostates with high grade prostatic intraepithelial neoplasia (PIN), 24 prostates with primary prostate cancer, 10 metastatic lesions from 50 pure C57BL/6 TRAMP mice (Wu colony) and 2 normal prostates, 2 prostates with high grade PIN, 6 prostates with primary prostate cancer and 4 metastatic lesions from 10 [C57BL/6 TRAMP x FVB] F1 mice (NMG colony) were used.
  • All mice bearing primary prostate tumors had prostate cancer metastatic to the peri-aortic lymph nodes and some had it to other organs (liver, lung, kidney, testes, seminal vesicles and abdominal cavity).
  • CONCLUSIONS: MUC18 expression is up-regulated in the TRAMP model and it correlates with the malignant progression of mouse prostate adenocarcinoma in this transgenic model.
  • This further strengthens the hypothesis that MUC18 has an important role in increasing the metastatic potential of prostate cancer cells.
  • [MeSH-major] Adenocarcinoma / metabolism. Adenocarcinoma / secondary. Antigens, CD / biosynthesis. Biomarkers, Tumor / biosynthesis. Neural Cell Adhesion Molecules / biosynthesis. Prostatic Neoplasms / metabolism. Prostatic Neoplasms / pathology

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  • (PMID = 15821586.001).
  • [ISSN] 0022-5347
  • [Journal-full-title] The Journal of urology
  • [ISO-abbreviation] J. Urol.
  • [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 / Antigens, CD; 0 / Antigens, CD146; 0 / Biomarkers, Tumor; 0 / Mcam protein, mouse; 0 / Neural Cell Adhesion Molecules
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42. Fujimoto N, Miyamoto H, Mizokami A, Harada S, Nomura M, Ueta Y, Sasaguri T, Matsumoto T: Prostate cancer cells increase androgen sensitivity by increase in nuclear androgen receptor and androgen receptor coactivators; a possible mechanism of hormone-resistance of prostate cancer cells. Cancer Invest; 2007 Feb;25(1):32-7
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  • [Title] Prostate cancer cells increase androgen sensitivity by increase in nuclear androgen receptor and androgen receptor coactivators; a possible mechanism of hormone-resistance of prostate cancer cells.
  • Although androgen-hypersensitivity is one of the possible pathways of hormone-resistance in prostate cancer, the mechanisms of androgen-hypersensitivity are still largely unknown.
  • Using androgen-hypersensitive prostate cancer cells LN-TR2, established from androgen-sensitive LNCaP cells by the long term treatment with tumor necrosis factor alpha, we explored the mechanisms of androgen-hypersensitivity in prostate cancer cells which may thus play a role in hormone-resistance.
  • In 2 of 6 patients, the expression level of ARA55 was higher in cancer cells in hormone-resistant tumor than those in hormone-sensitive tumor.
  • Taken together, our results suggest that prostate cancer cells change androgen-sensitivity by an overexpression of nuclear AR and AR coactivators, thus, resulting in transition from androgen-dependent to androgen-independent prostate cancer cells.
  • An increase in nuclear AR and AR coactivators may cause androgen-hypersensitivity of prostate cancer cells and thus play a role in hormone-resistance, at least in some patients with prostate cancer.
  • [MeSH-major] Drug Resistance, Neoplasm / physiology. Neoplasms, Hormone-Dependent / metabolism. Prostatic Neoplasms / metabolism. Receptors, Androgen / metabolism
  • [MeSH-minor] Androgen Antagonists / pharmacology. Antineoplastic Agents, Hormonal / pharmacology. Blotting, Western. Cell Line, Tumor. Cell Nucleus / metabolism. Humans. Immunohistochemistry. Intracellular Signaling Peptides and Proteins / metabolism. LIM Domain Proteins. Male. Nuclear Receptor Coactivator 2 / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Transfection. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 17364555.001).
  • [ISSN] 0735-7907
  • [Journal-full-title] Cancer investigation
  • [ISO-abbreviation] Cancer Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Antineoplastic Agents, Hormonal; 0 / Intracellular Signaling Peptides and Proteins; 0 / LIM Domain Proteins; 0 / NCOA2 protein, human; 0 / Nuclear Receptor Coactivator 2; 0 / Receptors, Androgen; 0 / TGFB1I1 protein, human; 0 / Tumor Necrosis Factor-alpha
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43. Kalender ME, Sevinc A, Kucukdurmaz Z, Balik A, Sari I, Camci C: Gastric and prostate adenocarcinoma in a patient with metastatic gastrointestinal stromal tumor. Onkologie; 2007 Nov;30(11):568-70
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  • [Title] Gastric and prostate adenocarcinoma in a patient with metastatic gastrointestinal stromal tumor.
  • BACKGROUND: Gastrointestinal stromal tumor (GIST) is the most common mesenchymal malignancy of the gastrointestinal tract.
  • Gastric cancer is the second most common neoplasm worldwide.
  • Prostate cancer is the most common non-cutaneous cancer.
  • The most frequently encountered second malignancies in patients with prostate adenocarcinoma include carcinomas of the bladder, stomach, and colon, followed by cutaneous and hematolymphoid malignancies.
  • At followup 6 months later, prostate-specific antigen (PSA) levels were elevated, and a prostate biopsy showed a prostate adenocarcinoma.
  • CONCLUSION: This is the second report of metachronous prostate cancer, gastric cancer, and GIST in the English language literature.
  • [MeSH-major] Gastrointestinal Stromal Tumors / diagnosis. Prostatic Neoplasms / diagnosis. Prostatic Neoplasms / secondary. Stomach Neoplasms / diagnosis. Stomach Neoplasms / secondary


44. Zeliadt SB, Ramsey SD: Cost-effectiveness of prostate cancer chemoprevention among high-risk men. Expert Rev Pharmacoecon Outcomes Res; 2010 Oct;10(5):505-8
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  • [Title] Cost-effectiveness of prostate cancer chemoprevention among high-risk men.
  • Cost effectiveness of 5-α reductase inhibitors for the prevention of prostate cancer in multiple patient populations.
  • Chemoprevention with 5-α reductase inhibitors (5ARIs) has been shown in clinical trials to reduce the incidence of prostate cancer.
  • Although avoiding or delaying a diagnosis of prostate cancer through chemoprevention is attractive, it is unknown whether 5ARI chemoprevention reduces the number of prostate cancer deaths.
  • The current study examines the cost-effectiveness of 5ARIs for men with multiple risk factors, including an elevated prostate-specific antigen and a prior negative biopsy.

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  • [CommentOn] Pharmacoeconomics. 2010;28(6):489-505 [20196623.001]
  • (PMID = 20950065.001).
  • [ISSN] 1744-8379
  • [Journal-full-title] Expert review of pharmacoeconomics & outcomes research
  • [ISO-abbreviation] Expert Rev Pharmacoecon Outcomes Res
  • [Language] eng
  • [Publication-type] Comment; Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
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45. Han B, Mehra R, Suleman K, Tomlins SA, Wang L, Singhal N, Linetzky KA, Palanisamy N, Zhou M, Chinnaiyan AM, Shah RB: Characterization of ETS gene aberrations in select histologic variants of prostate carcinoma. Mod Pathol; 2009 Sep;22(9):1176-85
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  • [Title] Characterization of ETS gene aberrations in select histologic variants of prostate carcinoma.
  • Histologic variants of prostate carcinoma account for 5-10% of the disease and are typically seen in association with conventional acinar carcinoma.
  • Recently, recurrent gene fusions between the androgen-regulated gene TMPRSS2 and the ETS transcription factors ERG, ETV1, ETV4, or ETV5 have been identified in a majority of conventional prostate carcinomas.
  • However, the frequency and significance of this critical molecular event is unknown in the histologic variants of prostate carcinoma.
  • Here, we used break-apart fluorescence in situ hybridization to assess TMPRSS2 and ETS aberrations in a series of select histologic variants: foamy gland carcinoma (N=17), ductal adenocarcinoma (N=18), mucinous carcinoma (N=18), and small cell carcinoma (N=7).
  • TMPRSS2:ERG fusion was identified in 83% (15/18), 71% (5/7), 50% (9/18), 33% (3/9), and 29% (5/17) of mucinous, small cell, ductal, glomeruloid, and foamy gland prostate carcinomas, respectively.
  • Previously, we reported that 100% of androgen-independent metastatic prostate carcinomas harboring TMPRSS2:ERG gene fusion were associated with interstitial deletion (Edel).
  • SPINK1, a biomarker expressed exclusively in a subset of ETS negative prostate carcinomas, was expressed in 6% of ETS negative histologic variants, specifically in ductal adenocarcinoma.
  • Overall, our data provide insight into the origin, molecular mechanism, and phenotypic association of ETS fusions in histologic variants of prostate carcinoma.

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  • (PMID = 19465903.001).
  • [ISSN] 1530-0285
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA069568-110020; United States / NCI NIH HHS / CA / U01 CA111275-01; United States / NCI NIH HHS / CA / R01 CA102872; United States / NCI NIH HHS / CA / P50CA69568; United States / NCI NIH HHS / CA / CA069568-110020; United States / NCI NIH HHS / CA / UO1 CA111275-01; United States / NCI NIH HHS / CA / P50 CA069568; United States / NCI NIH HHS / CA / U01 CA111275
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Carrier Proteins; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins c-ets; 0 / SPINK1 protein, human; 0 / TMPRSS2-ERG fusion protein, human; 0 / TMPRSS2-ETV1 fusion protein, human
  • [Other-IDs] NLM/ NIHMS148618; NLM/ PMC2760291
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46. van der Wielen GJ, Mutanga TF, Incrocci L, Kirkels WJ, Vasquez Osorio EM, Hoogeman MS, Heijmen BJ, de Boer HC: Deformation of prostate and seminal vesicles relative to intraprostatic fiducial markers. Int J Radiat Oncol Biol Phys; 2008 Dec 1;72(5):1604-1611.e3
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  • [Title] Deformation of prostate and seminal vesicles relative to intraprostatic fiducial markers.
  • PURPOSE: To quantify the residual geometric uncertainties after on-line corrections with intraprostatic fiducial markers, this study analyzed the deformation of the prostate and, in particular, the seminal vesicles relative to such markers.
  • PATIENTS AND METHODS: A planning computed tomography (CT) scan and three repeat CT scans were obtained for 21 prostate cancer patients who had had three to four cylindrical gold markers placed.
  • The prostate and whole seminal vesicles (clinical target volume [CTV]) were delineated on each scan at a slice thickness of 1.5 mm.
  • Prostate deformation was small (standard deviation </=1 mm).
  • CONCLUSION: Although prostate deformation with respect to implanted fiducial markers was small, the corresponding deformation of the seminal vesicles was considerable.
  • [MeSH-major] Prostate / abnormalities. Prostate / radiography. Prostatic Neoplasms / radiotherapy. Seminal Vesicles / pathology. Seminal Vesicles / radiography

