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6. Cao KY, Mao XP, Wang DH, Xu L, Yuan GQ, Dai SQ, Zheng BJ, Qiu SP: High expression of PSM-E correlated with tumor grade in prostate cancer: a new alternatively spliced variant of prostate-specific membrane antigen. Prostate; 2007 Dec 1;67(16):1791-800
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High expression of PSM-E correlated with tumor grade in prostate cancer: a new alternatively spliced variant of prostate-specific membrane antigen.
  • BACKGROUND: Prostate-specific membrane antigen (PSMA) overexpressed in prostate cancer (PCa) has been targeted for therapy and diagnosis of PCa.
  • METHODS: PSM-E and PSMA mRNA were measured in LNCaP, PC-3 and prostate or nonprostatic malignancies.
  • PSM-E and PSMA mRNA levels were quantified by a real-time PCR assay in normal prostate (n = 7), benign prostatic hyperplasia (BPH) (n = 22) and PCa (n = 41).
  • The correlation between their levels and tumor grade was analyzed.
  • Significant difference of PSM-E mRNA levels was observed among normal prostate, BPH and PCa (P < 0.001), and PSM-E levels increased with increasing Gleason score (r = 0.514, P < 0.001).
  • PSMA mRNA levels were higher in BPH and PCa than in normal prostate (P < 0.001), but no difference between BPH and PCa, no significant correlation was observed between PSMA levels and Gleason score (r = 0.229, P = 0.057).
  • [MeSH-major] Antigens, Surface / biosynthesis. Glutamate Carboxypeptidase II / biosynthesis. Prostatic Neoplasms / metabolism
  • [MeSH-minor] Alternative Splicing. Base Sequence. Blotting, Western. Cell Line, Tumor. Cloning, Molecular. Humans. Male. Microscopy, Fluorescence. Molecular Sequence Data. Protein Isoforms. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction. Sequence Alignment. Sequence Analysis, DNA. Statistics, Nonparametric. Transfection

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  • (PMID = 17929272.001).
  • [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, Surface; 0 / Protein Isoforms; 0 / RNA, Messenger; EC 3.4.17.21 / Glutamate Carboxypeptidase II; EC 3.4.17.21 / glutamate carboxypeptidase II, human
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7. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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8. Thomas S, Chigurupati S, Anbalagan M, Shah G: Calcitonin increases tumorigenicity of prostate cancer cells: evidence for the role of protein kinase A and urokinase-type plasminogen receptor. Mol Endocrinol; 2006 Aug;20(8):1894-911
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  • [Title] Calcitonin increases tumorigenicity of prostate cancer cells: evidence for the role of protein kinase A and urokinase-type plasminogen receptor.
  • The expression of human (h) calcitonin (CT) and its receptor (CTR) is localized to basal epithelium in benign prostates but is distributed in whole epithelium of malignant prostates.
  • Moreover, the abundance of hCT and CTR mRNA in primary prostate tumors positively correlates with the tumor grade.
  • We tested the hypothesis that the modulation of endogenous hCT expression of prostate cancer (PC) cell lines alters their oncogenicity.
  • These results, when combined with our other results, that the expression of hCT in primary PCs increase with tumor grade, suggest an important role for hCT in the progression of PC to a metastatic phenotype.

