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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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[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

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(PMID = 18265484.001).

[ISSN] 0002-9165

[Journal-full-title] The American journal of clinical nutrition

[ISO-abbreviation] Am. J. Clin. Nutr.

[Language] eng

[Grant] United States / NCI NIH HHS / CA / P50 CA-921310-01A1; United States / NCI NIH HHS / CA / R01 CA-100938

[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 / Insulin-Like Growth Factor Binding Protein 3; 67763-96-6 / Insulin-Like Growth Factor I

[Number-of-references] 62

   

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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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[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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Archivio Istituzionale della Ricerca Unimi. Full text from AIR - Univ. Milan .

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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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[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

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(PMID = 20225559.001).

[ISSN] 0035-2640

[Journal-full-title] La Revue du praticien

[ISO-abbreviation] Rev Prat

[Language] fre

[Publication-type] English Abstract; Journal Article

[Publication-country] France

   

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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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[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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[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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[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

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(PMID = 16195861.001).

[ISSN] 0172-8113

[Journal-full-title] Der Pathologe

[ISO-abbreviation] Pathologe

[Language] ger

[Publication-type] English Abstract; Journal Article

[Publication-country] Germany

[Chemical-registry-number] 0 / Biomarkers, Tumor; EC 3.4.21.77 / Prostate-Specific Antigen

   

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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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[Copyright] ©2010 AACR.

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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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[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.

[Cites] Nat Rev Cancer. 2007 Apr;7(4):256-69 [17384581.001]

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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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[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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[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

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(PMID = 17304503.001).

[ISSN] 0020-7136

[Journal-full-title] International journal of cancer

[ISO-abbreviation] Int. J. Cancer

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] DH2M523P0H / Genistein

   

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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

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(PMID = 16697804.001).

[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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[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

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(PMID = 20356946.001).

[ISSN] 1475-5793

[Journal-full-title] Journal of medical screening

[ISO-abbreviation] J Med Screen

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Chemical-registry-number] EC 3.4.21.77 / Prostate-Specific Antigen

   

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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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[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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[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

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(PMID = 15632264.001).

[ISSN] 0002-9262

[Journal-full-title] American journal of epidemiology

[ISO-abbreviation] Am. J. Epidemiol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

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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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[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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[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

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(PMID = 20208477.001).

[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

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 3.1.3.67 / PTEN Phosphohydrolase

   

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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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[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

[Chemical-registry-number] EC 3.4.21.77 / Prostate-Specific Antigen

   

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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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[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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[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

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(PMID = 17382156.001).

[ISSN] 1527-9995

[Journal-full-title] Urology

[ISO-abbreviation] Urology

[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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[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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[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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[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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[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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[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

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(PMID = 17382159.001).

[ISSN] 1527-9995

[Journal-full-title] Urology

[ISO-abbreviation] Urology

[Language] eng

[Publication-type] Journal Article; Multicenter Study

[Publication-country] United States

[Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / RNA, Messenger; 0 / prostate cancer antigen 3, human; EC 3.4.21.77 / Prostate-Specific Antigen

   

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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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[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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[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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[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.

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(PMID = 18560003.001).

[ISSN] 1538-3598

[Journal-full-title] JAMA

[ISO-abbreviation] JAMA

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / P30 CA006973; United States / NCI NIH HHS / CA / P50 CA058236; United States / NCI NIH HHS / CA / P50 CA058236-13; United States / NCI NIH HHS / CA / CA58236

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.

[Publication-country] United States

[Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; EC 3.4.21.77 / Prostate-Specific Antigen

[Other-IDs] NLM/ NIHMS283299; NLM/ PMC3076799

   

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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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[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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[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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[Cites] J Gerontol Nurs. 2000 Jan;26(1):6-15; quiz 54-5 [10776164.001]

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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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[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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[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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[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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[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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[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

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(PMID = 17992028.001).

[ISSN] 1423-0240

[Journal-full-title] Onkologie

[ISO-abbreviation] Onkologie

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Switzerland

   

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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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[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