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  • (PMID = 19028284.001).
  • [ISSN] 1879-355X
  • [Journal-full-title] International journal of radiation oncology, biology, physics
  • [ISO-abbreviation] Int. J. Radiat. Oncol. Biol. Phys.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers
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47. Chodak GW, Warren KS: Watchful waiting for prostate cancer: a review article. Prostate Cancer Prostatic Dis; 2006;9(1):25-9
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  • [Title] Watchful waiting for prostate cancer: a review article.
  • As earlier detection of prostate cancer increases because of prostate-specific antigen (PSA) testing, appropriate use for watchful waiting warrants re-evaluation.
  • Watchful waiting has the potential to play an increasingly important role in prostate cancer as less advanced disease is detected and methods are refined for identifying low-risk patients.
  • [MeSH-major] Prostate-Specific Antigen / blood. Prostatic Neoplasms / therapy


48. Breyer JP, McReynolds KM, Yaspan BL, Bradley KM, Dupont WD, Smith JR: Genetic variants and prostate cancer risk: candidate replication and exploration of viral restriction genes. Cancer Epidemiol Biomarkers Prev; 2009 Jul;18(7):2137-44
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  • [Title] Genetic variants and prostate cancer risk: candidate replication and exploration of viral restriction genes.
  • The genetic variants underlying the strong heritable component of prostate cancer remain largely unknown.
  • Genome-wide association studies of prostate cancer have yielded several variants that have significantly replicated across studies, predominantly in cases unselected for family history of prostate cancer.
  • Additional candidate gene variants have also been proposed, many evaluated within familial prostate cancer study populations.
  • Such variants hold great potential value for risk stratification, particularly for early-onset or aggressive prostate cancer, given the comorbidities associated with current therapies.
  • Here, we investigate a Caucasian study population of 523 independent familial prostate cancer cases and 523 age-matched controls without a personal or family history of prostate cancer.
  • [MeSH-major] Chromosomes, Human, X / genetics. European Continental Ancestry Group / genetics. Genetic Predisposition to Disease / genetics. Polymorphism, Single Nucleotide / genetics. Prostatic Neoplasms / genetics

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  • (PMID = 19567509.001).
  • [ISSN] 1538-7755
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA068485; United States / NCI NIH HHS / CA / P30 CA068485; United States / NCI NIH HHS / CA / P30 CA068485-13; United States / NCI NIH HHS / CA / T32 CA009592
  • [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
  • [Other-IDs] NLM/ NIHMS154795; NLM/ PMC2813685
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49. Miyagawa T, Tsutsumi M, Matsumura T, Kawazoe N, Ishikawa S, Shimokama T, Miyanaga N, Akaza H: Real-time elastography for the diagnosis of prostate cancer: evaluation of elastographic moving images. Jpn J Clin Oncol; 2009 Jun;39(6):394-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Real-time elastography for the diagnosis of prostate cancer: evaluation of elastographic moving images.
  • We applied elastography for the diagnosis of prostate cancer and evaluated the usefulness of elastography for prostate biopsy.
  • METHODS: The subjects of this study were 311 patients who underwent elastography during prostate needle biopsy at Hitachi General Hospital.
  • Strain images obtained during compression of the prostate tissue were displayed on a monitor and recorded on the computer.
  • RESULTS: The median patient age was 67 years (range 50-85 years), the median serum level of prostate-specific antigen was 8.4 ng/ml (range 0.3-82.5 ng/ml) and the median prostate volume was 42.6 ml (range 12-150 ml).
  • Among the 311 patients, prostate cancer was detected in 95 patients (30%) by biopsy.
  • Elastography-positive EMIs with negative biopsies were eventually determined to be due to benign prostatic hyperplasia.
  • CONCLUSION: Elastography has a significantly higher sensitivity for the detection of prostate cancer than the conventionally used examinations including DRE and TRUS.
  • [MeSH-major] Diagnostic Imaging / methods. Elasticity Imaging Techniques / methods. Prostatic Neoplasms / diagnosis

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  • (PMID = 19359330.001).
  • [ISSN] 1465-3621
  • [Journal-full-title] Japanese journal of clinical oncology
  • [ISO-abbreviation] Jpn. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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50. Yang TH, Leung SK, Phipps S, Reuben RL, McNeill SA, Habib FK, Schnieder A, Stevens R: In-vitro dynamic micro-probing and the mechanical properties of human prostate tissues. Technol Health Care; 2006;14(4-5):281-96
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  • [Title] In-vitro dynamic micro-probing and the mechanical properties of human prostate tissues.
  • In vitro macro- and micro-indentation test systems have been designed to measure the dynamic micro-mechanical properties of human prostate tissues at actuation frequencies between 5 Hz and 30 Hz, and 0.5 Hz and 20 Hz, respectively.
  • The development of in vitro test systems was aimed at assessing the capacity of such an in vivo medical probe to provide information useful for the diagnosis of various prostate diseases.
  • The macro-indentation test system is an established one, which we have used to determine structure-property relationships in human and canine prostate tissues and here we use it to validate a newly-developed micro-indentation test system using a tissue phantom.
  • Mechanical testing was also carried out on sections of prostate tissue harvested from cystectomy and radical prostatectomy, diagnosed with bladder cancer and benign prostatic hyperplasia.
  • Dynamic probing under displacement control was carried at pre-strains between 5% and 8% for macro-probing and at 5% pre-strain for micro-probing, and the general effect of pre-strain on the dynamic mechanical properties (described by the amplitude ratio between stress and strain, and the phase lag between strain and stress) of phantom and prostate tissues is presented.
  • [MeSH-major] Biomechanical Phenomena. Prostatic Hyperplasia / physiopathology. Prostatic Neoplasms / physiopathology. Silicones / analysis
  • [MeSH-minor] Compressive Strength. Diagnosis, Differential. Epithelial Cells / pathology. Humans. Immunohistochemistry. Male. Phantoms, Imaging. Prostate / chemistry. Prostate / pathology. Stromal Cells / pathology. Tissue Engineering

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  • (PMID = 17065751.001).
  • [ISSN] 0928-7329
  • [Journal-full-title] Technology and health care : official journal of the European Society for Engineering and Medicine
  • [ISO-abbreviation] Technol Health Care
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Silicones
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51. Garrison JB, Shaw YJ, Chen CS, Kyprianou N: Novel quinazoline-based compounds impair prostate tumorigenesis by targeting tumor vascularity. Cancer Res; 2007 Dec 1;67(23):11344-52
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  • [Title] Novel quinazoline-based compounds impair prostate tumorigenesis by targeting tumor vascularity.
  • Previous evidence showed the ability of the quinazoline-based alpha(1)-adrenoreceptor antagonist doxazosin to suppress prostate tumor growth via apoptosis.
  • Confocal microscopy revealed a significantly reduced ability of tumor cells to attach to extracellular matrix and migrate through endothelial cells in the presence of DZ-50.
  • In vivo tumorigenicty studies using two androgen-independent human prostate cancer xenografts, PC-3 and DU-145, showed that DZ-50 treatment leads to significant suppression of tumorigenic growth.
  • Exposure to the drug at the time of tumor cell inoculation led to prevention of prostate cancer initiation.
  • Furthermore, DZ-50 resulted in a reduced formation of prostate-tumor derived metastatic lesions to the lungs in an in vivo spontaneous metastasis assay.
  • Thus, our drug discovery approach led to the development of a class of lead (quinazoline-based) compounds with higher potency than doxazosin in suppressing prostate growth by targeting tissue vascularity.
  • This new class of quinazoline-based compounds provides considerable promise as antitumor drugs for the treatment of advanced prostate cancer.

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  • (PMID = 18056461.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA107575; United States / NCI NIH HHS / CA / R01 CA107575-01; United States / NCI NIH HHS / CA / CA112250-02; United States / NCI NIH HHS / CA / CA112250; United States / NCI NIH HHS / CA / R01 CA112250; United States / NCI NIH HHS / CA / CA107575-01; United States / NCI NIH HHS / CA / R01 CA112250-02
  • [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 / 2-(4-(biphenyl-4-sulfonyl)-piperazin-1-yl)-6,7-dipropoxyquinazolin-4-yl-amine; 0 / Adrenergic alpha-Antagonists; 0 / Antigens, CD29; 0 / Quinazolines; NW1291F1W8 / Doxazosin
  • [Other-IDs] NLM/ NIHMS19064; NLM/ PMC2194658
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52. Seki N, Tatsugami K, Naito S: Holmium laser enucleation of the prostate: comparison of outcomes according to prostate size in 97 Japanese patients. J Endourol; 2007 Feb;21(2):192-6
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  • [Title] Holmium laser enucleation of the prostate: comparison of outcomes according to prostate size in 97 Japanese patients.
  • PURPOSE: To review the outcomes associated with holmium laser enucleation of the prostate (HoLEP) to identify the efficacy and safety in relation to the prostate size in subjects with symptomatic benign prostatic hyperplasia (BPH).
  • The morbidity and improvement in the outcome variables were compared in groups classified according to the baseline prostate volume: <50 cm3 (group 1), >or=50 cm3-<100 cm3 (group 2), and >or=100 cm3 (group 3).
  • RESULTS: The peak urinary flow rate (Qmax), postvoiding residual urine volume (PVR), International Prostate Symptom Score (IPSS) and quality of life (QoL) score all improved significantly after HoLEP, and no significant differences were observed among the groups.
  • CONCLUSIONS: Holmium laser enucleation is an effective treatment for symptomatic BPH independent of prostate size.