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  • (PMID = 16574742.001).
  • [ISSN] 0888-8809
  • [Journal-full-title] Molecular endocrinology (Baltimore, Md.)
  • [ISO-abbreviation] Mol. Endocrinol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA096534; United States / NCI NIH HHS / CA / CA96534
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / PLAUR protein, human; 0 / Plaur protein, mouse; 0 / RNA, Messenger; 0 / Receptors, Cell Surface; 0 / Receptors, Urokinase Plasminogen Activator; 9007-12-9 / Calcitonin; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases; EC 3.4.21.73 / Urokinase-Type Plasminogen Activator
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9. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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10. Chun FK, Müller I, Lange I, Friedrich MG, Erbersdobler A, Karakiewicz PI, Graefen M, Pantel K, Huland H, Schwarzenbach H: Circulating tumour-associated plasma DNA represents an independent and informative predictor of prostate cancer. BJU Int; 2006 Sep;98(3):544-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Circulating tumour-associated plasma DNA represents an independent and informative predictor of prostate cancer.
  • OBJECTIVE: To investigate whether preoperative plasma levels of free DNA can discriminate between men with localized prostate cancer and benign prostatic hyperplasia (BPH).
  • PATIENTS AND METHODS: In all, 161 referred patients suspicious for prostate cancer either by an elevated prostate-specific antigen (PSA) level and/or abnormal digital rectal examination (DRE) were included in this prospective study.
  • Peripheral plasma was taken before prostate biopsy and genomic DNA was extracted from the plasma using the a commercial kit and a vacuum chamber.
  • After controlling for age, PSA level, the percentage free/total (f/t) PSA and prostate volume, the median prostate cancer plasma DNA concentration served as diagnostic threshold in uni- and multivariate logistic regression models.
  • RESULTS: Subgroups consisted of 142 men with clinically localized prostate cancer and 19 with BPH.
  • The median plasma concentration of cell-free DNA was 267 ng/mL in men with BPH vs 709 ng/mL in men with prostate cancer.
  • In multivariate analyses, it remained statistically significant after controlling for age, tPSA, f/tPSA and prostate volume, increasing the predictive accuracy by 5.6%.
  • CONCLUSIONS: Our data suggest that plasma DNA level is a highly accurate and informative predictor in uni- and multivariate models for the presence of prostate cancer on needle biopsy.
  • However, larger-scale studies are needed to further confirm its clinical impact on prostate cancer detection.
  • [MeSH-major] Biomarkers, Tumor / blood. DNA, Neoplasm / blood. Prostatic Hyperplasia / diagnosis. Prostatic Neoplasms / diagnosis
  • [MeSH-minor] Adult. Aged. Humans. Male. Middle Aged. Predictive Value of Tests. Preoperative Care. Prospective Studies. Prostate-Specific Antigen / blood. Sensitivity and Specificity


11. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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12. 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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13. Raj GV, Brashears JH, Anand A, Paulson DF, Polascik TJ: Does prior benign prostate biopsy predict outcome for patients treated with radical perineal prostatectomy? Urology; 2005 Feb;65(2):332-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Does prior benign prostate biopsy predict outcome for patients treated with radical perineal prostatectomy?
  • OBJECTIVES: To determine the effect of prior benign prostate biopsies on the surgical and clinical outcomes of patients treated with radical perineal prostatectomy for prostate cancer.
  • METHODS: A total of 1369 patients with clinically localized prostate cancer underwent radical prostatectomy by a single surgeon between 1991 and 2001.
  • A subset of 203 patients (14.9%), who had undergone at least one prior benign prostate biopsy for a rising prostate-specific antigen and/or abnormal digital rectal examination, constituted our study population.
  • After prostatectomy, patients were evaluated at 6-month intervals for biochemical evidence of recurrence, defined as a prostate-specific antigen level of 0.5 ng/mL or greater.
  • RESULTS: Patients with a prior benign biopsy had more favorable pathologic features with more organ-confined (74% versus 64%; P <0.001) and less margin-positive (9.8% versus 18%) disease.
  • Kaplan-Meier analyses suggested that patients with prior benign biopsies have improved biochemical disease-free survival, especially for those with more aggressive disease (Gleason sum 7 or greater; P <0.01).
  • CONCLUSIONS: A prior benign prostate biopsy may be independently associated with more favorable surgical and biochemical outcomes after prostatectomy.
  • [MeSH-major] Adenocarcinoma / surgery. Biopsy. Prostate / pathology. Prostatectomy / methods. Prostatic Neoplasms / surgery
  • [MeSH-minor] Aged. Biomarkers, Tumor / blood. Cohort Studies. Disease-Free Survival. Follow-Up Studies. Humans. Life Tables. Male. Middle Aged. Neoplasm Proteins / blood. Proportional Hazards Models. Prostate-Specific Antigen / blood. Treatment Outcome

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  • (PMID = 15708048.001).
  • [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] 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins; EC 3.4.21.77 / Prostate-Specific Antigen
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4. 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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15. 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


16. 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


17. 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


18. 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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19. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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


20. 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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21. Moriceau G, Ory B, Gobin B, Verrecchia F, Gouin F, Blanchard F, Redini F, Heymann D: Therapeutic approach of primary bone tumours by bisphosphonates. Curr Pharm Des; 2010;16(27):2981-7
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  • Bone tumours can be dissociated in two main categories: i) primary bone tumours (benign or malignant) including mainly osteosarcoma and other sarcomas.ii)and giant cell tumour and bone metastases originate from others cancer (Breast, prostate, kidney cancer, etc).
  • However, the first step of bone tumour development is associated with an induction of bone resorption and the establishment of a vicious cycle between the osteoclasts and the tumour growth.
  • Indeed, bone resorption contributes to the pathogenesis of bone tumour by the release of cytokines (IL6, TNFα) which govern the bone tumour's development and which are trapped into the bone matrix.
  • BPs exert also indirect anti-tumour activities in vivo.
  • Indeed, BPs directly interfere with the bone microenvironment and target osteoclasts, endothelial cells and immune cells (tumour-associated macrophages, γ9δ2 T cells).
  • BPs induce tumour cell death in vitro and same activity is suspected in vivo.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Bone Neoplasms / drug therapy. Diphosphonates / pharmacology. Diphosphonates / therapeutic use. Drug Design
  • [MeSH-minor] Animals. Bone Density Conservation Agents / pharmacology. Bone Density Conservation Agents / therapeutic use. Chondrosarcoma / drug therapy. Giant Cell Tumor of Bone / drug therapy. Humans. Osteosarcoma / drug therapy


22. 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


23. 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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24. 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
  • [Chemical-registry-number] EC 3.4.21.77 / Prostate-Specific Antigen
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25. 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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26. D'Antonio KB, Toubaji A, Albadine R, Mondul AM, Platz EA, Netto GJ, Getzenberg RH: Extracellular matrix associated protein CYR61 is linked to prostate cancer development. J Urol; 2010 Apr;183(4):1604-10
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  • [Title] Extracellular matrix associated protein CYR61 is linked to prostate cancer development.
  • Depending on cancer type these changes are linked with enhanced or inhibited tumor growth.
  • We characterized Cyr61 in prostate cancer.
  • MATERIALS AND METHODS: Cyr61 expression in prostate cancer, benign prostatic hyperplasia and normal tissues was evaluated by microarray analysis, quantitative real-time polymerase chain reaction and tissue microarray.
  • Immunoblots were analyzed to assess endogenous protein expression in prostate cancer cell lines.
  • RESULTS: On genomic analysis Cyr61 up-regulation was observed in prostate cancer tissue and in normal prostate tissue adjacent to tumor vs that in prostate donor tissue.
  • In 174 matched tumors and normal prostate tissues adjacent to tumor tissue microarray revealed significantly up-regulated Cyr61 protein expression in cancer tissue vs normal prostate tissue adjacent to tumor.
  • Staining in high grade prostatic intraepithelial neoplasia was moderately up-regulated vs that in normal prostate tissue adjacent to tumor but generally less intense than in carcinoma tissue.
  • CONCLUSIONS: In addition to the correlation with more advanced disease, the strong association between Cyr61 expression and prostate cancer supports the potential usefulness of Cyr61 as a novel biomarker for prostate cancer.
  • This warrants further analysis to determine the mechanisms by which Cyr61 may contribute to prostate cancer development and progression.
  • [MeSH-major] Cysteine-Rich Protein 61 / physiology. Prostatic Neoplasms / etiology