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  • (PMID = 17338621.001).
  • [ISSN] 0892-7790
  • [Journal-full-title] Journal of endourology
  • [ISO-abbreviation] J. Endourol.
  • [Language] ENG
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] W1XX32SQN1 / Holmium
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53. Sadetsky N, Hubbard A, Carroll PR, Satariano W: Predictive value of serial measurements of quality of life on all-cause mortality in prostate cancer patients: data from CaPSURE (cancer of the prostate strategic urologic research endeavor) database. Qual Life Res; 2009 Oct;18(8):1019-27
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  • [Title] Predictive value of serial measurements of quality of life on all-cause mortality in prostate cancer patients: data from CaPSURE (cancer of the prostate strategic urologic research endeavor) database.
  • In light of the longer survival in patients with prostate cancer and importance of quality of life, we seek to evaluate the association between HRQOL and survival using traditional and novel techniques.
  • METHODS: Patients from CaPSURE (Cancer of the Prostate Strategic Urologic Research Endeavor) who were treated within 6 months of diagnosis and had pre-treatment and sufficient post-treatment follow-up information constituted the study population.
  • Association between HRQOL and survival (defined by all-cause mortality) in patients with prostate cancer was evaluated using Cox proportional hazards models controlling for age at diagnosis, type of treatment received, clinical risk classification, and number of comorbidities.
  • CONCLUSION: This study demonstrated that several domains of HRQOL were significantly associated with survival in a large group of patients with localized prostate cancer.
  • [MeSH-major] Prostatic Neoplasms / diagnosis. Quality of Life

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  • (PMID = 19697155.001).
  • [ISSN] 1573-2649
  • [Journal-full-title] Quality of life research : an international journal of quality of life aspects of treatment, care and rehabilitation
  • [ISO-abbreviation] Qual Life Res
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Other-IDs] NLM/ PMC2744792
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54. Heitzer MD, DeFranco DB: Hic-5/ARA55, a LIM domain-containing nuclear receptor coactivator expressed in prostate stromal cells. Cancer Res; 2006 Jul 15;66(14):7326-33
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  • [Title] Hic-5/ARA55, a LIM domain-containing nuclear receptor coactivator expressed in prostate stromal cells.
  • Prostate gland development and growth requires both androgen action and epithelial-stromal communications.
  • In fact, androgen signaling through the androgen receptor (AR) may be important in both stromal and epithelial cells of the prostate.
  • Because interaction of AR with the coactivator, Hic-5/ARA55, results in enhanced androgen-induced transcription, we analyzed Hic-5/ARA55 expression in prostate tissue sections from normal human donors and prostate cancer patients.
  • In each sample, Hic-5/ARA55 expression was confined to the stromal compartment of the prostate.
  • Furthermore, a prostate stromal cell line, WPMY-1 cells, expresses Hic-5/ARA55, which is localized both at focal adhesion complexes and within the soluble cytoplasmic compartment.
  • These data provide the first demonstration of a stromal-specific AR coactivator that has an effect on an androgen-regulated growth factor that is essential for stromal/epithelial cell communication in the prostate.
  • [MeSH-major] Cytoskeletal Proteins / biosynthesis. DNA-Binding Proteins / biosynthesis. Prostate / metabolism. Prostatic Neoplasms / metabolism

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  • (PMID = 16849583.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA43037
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytoskeletal Proteins; 0 / DNA-Binding Proteins; 0 / Intracellular Signaling Peptides and Proteins; 0 / LIM Domain Proteins; 0 / Receptors, Androgen; 0 / TGFB1I1 protein, human; 126469-10-1 / Fibroblast Growth Factor 7
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55. Jackson MD, McFarlane-Anderson ND, Simon GA, Bennett FI, Walker SP: Urinary phytoestrogens and risk of prostate cancer in Jamaican men. Cancer Causes Control; 2010 Dec;21(12):2249-57
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  • [Title] Urinary phytoestrogens and risk of prostate cancer in Jamaican men.
  • We evaluated the relationship of spot urinary concentrations of phytoestrogens with total prostate cancer and tumor grade in a hospital-based case-control study in Jamaica.
  • Compared with non-producers of equol (reference tertile), men who produced equol were at decreased risk of total prostate cancer (tertile 2: OR, 0.42; CI, 0.23-0.75) (tertile 3: OR, 0.48; CI, 0.26-0.87) (p (trend), 0.020) and high-grade disease (tertile 2: OR, 0.31; CI, 0.15-0.61) (tertile 3: OR, 0.29; CI, 0.13-0.60) (p (trend), 0.001).
  • Higher concentrations of enterolactone were positively related to total prostate cancer (OR, 1.85; CI, 1.01-3.44; p (trend), 0.027) as well as high-grade disease (OR, 2.46; CI, 1.11-5.46; p (trend), 0.023).
  • There were no associations between urinary excretion of genistein and daidzein with risk of prostate cancer.
  • Producers of equol (isoflavone) may be at reduced risk of total- and high-grade prostate cancer whereas enterolactone may increase the likelihood of disease.
  • [MeSH-major] Carcinoma / etiology. Phytoestrogens / urine. Prostatic Neoplasms / etiology

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  • (PMID = 20924663.001).
  • [ISSN] 1573-7225
  • [Journal-full-title] Cancer causes & control : CCC
  • [ISO-abbreviation] Cancer Causes Control
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / 4',7-dihydroxy-3,4-dihydroisoflavone; 0 / Isoflavones; 0 / Lignans; 0 / Phytoestrogens; 531-95-3 / Equol; 6287WC5J2L / daidzein; DH2M523P0H / Genistein
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56. Nagata Y, Sonoda T, Mori M, Miyanaga N, Okumura K, Goto K, Naito S, Fujimoto K, Hirao Y, Takahashi A, Tsukamoto T, Akaza H: Dietary isoflavones may protect against prostate cancer in Japanese men. J Nutr; 2007 Aug;137(8):1974-9
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  • [Title] Dietary isoflavones may protect against prostate cancer in Japanese men.
  • We examined associations between nutritional and other lifestyle factors and the prevalence of prostate cancer in a case-control study of Japanese men.
  • BMI, physical activity, occupation, family history of prostate cancer, and medical history were not associated with prostate cancer risk.
  • On the other hand, isoflavone significantly decreased the risk of prostate cancer regardless of adjustment by PUFA, (n-6) fatty acids or magnesium.
  • In conclusion, our findings indicate that isoflavones might be an effective dietary protective factor against prostate cancer in Japanese men.
  • [MeSH-major] Diet. Isoflavones / pharmacology. Prostatic Neoplasms / prevention & control

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  • (PMID = 17634273.001).
  • [ISSN] 0022-3166
  • [Journal-full-title] The Journal of nutrition
  • [ISO-abbreviation] J. Nutr.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Isoflavones
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57. Saeki N, Gu J, Yoshida T, Wu X: Prostate stem cell antigen: a Jekyll and Hyde molecule? Clin Cancer Res; 2010 Jul 15;16(14):3533-8
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  • [Title] Prostate stem cell antigen: a Jekyll and Hyde molecule?
  • Prostate stem cell antigen (PSCA) is a glycosylphosphatidylinositol (GPI)-anchored cell surface protein.
  • It is up-regulated in several major cancers including prostate, bladder, and pancreatic cancers.
  • The expression of PSCA is positively correlated with advanced clinical stage and metastasis in prostate cancers and is also associated with malignant progression of premalignant prostate lesions.
  • Therefore, PSCA has been proposed as a biomarker of diagnosis and prognosis, as well as a target of therapy for these cancers.
  • In addition, PSCA has also shown clinical potential in immunotherapy as a prostate-specific antigen, which, when presented by dendritic cells, may elicit strong tumor-specific immunity.
  • In contrast, PSCA is down-regulated in esophageal and gastric cancer and may have a tumor-suppressing function in the gastric epithelium.
  • PSCA seems to be a Jekyll and Hyde molecule that plays differential roles, tumor promoting or suppressing, depending on the cellular context.

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  • [Copyright] Copyright 2010 AACR.
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  • (PMID = 20501618.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA091846; United States / NCI NIH HHS / CA / R01 CA074880; United States / NCI NIH HHS / CA / U01 CA127615; United States / NCI NIH HHS / CA / CA127615-02; United States / NCI NIH HHS / CA / R01CA74880; United States / NCI NIH HHS / CA / R01 CA131335; United States / NCI NIH HHS / CA / P50CA91846; United States / NCI NIH HHS / CA / R01 CA131335-02; United States / NCI NIH HHS / CA / R01 CA074880-10; United States / NCI NIH HHS / CA / CA091846-090007; United States / NCI NIH HHS / CA / U01 CA127615-02; United States / NCI NIH HHS / CA / R01CA131335; United States / NCI NIH HHS / CA / P50 CA091846-090007; United States / NCI NIH HHS / CA / U01CA127615; United States / NCI NIH HHS / CA / CA074880-10; United States / NCI NIH HHS / CA / R01 CA111922; United States / NCI NIH HHS / CA / CA131335-02
  • [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 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / GPI-Linked Proteins; 0 / Neoplasm Proteins; 0 / PSCA protein, human
  • [Other-IDs] NLM/ NIHMS204237; NLM/ PMC2905486
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58. Wong PF, Abubakar S: Comparative transcriptional study of the effects of high intracellular zinc on prostate carcinoma cells. Oncol Rep; 2010 Jun;23(6):1501-16
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  • [Title] Comparative transcriptional study of the effects of high intracellular zinc on prostate carcinoma cells.
  • The normally high concentration of zinc in normal prostate gland is significantly reduced in malignant prostate tissues, but its precise role in prostate tumorigenesis remains unclear.
  • The present study investigates the growth and transcriptional responses of LNCaP prostate cancer cells to prolonged high Zn2+ treatment.
  • FBL and CD164 were responsive to the treatment with Zn2+ in PNT2 prostate normal cells and were further overexpressed in the prolonged Zn2+-treated LNCaP cells.
  • These observations suggest that in general high Zn2+ has suppressive effects on prostate cancer cell growth but continuous exposure to an environment of high Zn2+ can lead to the overexpression of cancer promoting genes such as FBL and CD164.
  • These findings support a potential detrimental role of Zn2+ in prostate cancer.
  • [MeSH-major] Biomarkers, Tumor / genetics. Prostatic Neoplasms / metabolism. RNA, Messenger / genetics. Trace Elements / pharmacology. Transcription, Genetic / drug effects. Zinc / pharmacology
  • [MeSH-minor] Cell Proliferation / drug effects. Colony-Forming Units Assay. Gene Expression Profiling. Humans. Male. Oligonucleotide Array Sequence Analysis. Reverse Transcriptase Polymerase Chain Reaction. Tumor Cells, Cultured

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  • (PMID = 20428803.001).
  • [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 / Biomarkers, Tumor; 0 / RNA, Messenger; 0 / Trace Elements; J41CSQ7QDS / Zinc
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59. Frattaroli J, Weidner G, Dnistrian AM, Kemp C, Daubenmier JJ, Marlin RO, Crutchfield L, Yglecias L, Carroll PR, Ornish D: Clinical events in prostate cancer lifestyle trial: results from two years of follow-up. Urology; 2008 Dec;72(6):1319-23
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical events in prostate cancer lifestyle trial: results from two years of follow-up.
  • OBJECTIVES: Previous research has demonstrated that patients with prostate cancer participating in the Prostate Cancer Lifestyle Trial had a reduction in prostate-specific antigen (PSA) levels, inhibition of LNCaP cell growth, and fewer prostate cancer-related clinical events at the end of 1 year compared with controls.
  • METHODS: The Prostate Cancer Lifestyle Trial was a 1-year randomized controlled clinical trial of 93 patients with early-stage prostate cancer (Gleason score <7, PSA 4-10 ng/mL) undergoing active surveillance.
  • RESULTS: By 2 years of follow-up, 13 of 49 (27%) control patients and 2 of 43 (5%) experimental patients had undergone conventional prostate cancer treatment (radical prostatectomy, radiotherapy, or androgen deprivation, P < .05).
  • CONCLUSIONS: Patients with early-stage prostate cancer choosing active surveillance might be able to avoid or delay conventional treatment for at least 2 years by making changes in their diet and lifestyle.
  • [MeSH-major] Life Style. Prostatic Neoplasms / therapy
  • [MeSH-minor] Aged. Biopsy. Cell Line, Tumor. Diet. Exercise. Follow-Up Studies. Humans. Male. Medical Oncology / methods. Middle Aged. Prostate-Specific Antigen / biosynthesis. Self-Help Groups. Treatment Outcome