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  • [Copyright] Copyright (c) 2010 American Urological Association Education and Research, Inc. Published by Elsevier Inc. All rights reserved.
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  • (PMID = 20172544.001).
  • [ISSN] 1527-3792
  • [Journal-full-title] The Journal of urology
  • [ISO-abbreviation] J. Urol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / T32 CA009314; United States / NCI NIH HHS / CA / T32 CA009314; United States / NCI NIH HHS / CA / T32 CA009314-27S1
  • [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 / CYR61 protein, human; 0 / Cysteine-Rich Protein 61
  • [Other-IDs] NLM/ NIHMS371120; NLM/ PMC3349619
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27. Huo Q: Protein complexes/aggregates as potential cancer biomarkers revealed by a nanoparticle aggregation immunoassay. Colloids Surf B Biointerfaces; 2010 Jul 1;78(2):259-65
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  • This study examined four biomarkers proteins, CA125, CEA (carcinoembryonic antigen), CA19-9 and PAP (prostatic acid phosphatase) in ovarian, colon and prostate tissue lysates.
  • The most exciting results were observed from the PAP assay of prostate tissues: prostate cancer can be clearly distinguished from normal prostate and prostate with benign conditions such as BPH (benign prostate hyperplasia) based on the complex/aggregation level of PAP in prostate tissue lysates.
  • The complex/aggregate level of a protein can be potential biomarkers for cancer detection and diagnosis.
  • [MeSH-major] Biomarkers, Tumor / analysis. Immunoassay / methods. Metal Nanoparticles / chemistry. Neoplasms / metabolism. Proteins / analysis
  • [MeSH-minor] Acid Phosphatase. Adult. Aged. Aged, 80 and over. Antibodies / chemistry. CA-125 Antigen / analysis. CA-125 Antigen / chemistry. CA-19-9 Antigen / analysis. CA-19-9 Antigen / chemistry. Carcinoembryonic Antigen / analysis. Carcinoembryonic Antigen / chemistry. Colonic Neoplasms / diagnosis. Colonic Neoplasms / metabolism. Diagnosis, Differential. Female. Gold / chemistry. Humans. Male. Membrane Proteins / analysis. Membrane Proteins / chemistry. Middle Aged. Ovarian Neoplasms / diagnosis. Ovarian Neoplasms / metabolism. Prostatic Hyperplasia / diagnosis. Prostatic Hyperplasia / metabolism. Prostatic Neoplasms / diagnosis. Prostatic Neoplasms / metabolism. Protein Binding. Protein Conformation. Protein Tyrosine Phosphatases / analysis. Protein Tyrosine Phosphatases / chemistry. Sensitivity and Specificity

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  • [Copyright] 2010 Elsevier B.V. All rights reserved.
  • (PMID = 20392611.001).
  • [ISSN] 1873-4367
  • [Journal-full-title] Colloids and surfaces. B, Biointerfaces
  • [ISO-abbreviation] Colloids Surf B Biointerfaces
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antibodies; 0 / Biomarkers, Tumor; 0 / CA-125 Antigen; 0 / CA-19-9 Antigen; 0 / Carcinoembryonic Antigen; 0 / MUC16 protein, human; 0 / Membrane Proteins; 0 / Proteins; 7440-57-5 / Gold; EC 3.1.3.2 / Acid Phosphatase; EC 3.1.3.2 / prostatic acid phosphatase; EC 3.1.3.48 / Protein Tyrosine Phosphatases
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28. 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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  • [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


29. 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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30. 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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31. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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32. 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


33. 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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34. 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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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. Abdul M, Hoosein N: Reduced Kv1.3 potassium channel expression in human prostate cancer. J Membr Biol; 2006;214(2):99-102
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  • [Title] Reduced Kv1.3 potassium channel expression in human prostate cancer.
  • The presence of Kv1.3 voltage-gated potassium channels in rat and human prostate epithelial cells has been previously reported.
  • We examined, by immunohistochemistry, Kv1.3 levels in 10 normal human prostate, 18 benign prostatic hyperplasia (BPH) and 147 primary human prostate cancer (Pca) specimens.
  • We found high epithelial expression of Kv1.3 in all normal prostate, 16 BPH and 77 (52%) Pca specimens.
  • We found a significant inverse correlation between Kv1.3 levels and tumor grade (r = -0.25, P = 0.003) as well as tumor stage (r = -0.27, P = 0.001).
  • Study of an additional 30 primary Pca specimens showed that 15 (50%) had reduced Kv1.3 immunostaining compared to matched normal prostate tissue.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Kv1.3 Potassium Channel / biosynthesis. Prostate-Specific Antigen / biosynthesis. Prostatic Hyperplasia / metabolism. Prostatic Neoplasms / metabolism
  • [MeSH-minor] Adult. Aged. Animals. Humans. Male. Middle Aged. Neoplasm Staging. Neoplasms / diagnosis. Neoplasms / metabolism. Neoplasms / pathology. Prognosis. Rats