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  • (PMID = 18602144.001).
  • [ISSN] 1527-9995
  • [Journal-full-title] Urology
  • [ISO-abbreviation] Urology
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 5P50CA089520-02; United States / PHS HHS / / C76HF00803
  • [Publication-type] Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] EC 3.4.21.77 / Prostate-Specific Antigen
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60. Thompson IM, Ankerst DP: Prostate-specific antigen in the early detection of prostate cancer. CMAJ; 2007 Jun 19;176(13):1853-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prostate-specific antigen in the early detection of prostate cancer.
  • Throughout Canada, the United States and much of Europe, prostate-specific antigen (PSA) screening for prostate cancer has proliferated over the past 2 decades, leading to dramatic increases in detection rates of prostate cancer.
  • Although it has unquestionably led to increased detection of cancer and a migration to lower-stage and -volume tumours, it is still unknown whether PSA screening significantly reduces mortality from prostate cancer.
  • The recently developed risk calculator from the Prostate Cancer Prevention Trial, which integrates family history of prostate cancer, digital rectal examination findings, PSA test result, age, ethnicity, and history of a prior prostate biopsy with a negative result, allows clinicians to assess a patient's individual risk of cancer.
  • This risk should be examined in the context of a patient's life expectancy and comorbidity as well as his concern about the possibility of prostate cancer.

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  • (PMID = 17576986.001).
  • [ISSN] 1488-2329
  • [Journal-full-title] CMAJ : Canadian Medical Association journal = journal de l'Association medicale canadienne
  • [ISO-abbreviation] CMAJ
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U01 CA086402; United States / NCI NIH HHS / CA / UO1 CA 86402
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] Canada
  • [Chemical-registry-number] 0 / Biomarkers; EC 3.4.21.77 / Prostate-Specific Antigen
  • [Number-of-references] 48
  • [Other-IDs] NLM/ PMC1891131
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61. Phan TP, Syed AM, Puthawala A, Sharma A, Khan F: High dose rate brachytherapy as a boost for the treatment of localized prostate cancer. J Urol; 2007 Jan;177(1):123-7; discussion 127
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  • [Title] High dose rate brachytherapy as a boost for the treatment of localized prostate cancer.
  • PURPOSE: We report the outcome and toxicities of high dose rate brachytherapy as a boost for localized prostate cancer.
  • MATERIALS AND METHODS: Between 1996 and 2003, 309 patients with prostate carcinoma were treated with external beam radiation therapy and high dose rate brachytherapy.
  • Group 1 of 67 patients had Gleason score 6 or less, pretreatment prostate specific antigen 10 ng/ml or less and clinical stage T2a or less.
  • Group 2 of 109 patients had Gleason score 7 or greater, pretreatment prostate specific antigen greater than 10 ng/ml and clinical stage T2b or greater.
  • On univariate analysis risk group, pretreatment prostate specific antigen and Gleason score were significant predictors of biochemical control.
  • However, on multivariate analysis only risk group and pretreatment prostate specific antigen were significant.
  • CONCLUSIONS: External beam radiation therapy and high dose rate brachytherapy for prostate cancer resulted in excellent biochemical control, cause specific survival and overall survival with minimal severe acute or late complications.
  • [MeSH-major] Adenocarcinoma / radiotherapy. Brachytherapy / methods. Prostatic Neoplasms / radiotherapy

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  • (PMID = 17162020.001).
  • [ISSN] 0022-5347
  • [Journal-full-title] The Journal of urology
  • [ISO-abbreviation] J. Urol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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62. Marcu M, Radu E, Sajin M: Neuroendocrine transdifferentiation of prostate carcinoma cells and its prognostic significance. Rom J Morphol Embryol; 2010;51(1):7-12
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  • [Title] Neuroendocrine transdifferentiation of prostate carcinoma cells and its prognostic significance.
  • Neuroendocrine (NE) cells are a distinct epithelial cell compartment of the normal human prostate gland.
  • Their phenotype and range of endocrine secretion products are similar, but not identical to those of NE-like cells from prostate carcinoma.
  • Neuroendocrine differentiation (NED) is a feature commonly seen in prostate carcinoma and a number of studies pointed out that its extent is associated to hormone therapy refractory and aggressive disease.
  • However, less information is available on the significance of NED in organ-confined prostate cancer, although identification of early predictors of aggressive disease would obviously allow for more adequate therapy.
  • [MeSH-major] Carcinoma / diagnosis. Carcinoma / pathology. Cell Transdifferentiation / physiology. Neuroendocrine Cells / physiology. Prostatic Neoplasms / diagnosis. Prostatic Neoplasms / pathology
  • [MeSH-minor] Biomarkers, Tumor. Humans. Male. Neoplasm Invasiveness. Prognosis

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  • (PMID = 20191113.001).
  • [ISSN] 1220-0522
  • [Journal-full-title] Romanian journal of morphology and embryology = Revue roumaine de morphologie et embryologie
  • [ISO-abbreviation] Rom J Morphol Embryol
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Review
  • [Publication-country] Romania
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 53
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63. Adhami VM, Mukhtar H: Anti-oxidants from green tea and pomegranate for chemoprevention of prostate cancer. Mol Biotechnol; 2007 Sep;37(1):52-7
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  • [Title] Anti-oxidants from green tea and pomegranate for chemoprevention of prostate cancer.
  • Among males, prostate cancer has become the second leading cause of cancer-related deaths in North America, with similar trends in many Western and developing countries.
  • One way to control prostate cancer is through chemoprevention, which refers to the administration of synthetic or naturally occurring agents to block, reverse, or delay the process of carcinogenesis.
  • Prostate cancer is an ideal candidate disease for chemopreventive intervention, because it grows very slowly, likely for decades, before symptoms arise and a diagnosis is finally established, it has a long latency period, and it is typically diagnosed in men >50 years of age.
  • We have been defining the usefulness of dietary anti-oxidants for chemoprevention of prostate and other cancers.
  • This review will focus on prostate cancer chemopreventive effects of polyphenolic anti-oxidants derived from green tea and pomegranate.
  • It is a challenge to custom-tailor these gift molecules as cocktails in concentrations that can easily be consumed by humans for delaying prostate and other cancers.
  • [MeSH-major] Antioxidants / administration & dosage. Camellia sinensis / chemistry. Flavonoids / administration & dosage. Phenols / administration & dosage. Prostatic Neoplasms / prevention & control. Punicaceae / chemistry. Tea / chemistry

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  • (PMID = 17914164.001).
  • [ISSN] 1073-6085
  • [Journal-full-title] Molecular biotechnology
  • [ISO-abbreviation] Mol. Biotechnol.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / P50 DK065303-019; United States / NCI NIH HHS / CA / R01 CA 101039; United States / NCI NIH HHS / CA / R01 CA 120451; United States / NCI NIH HHS / CA / R01 CA 78809
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antioxidants; 0 / Flavonoids; 0 / Phenols; 0 / Polyphenols; 0 / Tea
  • [Number-of-references] 52
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64. Setlur SR, Mertz KD, Hoshida Y, Demichelis F, Lupien M, Perner S, Sboner A, Pawitan Y, Andrén O, Johnson LA, Tang J, Adami HO, Calza S, Chinnaiyan AM, Rhodes D, Tomlins S, Fall K, Mucci LA, Kantoff PW, Stampfer MJ, Andersson SO, Varenhorst E, Johansson JE, Brown M, Golub TR, Rubin MA: Estrogen-dependent signaling in a molecularly distinct subclass of aggressive prostate cancer. J Natl Cancer Inst; 2008 Jun 4;100(11):815-25
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  • [Title] Estrogen-dependent signaling in a molecularly distinct subclass of aggressive prostate cancer.
  • BACKGROUND: The majority of prostate cancers harbor gene fusions of the 5'-untranslated region of the androgen-regulated transmembrane protease serine 2 (TMPRSS2) promoter with erythroblast transformation-specific transcription factor family members.
  • The common fusion between TMPRESS2 and v-ets erythroblastosis virus E26 oncogene homolog (avian) (ERG) is associated with a more aggressive clinical phenotype, implying the existence of a distinct subclass of prostate cancer defined by this fusion.
  • METHODS: We used complementary DNA-mediated annealing, selection, ligation, and extension to determine the expression profiles of 6144 transcriptionally informative genes in archived biopsy samples from 455 prostate cancer patients in the Swedish Watchful Waiting cohort (1987-1999) and the United States-based Physicians(') Health Study cohort (1983-2003).
  • A gene expression signature for prostate cancers with the TMPRSS2-ERG fusion was determined using partitioning and classification models and used in computational functional analysis.
  • Cell proliferation and TMPRSS2-ERG expression in androgen receptor-negative (NCI-H660) prostate cancer cells after treatment with vehicle or estrogenic compounds were assessed by viability assays and quantitative polymerase chain reaction, respectively.
  • RESULTS: We identified an 87-gene expression signature that distinguishes TMPRSS2-ERG fusion prostate cancer as a discrete molecular entity (area under the curve = 0.80, 95% confidence interval [CI] = 0.792 to 0.81; P < .001).
  • CONCLUSIONS: TMPRSS2-ERG fusion prostate cancer is a distinct molecular subclass.