37. 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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38. 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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  • [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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39. Iczkowski KA: Cell adhesion molecule CD44: its functional roles in prostate cancer. Am J Transl Res; 2010;3(1):1-7
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  • [Title] Cell adhesion molecule CD44: its functional roles in prostate cancer.
  • Dysregulated CD44 expression characterizes most human cancers, including prostate cancer (PCa).
  • PCa loses expression of CD44 standard (CD44s) that is present in benign epithelium, and overexpresses the novel splice variant (v) isoform, CD44v7-10.
  • Phenyl-methylene hydantoins (PMH), guanidine alkaloids derived from Red Sea sponges, have the ability to increase cell-cell adhesion in prostate cancer cells and reduce invasion.
  • The oncogenic mi-croRNAs, miR-373 and miR-520c, which interact with CD44, were studied in prostate cancer cells and human tissues.
  • We found that they bound the 3' untranslated region of the CD44 RNA, and suppressed CD44 in prostate cancer, by preventing the translation of CD44 RNA, rather than by degrading the RNA.
  • Finally, CD44v7-10 may be a target for chemosensitization, and plays a role in nutraceutical abrogation of tumor development.

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  • (PMID = 21139802.001).
  • [ISSN] 1943-8141
  • [Journal-full-title] American journal of translational research
  • [ISO-abbreviation] Am J Transl Res
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2981422
  • [Keywords] NOTNLM ; CD44 / phenyl-methylene hydantoins / prostate / silibinin / splicing / standard / variant / xenografts
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40. 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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41. 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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42. Rubin MA, Bismar TA, Andrén O, Mucci L, Kim R, Shen R, Ghosh D, Wei JT, Chinnaiyan AM, Adami HO, Kantoff PW, Johansson JE: Decreased alpha-methylacyl CoA racemase expression in localized prostate cancer is associated with an increased rate of biochemical recurrence and cancer-specific death. Cancer Epidemiol Biomarkers Prev; 2005 Jun;14(6):1424-32
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  • [Title] Decreased alpha-methylacyl CoA racemase expression in localized prostate cancer is associated with an increased rate of biochemical recurrence and cancer-specific death.
  • Alpha-methylacyl CoA racemase (AMACR) is overexpressed in prostate cancer relative to benign prostatic tissue.
  • AMACR expression is highest in localized prostate cancer and decreases in metastatic prostate cancer.
  • Herein, we explored the use of AMACR as a biomarker for aggressive prostate cancer.
  • AMACR protein expression was determined by immunohistochemistry using an image analysis system on two localized prostate cancer cohorts consisting of 204 men treated by radical prostatectomy and 188 men followed expectantly.
  • The end points for the cohorts were time to prostate-specific antigen (PSA) failure (i.e., elevation >0.2 ng/mL) and time to prostate cancer death in the watchful waiting cohort.
  • Using a regression tree method, optimal AMACR protein expression cut-points were determined to best differentiate prostate cancer outcome in each of the cohorts separately.
  • Cox proportional hazard models were then employed to examine the effect of the AMACR cut-point on prostate cancer outcome, and adjusted for clinical variables.
  • Lower AMACR tissue expression was associated with worse prostate cancer outcome, independent of clinical variables (hazard ratio, 3.7 for PSA failure; P = 0.018; hazard ratio, 4.1 for prostate cancer death, P = 0.0006).
  • Among those with both low AMACR expression and high Gleason score, the risk of prostate cancer death was 18-fold higher (P = 0.006).
  • The AMACR cut-point developed using prostate cancer-specific death as the end point predicted PSA failures independent of Gleason score, PSA, and margin status.
  • This is the first study to show that AMACR expression is significantly associated with prostate cancer progression and suggests that not all surrogate end points may be optimal to define biomarkers of aggressive prostate cancer.
  • [MeSH-major] Biomarkers, Tumor / blood. Gene Expression Profiling. Prostatic Neoplasms / genetics. Racemases and Epimerases / biosynthesis

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  • (PMID = 15941951.001).
  • [ISSN] 1055-9965
  • [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 / CA 97063; United States / NCI NIH HHS / CA / P50CA69568; United States / NCI NIH HHS / CA / P50CA90381; United States / NIA NIH HHS / AG / R01AG21404
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
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43. 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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44. 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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45. 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