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  • (PMID = 18505969.001).
  • [ISSN] 1460-2105
  • [Journal-full-title] Journal of the National Cancer Institute
  • [ISO-abbreviation] J. Natl. Cancer Inst.
  • [Language] ENG
  • [Grant] United States / NIA NIH HHS / AG / R01AG21404; United States / NCI NIH HHS / CA / P50 CA090381; United States / NIA NIH HHS / AG / R01 AG021404; United States / NIA NIH HHS / AG / R01 AG021404-05; United States / NCI NIH HHS / CA / P50 CA090381-10; United States / NIA NIH HHS / AG / AG021404-05
  • [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 / 1,3,5-tris(4-hydroxyphenyl)-4-propyl-1H-pyrazole; 0 / Antineoplastic Agents, Hormonal; 0 / DNA, Complementary; 0 / Estrogen Receptor alpha; 0 / Estrogen Receptor beta; 0 / Estrogens; 0 / Nitriles; 0 / Oncogene Proteins, Fusion; 0 / Phenols; 0 / Propionates; 0 / Pyrazoles; 0 / TMPRSS2-ERG fusion protein, human; 0 / diarylpropionitrile; 4TI98Z838E / Estradiol; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.- / TMPRSS2 protein, human
  • [Other-IDs] NLM/ NIHMS272096; NLM/ PMC3073404
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65. Nishiyama T, Suzuki K, Yamana K, Tonegawa E, Wako K, Takahashi K: Stepping-stones to the further advancement of androgen-deprivation therapy for prostate cancer. Expert Rev Anticancer Ther; 2006 Feb;6(2):259-68
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Stepping-stones to the further advancement of androgen-deprivation therapy for prostate cancer.
  • Androgen-deprivation therapy has remained the critical therapeutic option for patients with advanced prostate cancer for over 60 years.
  • Patients with poorly differentiated prostate cancer have low dihydrotestosterone levels in the prostate.
  • After androgen-deprivation therapy, dihydrotestosterone levels in the prostate remain at approximately 25% of the level measured before therapy.
  • The biologically aggressive prostate cancer cells may have an androgen receptor with heightened sensitivity to low dihydrotestosterone levels from the early stage of androgen-dependent disease.
  • It is necessary to consider the androgen environment and the status of the androgen receptor in the prostate in order to improve the clinical efficacy of androgen-deprivation therapy and the quality of life of patients.
  • [MeSH-major] Androgen Antagonists / therapeutic use. Prostatic Neoplasms / drug therapy. Receptors, Androgen / physiology

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  • (PMID = 16445378.001).
  • [ISSN] 1744-8328
  • [Journal-full-title] Expert review of anticancer therapy
  • [ISO-abbreviation] Expert Rev Anticancer Ther
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Androgens; 0 / Receptors, Androgen; 08J2K08A3Y / Dihydrotestosterone
  • [Number-of-references] 71
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66. Bruxvoort KJ, Charbonneau HM, Giambernardi TA, Goolsby JC, Qian CN, Zylstra CR, Robinson DR, Roy-Burman P, Shaw AK, Buckner-Berghuis BD, Sigler RE, Resau JH, Sullivan R, Bushman W, Williams BO: Inactivation of Apc in the mouse prostate causes prostate carcinoma. Cancer Res; 2007 Mar 15;67(6):2490-6
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  • [Title] Inactivation of Apc in the mouse prostate causes prostate carcinoma.
  • Alterations of the Wnt/beta-catenin signaling pathway are positively associated with the development and progression of human cancer, including carcinoma of the prostate.
  • To determine the role of activated Wnt/beta-catenin signaling in mouse prostate carcinogenesis, we created a mouse prostate tumor model using probasin-Cre-mediated deletion of Apc.
  • Prostate tumors induced by the deletion of Apc have elevated levels of beta-catenin protein and are highly proliferative.
  • Tumor formation is fully penetrant and follows a consistent pattern of progression.
  • Continued tumor growth usually necessitated sacrifice between 12 and 15 months of age.
  • Surgical castration of 6-week-old mice inhibited tumor formation, and castration of mice with more advanced tumors resulted in the partial regression of specific prostate glands.
  • We conclude that the prostate-specific deletion of Apc and the increased expression of beta-catenin associated with prostate carcinoma suggests a role for beta-catenin in prostate cancer and offers an appropriate animal model to investigate the interaction of Wnt signaling with other genetic and epigenetic signals in prostate carcinogenesis.
  • [MeSH-major] Cell Transformation, Neoplastic / genetics. Genes, APC. Prostatic Neoplasms / genetics
  • [MeSH-minor] Alleles. Androgens / deficiency. Androgens / metabolism. Animals. Cell Nucleus / metabolism. Female. Gene Deletion. Gene Expression Regulation, Neoplastic. Gene Silencing. Immunohistochemistry. Male. Mice. Mice, Inbred C57BL. Mice, Transgenic. Neoplasms, Hormone-Dependent / genetics. Neoplasms, Hormone-Dependent / metabolism. Organ Specificity. Prostatic Hyperplasia / genetics. Prostatic Hyperplasia / metabolism. beta Catenin / metabolism


67. Biundo B: Hormonal influences in prostate cancer: an update of a complex subject. Int J Pharm Compd; 2010 Mar-Apr;14(2):100-4
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  • [Title] Hormonal influences in prostate cancer: an update of a complex subject.
  • Pharmacists who are involved with patients and physicians have a tremendous opportunity to serve in the realm of prostate cancer, and there are numerous compounding opportunities.
  • Nutraceuticals such as omega-3 fatty acids, vitamin D, zinc, and selenium all play an important role in prostate health, as these agents have 5a-reductase inhibiting and anti-inflammatory properties.
  • More than anything else, we see that the pathophysiology of prostate cancer, although quite complex, is being explored at an amazing rate.
  • The author believes that hormonal balance is critical, and that it is largely hormonal imbalance that is involved in prostate disease.
  • In that regard, the author concludes that the levels of testosterone, estradiol, and drotestosterone, experienced at a more youthful age are vital if we are to improve prostate health.

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  • (PMID = 23965417.001).
  • [ISSN] 1092-4221
  • [Journal-full-title] International journal of pharmaceutical compounding
  • [ISO-abbreviation] Int J Pharm Compd
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
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68. Crook J, Patil N, Wallace K, Borg J, Zhou D, Ma C, Pond G: A phase III randomized trial of the timing of meloxicam with iodine-125 prostate brachytherapy. Int J Radiat Oncol Biol Phys; 2010 Jun 1;77(2):496-501
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  • [Title] A phase III randomized trial of the timing of meloxicam with iodine-125 prostate brachytherapy.
  • PURPOSE: Nonsteroidal anti-inflammatory medication is used to reduce prostate edema and urinary symptoms following prostate brachytherapy.
  • Prostate volume obtained by MR imaging at 1 month was compared to baseline prostate volume obtained by TRUS planimetry and expressed as an edema factor.
  • The trial endpoints were prostate edema at 1 month, International Prostate Symptom Score (IPSS) questionnaire results at 1 and 3 months, and any need for catheterization.
  • Median age was 61 (range, 45-79 years), and median TRUS prostate volume was 35.7 cc (range, 18.1-69.5 cc).
  • Baseline prostate volume remained the primary predictor of postimplant urinary retention.
  • [MeSH-minor] Administration, Oral. Aged. Anti-Inflammatory Agents, Non-Steroidal / administration & dosage. Drug Administration Schedule. Edema / drug therapy. Edema / etiology. Humans. Male. Middle Aged. Ontario. Prostatic Diseases / drug therapy. Prostatic Diseases / etiology

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  • [Copyright] Copyright 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20350785.001).
  • [ISSN] 1879-355X
  • [Journal-full-title] International journal of radiation oncology, biology, physics
  • [ISO-abbreviation] Int. J. Radiat. Oncol. Biol. Phys.
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00152919
  • [Publication-type] Clinical Trial, Phase III; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Cyclooxygenase 2 Inhibitors; 0 / Iodine Radioisotopes; 0 / Thiazines; 0 / Thiazoles; 71125-38-7 / meloxicam
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69. Famili P, Cauley JA, Greenspan SL: The effect of androgen deprivation therapy on periodontal disease in men with prostate cancer. J Urol; 2007 Mar;177(3):921-4
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  • [Title] The effect of androgen deprivation therapy on periodontal disease in men with prostate cancer.
  • PURPOSE: We tested the hypothesis that men undergoing androgen deprivation therapy as treatment for prostate cancer are at greater risk for periodontitis and tooth loss.
  • MATERIALS AND METHODS: A total of 81 men with a mean age of 68.5 years who had prostate cancer were consecutively recruited among 325 enrolled in an academic osteoporosis study.
  • The prevalence of periodontal disease in 41 men with prostate cancer undergoing androgen deprivation for a mean of 1.5 years was compared to that in 27 with prostate cancer not undergoing androgen deprivation, who served as controls.
  • The prevalence of periodontal disease was examined in relation to bone mineral density in men with prostate cancer with and without androgen deprivation therapy.
  • Linear regression models were used to assess the association between periodontal disease and bone mineral density in the 2 groups with prostate cancer (treated/untreated).
  • CONCLUSIONS: Men with prostate cancer undergoing androgen deprivation therapy were more likely to have periodontal disease than men not on androgen deprivation therapy.
  • If confirmed in larger studies, this observation could have important public health implications, given the increasing use of androgen deprivation therapy to treat prostate cancer.

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  • (PMID = 17296376.001).
  • [ISSN] 0022-5347
  • [Journal-full-title] The Journal of urology
  • [ISO-abbreviation] J. Urol.
  • [Language] ENG
  • [Grant] United States / NIA NIH HHS / AG / P30 AG024827; United States / NCATS NIH HHS / TR / UL1 TR000005; United States / NCRR NIH HHS / RR / M01-RR0056; United States / NCRR NIH HHS / RR / M01 RR000056; United States / NIDDK NIH HHS / DK / K24 DK062895; United States / NIDDK NIH HHS / DK / K24 DK 062895-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgen Antagonists
  • [Other-IDs] NLM/ NIHMS19813; NLM/ PMC1934505
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70. Basu HS, Thompson TA, Church DR, Clower CC, Mehraein-Ghomi F, Amlong CA, Martin CT, Woster PM, Lindstrom MJ, Wilding G: A small molecule polyamine oxidase inhibitor blocks androgen-induced oxidative stress and delays prostate cancer progression in the transgenic adenocarcinoma of the mouse prostate model. Cancer Res; 2009 Oct 1;69(19):7689-95
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  • [Title] A small molecule polyamine oxidase inhibitor blocks androgen-induced oxidative stress and delays prostate cancer progression in the transgenic adenocarcinoma of the mouse prostate model.
  • High levels of reactive oxygen species (ROS) present in human prostate epithelia are an important etiologic factor in prostate cancer (CaP) occurrence, recurrence, and progression.
  • Androgen induces ROS production in the prostate by a yet unknown mechanism.
  • As prostatic epithelia produce a large excess of polyamines, the androgen-induced polyamine oxidation that produces H2O2 could be a major reason for the high ROS levels in the prostate epithelia.
  • These data show that polyamine oxidation is not only a major pathway for ROS production in prostate, but inhibiting this pathway also successfully delays CaP progression.

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  • (PMID = 19773450.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R03 CA121367-02; United States / NCI NIH HHS / CA / CA121367-02; United States / NCI NIH HHS / CA / R03 CA121367-01; United States / NCI NIH HHS / CA / CA121367-01; United States / NCI NIH HHS / CA / R03 CA121367; United States / NCI NIH HHS / CA / R01 CA085509
  • [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 / Enzyme Inhibitors; 0 / RNA, Small Interfering; 0 / Reactive Oxygen Species; 93565-01-6 / MDL 72527; EC 1.5.- / Oxidoreductases Acting on CH-NH Group Donors; EC 1.5.3.- / polyamine oxidase; EC 2.3.1.- / Acetyltransferases; EC 2.3.1.57 / diamine N-acetyltransferase; V10TVZ52E4 / Putrescine
  • [Other-IDs] NLM/ NIHMS140232; NLM/ PMC2756327
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71. Schroeder JC, Bensen JT, Su LJ, Mishel M, Ivanova A, Smith GJ, Godley PA, Fontham ET, Mohler JL: The North Carolina-Louisiana Prostate Cancer Project (PCaP): methods and design of a multidisciplinary population-based cohort study of racial differences in prostate cancer outcomes. Prostate; 2006 Aug 1;66(11):1162-76
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  • [Title] The North Carolina-Louisiana Prostate Cancer Project (PCaP): methods and design of a multidisciplinary population-based cohort study of racial differences in prostate cancer outcomes.
  • BACKGROUND: The North Carolina-Louisiana Prostate Cancer Project (PCaP) is a multidisciplinary study of social, individual, and tumor-level causes of racial differences in prostate cancer aggressiveness.
  • METHODS: A population-based sample of incident prostate cancer cases from North Carolina and Louisiana will include 1,000 African Americans and 1,000 Caucasian Americans.
  • Prostate cancer aggressiveness is classified based on PSA, clinical stage, and Gleason grade.
  • CONCLUSIONS: Preliminary data support the feasibility of this comprehensive study to help determine the focus of public health efforts to reduce racial disparities in prostate cancer mortality.
  • [MeSH-major] Continental Population Groups. Prostatic Neoplasms / epidemiology
  • [MeSH-minor] African Continental Ancestry Group. Cohort Studies. European Continental Ancestry Group. Humans. Louisiana / epidemiology. Male. Microarray Analysis. North Carolina / epidemiology. Patient Acceptance of Health Care. Prostate-Specific Antigen / blood. Surveys and Questionnaires. Survival Rate. Treatment Outcome


72. Lum AM, Wang BB, Beck-Engeser GB, Li L, Channa N, Wabl M: Orphan receptor GPR110, an oncogene overexpressed in lung and prostate cancer. BMC Cancer; 2010 Feb 11;10:40
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  • [Title] Orphan receptor GPR110, an oncogene overexpressed in lung and prostate cancer.
  • GPR110 transcript and protein levels were measured in lung and prostate cancer cell lines and clinical samples, respectively, by quantitative PCR and immunohistochemistry.
  • However, it had higher than average gene expression in normal kidney tissue and in prostate tissues originating from older donors.
  • Although identified as an oncogene in murine T lymphomas, GPR110 is greatly overexpressed in human lung and prostate cancers.
  • As detected by immunohistochemistry, GPR110 was overexpressed in 20 of 27 (74%) lung adenocarcinoma tissue cores and in 17 of 29 (59%) prostate adenocarcinoma tissue cores.
  • Additionally, staining with a GPR110 antibody enabled us to differentiate between benign prostate hyperplasia and potential incipient malignancy.
  • CONCLUSION: Our work suggests a role for GPR110 in tumor physiology and supports it as a potential therapeutic candidate and disease marker for both lung and prostate cancer.


73. Pu H, Collazo J, Jones E, Gayheart D, Sakamoto S, Vogt A, Mitchell B, Kyprianou N: Dysfunctional transforming growth factor-beta receptor II accelerates prostate tumorigenesis in the TRAMP mouse model. Cancer Res; 2009 Sep 15;69(18):7366-74
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  • [Title] Dysfunctional transforming growth factor-beta receptor II accelerates prostate tumorigenesis in the TRAMP mouse model.
  • The contribution of a dysfunctional transforming growth factor-beta type II receptor (TGF beta RII) to prostate cancer initiation and progression was investigated in an in vivo mouse model.
  • Transgenic mice harboring the dominant-negative mutant TGF-beta type II receptor (DNTGF beta RII) in mouse epithelial cell were crossed with the TRAMP prostate cancer transgenic mouse to characterize the in vivo consequences of inactivated TGF-beta signaling on prostate tumor initiation and progression.
  • Histopathologic diagnosis of prostate specimens from the TRAMP+/DNTGF beta RII double transgenic mice revealed the appearance of early malignant changes and subsequently highly aggressive prostate tumors at a younger age, compared with littermates TRAMP+/Wt TGF beta RII mice.
  • A significant increase in the androgen receptor mRNA and protein levels was associated with the early onset of prostate tumorigenesis in TRAMP+/DNTGF beta RII mice.
  • Our results indicate that in vivo disruption of TGF-beta signaling accelerates the pathologic malignant changes in the prostate by altering the kinetics of prostate growth and inducing EMT.
  • The study also suggests that a dysfunctional TGF beta RII augments androgen receptor expression and promotes inflammation in early stage tumor growth, thus conferring a significant contribution by TGF-beta to prostate cancer progression.

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  • (PMID = 19738062.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK053525-07; United States / NIEHS NIH HHS / ES / T32 ES007266; United States / NIDDK NIH HHS / DK / R01 DK053525; United States / NIDDK NIH HHS / DK / R01 DK053525-07; United States / NIDDK NIH HHS / DK / R01 DK5355-12
  • [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 / Receptors, Androgen; 0 / Receptors, Transforming Growth Factor beta; 0 / Transforming Growth Factor beta; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.30 / transforming growth factor-beta type II receptor
  • [Other-IDs] NLM/ NIHMS135291; NLM/ PMC2747670
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74. Lawson DA, Zong Y, Memarzadeh S, Xin L, Huang J, Witte ON: Basal epithelial stem cells are efficient targets for prostate cancer initiation. Proc Natl Acad Sci U S A; 2010 Feb 9;107(6):2610-5
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  • [Title] Basal epithelial stem cells are efficient targets for prostate cancer initiation.
  • Prevailing theories suggest that luminal cells are the origin of prostate cancer because it is histologically defined by basal cell loss and malignant luminal cell expansion.
  • We introduced a series of genetic alterations into prospectively identified populations of murine basal/stem and luminal cells in an in vivo prostate regeneration assay.
  • Even though luminal cells fail to respond, basal/stem cells demonstrate efficient capacity for cancer initiation and can produce luminal-like disease characteristic of human prostate cancer in multiple models.
  • This finding provides evidence in support of basal epithelial stem cells as one target cell for prostate cancer initiation and demonstrates the propensity of primitive cells for tumorigenesis.

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  • (PMID = 20133806.001).
  • [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
  • [Grant] United States / NCI NIH HHS / CA / R00 CA125937-03; United States / NCI NIH HHS / CA / 1K99/R00 CA125937; United States / NCI NIH HHS / PC / PC061456; United States / NCI NIH HHS / CA / R00 CA125937; United States / NICHD NIH HHS / HD / K12 HD001400; United States / NCI NIH HHS / CA / K99 CA125937; United States / Howard Hughes Medical Institute / / ; United States / NCI NIH HHS / CA / CA125937-03; United States / NICHD NIH HHS / HD / 5 K12HD001400
  • [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 / Fibroblast Growth Factor 10; 0 / Fli1 protein, mouse; 0 / Proto-Oncogene Protein c-fli-1; 0 / Receptors, Androgen; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / Akt1 protein, mouse; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
  • [Other-IDs] NLM/ PMC2823887
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75. Sartor O: Prostate cancer. Saturation biopsy does not accurately localize tumors. Nat Rev Urol; 2010 Sep;7(9):479-80
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  • [Title] Prostate cancer. Saturation biopsy does not accurately localize tumors.
  • Precise localization of prostate cancer is essential for the success of focal therapies.
  • Despite suggestions that saturation biopsy might be useful in this regard, a new study implies it cannot accurately pinpoint prostate tumors. research efforts would perhaps be better focused on identifying which patients require treatment for clinically localized prostate cancer in the first place.
  • [MeSH-major] Biopsy, Needle / methods. Prostatic Neoplasms / pathology

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  • (PMID = 20818322.001).
  • [ISSN] 1759-4820
  • [Journal-full-title] Nature reviews. Urology
  • [ISO-abbreviation] Nat Rev Urol
  • [Language] eng
  • [Publication-type] News
  • [Publication-country] England
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76. Josifovski T, Radosević-Jelić L, Tulić C, Milosević A: [Disease relapses after radical radiotherapy of prostate cancer--analysis of prognostic factors]. Srp Arh Celok Lek; 2008 Jul-Aug;136(7-8):373-8
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  • [Title] [Disease relapses after radical radiotherapy of prostate cancer--analysis of prognostic factors].
  • INTRODUCTION: Although there is no consensus on which is the best option in prostate cancer treatment, these patients could be successfully treated with radiotherapy.
  • Regarding some prognostic factors, it is possible today to classify prostate cancer patients into several risk groups for clinical and biochemical relapse, and therefore to choose the right treatment modality.
  • OBJECTIVE: The objective in our study was to analyze the impact of tumour stage and grade, previous transurethral resection of the prostate (TUR), initial prostate specific antigen (PSA) level and age on disease relapse after radical radiotherapy of the prostate cancer.
  • METHOD: Between January 1991 and December 2005, a clinical, retrospective study was performed at the Radiotherapy Department of the Institute for Oncology and Radiology of Serbia, which included 283 patients with prostate cancer treated only with radical radiotherapy.
  • RESULTS: After radical radiotherapy disease relapse more often occurred (with statistical significance) in patients with locally advanced tumour (stage C 35% vs. A 13% vs. B 19%), low tumour grade (grade III 38% vs. grade II 23% vs. grade I 17%), initial PSA level over 10 ng/ml (29%) and over 20 ng/ml (37%) compared to 11% in the patients with initial PSA level below 10 ng/ml, and patients of lower age (less than 55 years 50% vs. 16% in patients over 70 years).
  • CONCLUSION: Tumour stage C, low tumour grade (grade II-III), initial PSA level over 10 ng/ml (over 20 ng/ml) and younger age are poor prognostic factors for disease relapse.
  • [MeSH-major] Carcinoma / radiotherapy. Carcinoma / secondary. Neoplasm Recurrence, Local. Prostatic Neoplasms / radiotherapy
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Humans. Male. Middle Aged. Prognosis. Prostate-Specific Antigen / blood


77. Miller DC, Spencer BA, Ritchey J, Stewart AK, Dunn RL, Sandler HM, Wei JT, Litwin MS: Treatment choice and quality of care for men with localized prostate cancer. Med Care; 2007 May;45(5):401-9
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  • [Title] Treatment choice and quality of care for men with localized prostate cancer.
  • BACKGROUND: Variations in patterns of care and treatment outcomes suggest differences in the quality of care for men treated for localized prostate cancer.
  • OBJECTIVE: We sought to compare adherence with quality indicators for prostate cancer care among men treated with radical prostatectomy or external beam radiation therapy.
  • RESEARCH DESIGN AND SUBJECTS: We sampled 5230 men diagnosed in 2000 or 2001 with early-stage prostate cancer from 984 facilities reporting to the National Cancer Data Base.
  • MAIN OUTCOME MEASURE: Subject-level compliance with the RAND quality indicators for localized prostate cancer care, stratified by treatment.
  • CONCLUSIONS: Documented compliance with process of care quality indicators among men with localized prostate cancer appears superior for those treated with external beam radiation compared with those treated surgically.
  • [MeSH-major] Choice Behavior. Guideline Adherence / statistics & numerical data. Prostatic Neoplasms / radiotherapy. Prostatic Neoplasms / surgery. Quality Indicators, Health Care

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  • (PMID = 17446826.001).
  • [ISSN] 0025-7079
  • [Journal-full-title] Medical care
  • [ISO-abbreviation] Med Care
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / 1-T-32 DK07782
  • [Publication-type] Comparative Study; 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
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78. Kane CJ, Bassett WW, Sadetsky N, Silva S, Wallace K, Pasta DJ, Cooperberg MR, Chan JM, Carroll PR: Obesity and prostate cancer clinical risk factors at presentation: data from CaPSURE. J Urol; 2005 Mar;173(3):732-6
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  • [Title] Obesity and prostate cancer clinical risk factors at presentation: data from CaPSURE.
  • PURPOSE: We investigated the association of obesity with prostate cancer case demographics and clinical disease features at presentation.
  • MATERIALS AND METHODS: Data were abstracted from CaPSURE (Cancer of the Prostate Strategic Urologic Research Endeavor), a disease registry of 10,018 men with prostate cancer.
  • The overweight group had a lower serum prostate specific antigen (p = 0.010) and lower stage disease (p = 0.030) at diagnosis, but there was no association between Gleason score and obesity (p = 0.57).
  • However, among men with a BMI of 25 kg/m or greater there was a positive correlation between increasing BMI and risk of being in a worse prognostic group at diagnosis (p = 0.018).
  • CONCLUSIONS: Overweight and obese patients are more likely to be young at diagnosis and have multiple comorbidities.
  • Men in the overweight and obese groups presented with lower risk prostate cancer at diagnosis.
  • Among overweight and obese patients increased obesity is associated with a slightly increased chance of having high risk prostate cancer at diagnosis.
  • [MeSH-major] Adenocarcinoma / complications. Obesity / complications. Prostatic Neoplasms / complications


79. Qu Y, Zhang L, Mao M, Zhao F, Huang X, Yang C, Xiong Y, Mu D: Effects of DNAzymes targeting Aurora kinase A on the growth of human prostate cancer. Cancer Gene Ther; 2008 Aug;15(8):517-25
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  • [Title] Effects of DNAzymes targeting Aurora kinase A on the growth of human prostate cancer.
  • Aurora kinase A has been demonstrated to be involved in the malignant progression of many types of cancer including prostate cancer, we therefore hypothesized that Aurora kinase A might work as a valuable target for prostate cancer treatment.
  • To test this hypothesis, we used DNAzyme technology to inhibit Aurora kinase A expression and evaluated the effects of DNAzymes as therapeutic agents to treat prostate cancer.
  • When transfected into the prostate cancer cell line PC3, DZ2 was found to strongly inhibit the expression of Aurora kinase A examined by western blot analysis, and thus suppressed cell growth, arrested the progression of cell cycle, induced cell apoptosis and attenuated cell migration, as measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium assay, flow cytometry and Boyden chamber assay.
  • Through in vivo study, we also found that DZ2 could significantly inhibit the growth of human prostate cancer xenografts in nude mice.
  • In conclusion, DZ2 could effectively attenuate malignant progression of prostate cancer both in vitro and in vivo, suggesting that DNAzyme targeting Aurora kinase A may be used as a valuable therapy to treat prostate cancer.
  • [MeSH-major] DNA, Catalytic / pharmacology. Prostatic Neoplasms / pathology. Protein-Serine-Threonine Kinases / antagonists & inhibitors
  • [MeSH-minor] Animals. Aurora Kinase A. Aurora Kinases. Base Sequence. Blotting, Western. Cell Cycle. Cell Line, Tumor. Cell Proliferation. Cloning, Molecular. DNA Primers. DNA, Complementary. Humans. Male. Mice. Mice, Nude

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  • (PMID = 18404163.001).
  • [ISSN] 1476-5500
  • [Journal-full-title] Cancer gene therapy
  • [ISO-abbreviation] Cancer Gene Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA Primers; 0 / DNA, Catalytic; 0 / DNA, Complementary; EC 2.7.11.1 / AURKA protein, human; EC 2.7.11.1 / Aurka protein, mouse; EC 2.7.11.1 / Aurora Kinase A; EC 2.7.11.1 / Aurora Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
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80. Drouin SJ, Rouprêt M: [Epidemiology, diagnosis and prognosis of localized prostate cancer: what's new?]. Prog Urol; 2009 Apr;19 Suppl 1:S3-7
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  • [Title] [Epidemiology, diagnosis and prognosis of localized prostate cancer: what's new?].
  • [Transliterated title] Epidemiologie, diagnostic et pronostic du cancer de prostate localisé : état des lieux.
  • Detection and diagnosis of prostate cancer has challenged researchers and clinicians for several years, particularly with the increase of its incidence.
  • With the advent of optimal treatments for each patient, diagnosis and prognostic tools arouse more and more interest.
  • Effectively, it becomes necessary to assess even better the aggressiveness of the tumour in order to choose the most appropriate treatment and, thus to make a correlation between the phenotype and the genotype.
  • The optimization of MRI allows more precise diagnosis of local invasion and is usefull to optimize.
  • [MeSH-major] Prostatic Neoplasms / epidemiology
  • [MeSH-minor] Antigens, Neoplasm / genetics. Antigens, Neoplasm / urine. Biopsy / methods. France / epidemiology. Genetic Markers. Humans. Incidence. Magnetic Resonance Imaging. Male. Phenotype. Prognosis. Reference Values

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  • (PMID = 19465334.001).
  • [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 / Antigens, Neoplasm; 0 / Genetic Markers; 0 / prostate cancer antigen 3, human
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81. Moreira Leite KR, Camara-Lopes LH, Dall'Oglio MF, Cury J, Antunes AA, Sañudo A, Srougi M: Upgrading the Gleason score in extended prostate biopsy: implications for treatment choice. Int J Radiat Oncol Biol Phys; 2009 Feb 1;73(2):353-6
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  • [Title] Upgrading the Gleason score in extended prostate biopsy: implications for treatment choice.
  • PURPOSE: To determine the incidence of overestimation of Gleason score (GS) in extended prostate biopsy, and consequently circumventing unnecessary aggressive treatment.
  • METHODS AND MATERIALS: This is a retrospective study of 464 patients who underwent prostate biopsy and radical prostatectomy between January 2001 and November 2007.
  • The incidence of overestimation of GS in biopsies and tumor volume were studied.
  • Multivariate analysis was applied to find parameters that predict upgrading the GS in prostate biopsy.
  • RESULTS: The exact agreement of GS between prostate biopsy and radical prostatectomy occurred in 56.9% of cases.
  • One hundred and six (22.8%) patients received a diagnosis of high GS (8, 9, or 10) in a prostate biopsy.
  • In multivariate analysis, the total percentage of tumor was the only independent factor in overestimation of GS.
  • This should be remembered by professionals involved with prostate cancer to avoid overtreatment and undesirable side effects.
  • [MeSH-major] Prostate / pathology. Prostatic Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Biopsy, Needle. Chi-Square Distribution. Humans. Male. Middle Aged. Prostatectomy. Regression Analysis. Retrospective Studies. Statistics, Nonparametric. Tumor Burden

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  • (PMID = 18774658.001).
  • [ISSN] 1879-355X
  • [Journal-full-title] International journal of radiation oncology, biology, physics
  • [ISO-abbreviation] Int. J. Radiat. Oncol. Biol. Phys.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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82. Reiner T, de Las Pozas A, Parrondo R, Perez-Stable C: Progression of prostate cancer from a subset of p63-positive basal epithelial cells in FG/Tag transgenic mice. Mol Cancer Res; 2007 Nov;5(11):1171-9
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  • [Title] Progression of prostate cancer from a subset of p63-positive basal epithelial cells in FG/Tag transgenic mice.
  • Transgenic mice that allow targeting of SV40 T antigen (Tag) to the prostate provide a unique model to identify cancer-initiating cells and follow their progression from a normal cell phenotype into prostate cancer cells.
  • We have developed the FG/Tag transgenic mouse model of prostate cancer using the human fetal globin (FG) promoter linked to Tag.
  • Immunohistochemistry results show that before the development of prostate intraepithelial neoplasia (PIN), a subset of p63(+) basal epithelial cells expresses Tag.
  • As in the case of human prostate cancer, there is a loss of p63(+) basal cells with neoplastic progression, and a long period of time is required for PIN lesions to develop into palpable prostate tumors.
  • Cell lines derived from primary prostate tumors showed characteristics of a neuroendocrine-epithelial intermediate cell type.
  • The FG promoter has high transcriptional activity in intermediate (DU 145, PC-3) and p63(+) basal epithelial (LHSR-AR) prostate cancer cells.
  • Therefore, the unexpected development of prostate cancer in the FG/Tag mice may be due to the presence of DNA elements in the FG promoter that can target Tag to specific basal or intermediate cells.
  • We conclude that FG/Tag mouse is a unique model of prostate cancer because the initiating cells are a subset of p63(+) basal (possibly stem cells), which may be the true cells of origin for carcinogenesis in aggressive human prostate cancer.
  • [MeSH-major] Antigens, Polyomavirus Transforming / genetics. Disease Models, Animal. Mice, Transgenic. Prostatic Neoplasms / pathology


83. Zhang J, Dhakal I, Stone A, Ning B, Greene G, Lang NP, Kadlubar FF: Plasma carotenoids and prostate cancer: a population-based case-control study in Arkansas. Nutr Cancer; 2007;59(1):46-53
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  • [Title] Plasma carotenoids and prostate cancer: a population-based case-control study in Arkansas.
  • Carotenoids possess antioxidant properties and thus may protect against prostate cancer.
  • In this study, we aimed to investigate the relation between plasma concentrations of carotenoids and the risk of prostate cancer in a population-based case-control study in Arkansas.
  • Cases (n = 193) were men with prostate cancer diagnosed in 3 major hospitals, and controls (n = 197) were matched to cases by age, race, and county of residence.
  • After adjustment for confounders, plasma levels of lycopene, lutein/zeaxanthin, and beta-cryptoxanthin were inversely associated with prostate cancer risk.
  • Subjects in the highest quartile of plasma lycopene (513.7 microg/l) had a 55% lower risk of prostate cancer than those in the lowest quartile (140.5 microg/l; P trend = 0.042).
  • This study added to the emerging evidence that high circulating levels of lycopene, lutein/zeaxanthin, and beta-cryptoxanthin are associated with a low risk of prostate cancer.
  • [MeSH-major] Antioxidants / metabolism. Carotenoids / blood. Prostatic Neoplasms / blood. Prostatic Neoplasms / epidemiology

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  • (PMID = 17927501.001).
  • [ISSN] 0163-5581
  • [Journal-full-title] Nutrition and cancer
  • [ISO-abbreviation] Nutr Cancer
  • [Language] eng
  • [Grant] United States / NIA NIH HHS / AG / 1 R01 AG15722
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antioxidants; 0 / Cryptoxanthins; 0 / Xanthophylls; 0 / Zeaxanthins; 01YAE03M7J / beta Carotene; 36-88-4 / Carotenoids; 45XWE1Z69V / alpha-carotene; SB0N2N0WV6 / lycopene; X72A60C9MT / Lutein
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84. Carver BS, Bianco FJ Jr, Scardino PT, Eastham JA: Long-term outcome following radical prostatectomy in men with clinical stage T3 prostate cancer. J Urol; 2006 Aug;176(2):564-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Long-term outcome following radical prostatectomy in men with clinical stage T3 prostate cancer.
  • PURPOSE: We evaluated patients at our institution who underwent radical prostatectomy for clinical stage T3 prostate cancer to determine their long-term clinical outcomes.
  • MATERIALS AND METHODS: We reviewed our prospective surgical database and identified 176 men who underwent radical retropubic prostatectomy for clinical stage T3 prostate cancer from 1983 to 2003.
  • Clinical progression following biochemical recurrence was evaluated and clinical failure was defined as the development of clinical metastases or progression to hormone refractory prostate cancer.
  • RESULTS: Of the 176 patients with cT3 prostate cancer 64 (36%) received neoadjuvant hormonal therapy.
  • On multivariate analysis biopsy Gleason score, pretreatment serum prostate specific antigen and year of surgery were independent predictors of biochemical recurrence.
  • Overall the 5, 10 and 15-year probabilities of death from prostate cancer were 6%, 15% and 24%, respectively.
  • Radical prostatectomy remains an integral component in the treatment of select patients with clinical stage T3 prostate cancer.
  • [MeSH-major] Prostatectomy. Prostatic Neoplasms / pathology. Prostatic Neoplasms / surgery
  • [MeSH-minor] Follow-Up Studies. Humans. Male. Middle Aged. Neoplasm Recurrence, Local / blood. Neoplasm Staging. Prospective Studies. Prostate-Specific Antigen / blood. Time Factors. Treatment Outcome

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  • (PMID = 16813890.001).
  • [ISSN] 0022-5347
  • [Journal-full-title] The Journal of urology
  • [ISO-abbreviation] J. Urol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 3.4.21.77 / Prostate-Specific Antigen
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85. Park H, Piert MR, Khan A, Shah R, Hussain H, Siddiqui J, Chenevert TL, Meyer CR: Registration methodology for histological sections and in vivo imaging of human prostate. Acad Radiol; 2008 Aug;15(8):1027-39
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Registration methodology for histological sections and in vivo imaging of human prostate.
  • Our objective is to register in vivo imaging with histologic sections of the human prostate so that histologic truth can be correlated with in vivo imaging features.
  • MATERIALS AND METHODS: In vivo imaging of the prostate included T2-weighted anatomic and diffusion weighted 3-T magnetic resonance imaging (MRI) as well as 11C-choline positron emission tomography (PET).
  • In addition, ex vivo 3-T MRI of the prostate specimen, histology, and associated block face photos of the prostate specimen were obtained.
  • An indirect validation of the registration accuracy has been proposed comparing tumor boundary markings found in diffusion MRI and histologic sections.
  • CONCLUSION: This proof of concept paper demonstrates a method based on intrinsic image information content for successfully registering in vivo imaging of the human prostate with its post-resection histology, which does not require the use of extrinsic fiducial markers.
  • The methodology is therefore the basis for a systematic comparison of in vivo imaging for staging of human prostate cancer.

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  • (PMID = 18620123.001).
  • [ISSN] 1076-6332
  • [Journal-full-title] Academic radiology
  • [ISO-abbreviation] Acad Radiol
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA087634-01A2; United States / NCI NIH HHS / CA / P01 CA087634; United States / NCI NIH HHS / CA / P50 CA069568-05; United States / NCI NIH HHS / CA / CA087634-01A2; United States / NCI NIH HHS / CA / P50CA069568; United States / NCI NIH HHS / CA / 1P01CA87684; United States / NCI NIH HHS / CA / P50 CA069568; None / None / / P50 CA069568-05
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carbon Radioisotopes
  • [Other-IDs] NLM/ NIHMS60416; NLM/ PMC2646010
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86. Forootan SS, Foster CS, Aachi VR, Adamson J, Smith PH, Lin K, Ke Y: Prognostic significance of osteopontin expression in human prostate cancer. Int J Cancer; 2006 May 01;118(9):2255-61
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  • [Title] Prognostic significance of osteopontin expression in human prostate cancer.
  • To test the hypothesis that expression of osteopontin (OPN), an integrin-binding glycoprotein, can independently predict the potential aggressiveness of prostate cancer, the status of OPN expression in benign and malignant prostate cancer cell lines and tissues was analysed by Western blot and immunohistochemistry.
  • Amongst the four prostate cell lines analysed, the level of OPN expressed in the benign PNT-2 cells was set at 1, the relative level of OPN expressed in the weakly malignant cell line LNCaP was increased to 1.5.
  • An increased expression of OPN was also observed in the prostate tissue samples.
  • When the level of OPN in normal tissue was set at 1, its level in benign prostate hyperplasia (BPH) was similar at 0.99 +/- 0.2, whereas the OPN level in the highly malignant carcinoma tissue was greatly increased by nearly 6-fold to 5.9 +/- 0.3.
  • The results in our study support our hypothesis and suggest that the increased OPN level may be involved in the malignant transformation of prostate epithelial cells and OPN expression level is an important determinant for patient survival.
  • [MeSH-major] Prostatic Neoplasms / pathology. Sialoglycoproteins / biosynthesis
  • [MeSH-minor] Aged. Blotting, Western. Cell Transformation, Neoplastic. Epithelial Cells. Gene Expression Profiling. Humans. Immunohistochemistry. Male. Osteopontin. Predictive Value of Tests. Prognosis. Prostate / cytology. Survival Analysis. Tumor Cells, Cultured

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  • [Copyright] 2005 Wiley-Liss, Inc.
  • (PMID = 16331611.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0501019
  • [Publication-type] Comparative Study; 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 / SPP1 protein, human; 0 / Sialoglycoproteins; 106441-73-0 / Osteopontin
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87. Antunes AA, Leite KR, Dall'Oglio MF, Cury J, Srougi M: The effect of the number of biopsy cores on the concordance between prostate biopsy and prostatectomy Gleason score: a prostate volume-controlled study. Arch Pathol Lab Med; 2008 Jun;132(6):989-92
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The effect of the number of biopsy cores on the concordance between prostate biopsy and prostatectomy Gleason score: a prostate volume-controlled study.
  • Some included 2 or more centers, used historical controls from the early prostate specific antigen era or lacked a clear definition of the biopsy schemes.
  • Furthermore, most did not control the results for prostate volume.
  • OBJECTIVE: To confirm whether prediction of RP Gleason score can be optimized by taking more biopsy cores in a contemporary series of patients, with pathologic samples analyzed by the same pathologist, and controlling these results for prostate volume.
  • DESIGN: The study comprised a retrospective case-control analysis of 393 patients with prostate cancer treated with RP.
  • When we analyzed patients with prostate volumes of less than 50 cm(3), concordance rates were 58.3%, 58.3%, and 65.1% for each group, respectively (P = .03).
  • Among patients with prostate volumes of 50 cm(3) or more, concordance rates were 70%, 58.1%, and 63.6%, respectively (P = .66).
  • CONCLUSIONS: Taking 10 or more cores can improve the prediction of RP Gleason score in patients with prostate volumes of less than 50 cm(3).
  • For patients with prostate volumes of 50 cm(3) or more, increasing the biopsy cores to 10 or more did not improve prediction of RP Gleason score.
  • [MeSH-major] Biopsy. Prostatectomy. Prostatic Neoplasms / pathology. Prostatic Neoplasms / surgery

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  • (PMID = 18517284.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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88. Raben A, Rusthoven KE, Sarkar A, Glick A, Benge B, Jacobs D, Raben D: Favorable toxicity and biochemical control using real-time inverse optimization technique for prostate brachytherapy. Brachytherapy; 2009 Jul-Sep;8(3):297-303
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Favorable toxicity and biochemical control using real-time inverse optimization technique for prostate brachytherapy.
  • PURPOSE: Favorable dosimetric results have been reported using intraoperative inverse optimization (IO) for permanent prostate brachytherapy.
  • METHODS AND MATERIALS: Between 2001 and 2007, 165 patients received permanent prostate implants using real-time IO and had >/=3 months of followup.
  • Dose constraints for inverse planning were: the prostate volume receiving 100% of the prescription dose [prostate V(100)] was >95%; the dose received by 90% of the gland [prostate D(90)] was within the 140-180 by dose range; the volume of urethra receiving 150% of the prescription dose [urethra V(150)] was <30%; and the volume of rectal wall receiving 110% of the prescription dose [rectal V(110)] was <1.0 cc.
  • Toxicity was prospectively scored using the Radiation Therapy Oncology Group toxicity scale and the International Prostate Symptom Score questionnaire.
  • The median number of seeds and total activity implanted were 61 and 999 MBq, respectively, for a median prostate volume of 33.6 cc.
  • CONCLUSIONS: IO technique for prostate brachytherapy is associated with low rates of late morbidity and excellent early biochemical control.
  • [MeSH-major] Brachytherapy / adverse effects. Brachytherapy / methods. Prostatic Neoplasms / radiotherapy
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Humans. Iodine Radioisotopes. Male. Middle Aged. Palladium. Prostate-Specific Antigen / blood. Radioisotopes. Radiotherapy Dosage. Risk Assessment