46. 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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47. 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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  • [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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48. Yang LP, Yang ZL, Huang JS, Fu X: [Expression of cancer stem cell antigens, prostate stem cell antigen and Oct-4, and its clinicopatholgical significances in benign and malignant lesions of gallbladder]. Zhonghua Bing Li Xue Za Zhi; 2008 Jan;37(1):56-7
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  • [Title] [Expression of cancer stem cell antigens, prostate stem cell antigen and Oct-4, and its clinicopatholgical significances in benign and malignant lesions of gallbladder].
  • [MeSH-major] Antigens, Neoplasm / immunology. Gallbladder Neoplasms / pathology. Neoplastic Stem Cells / immunology. Octamer Transcription Factor-3 / metabolism. Prostatic Neoplasms / pathology
  • [MeSH-minor] Antigens / immunology. Gene Expression Regulation, Neoplastic. Humans. Male. Tumor Cells, Cultured

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  • (PMID = 18509987.001).
  • [ISSN] 0529-5807
  • [Journal-full-title] Zhonghua bing li xue za zhi = Chinese journal of pathology
  • [ISO-abbreviation] Zhonghua Bing Li Xue Za Zhi
  • [Language] chi
  • [Publication-type] Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens; 0 / Antigens, Neoplasm; 0 / Octamer Transcription Factor-3
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49. Aitchison A, Warren A, Neal D, Rabbitts P: RASSF1A promoter methylation is frequently detected in both pre-malignant and non-malignant microdissected prostatic epithelial tissues. Prostate; 2007 May 01;67(6):638-44
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  • [Title] RASSF1A promoter methylation is frequently detected in both pre-malignant and non-malignant microdissected prostatic epithelial tissues.
  • BACKGROUND: The RASSF1A gene is a tumor suppressor gene inactivated by hypermethylation in a very wide variety of malignant tumors including prostate cancer.
  • METHODS: In this study we have used laser capture microdissection to provide pure cell populations to investigate the methylation status of 16 CpG sites in the promoter region of this gene in prostatic intra-epithelial neoplasia, in histologically normal epithelial cells associated with these lesions and in epithelial cells from benign prostatic hyperplasia.
  • RESULTS: Unexpectedly, frequent methylation, detected by sequence analysis following bisulphite treatment, was observed in benign epithelium as well as in the lesions associated with prostatic intra-epithelial neoplasia and at high risk of cancer formation.
  • Fifty percent or more CpG sites were methylated in 7/14 prostatic intra-epithelial neoplasms, 8/11 histologically normal epithelial cells and 8/12 specimens of benign prostatic tissue.
  • CONCLUSION: These observations suggest that methylation of the RASSF1A gene is present in both pre-malignant and benign epithelia and suggests quantitation is required for it to be an effective marker of early prostate cancer.
  • [MeSH-major] DNA Methylation. Gene Silencing. Promoter Regions, Genetic. Prostatic Intraepithelial Neoplasia / genetics. Prostatic Neoplasms / genetics. Tumor Suppressor Proteins / genetics
  • [MeSH-minor] Aged. Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. Biopsy, Needle. CpG Islands / genetics. DNA, Neoplasm / analysis. Humans. Lasers. Male. Microdissection. Middle Aged. Precancerous Conditions. Prostate / pathology. Sequence Analysis, DNA

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17342751.001).
  • [ISSN] 0270-4137
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0500966
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DNA, Neoplasm; 0 / RASSF1 protein, human; 0 / Tumor Suppressor Proteins
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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. 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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55. Ishiguro H, Nakaigawa N, Miyoshi Y, Fujinami K, Kubota Y, Uemura H: Receptor for advanced glycation end products (RAGE) and its ligand, amphoterin are overexpressed and associated with prostate cancer development. Prostate; 2005 Jun 15;64(1):92-100
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  • [Title] Receptor for advanced glycation end products (RAGE) and its ligand, amphoterin are overexpressed and associated with prostate cancer development.
  • METHODS: We investigated RAGE and amphoterin mRNA expression in prostate cancer cell lines (DU145, PC-3, and LNCaP cells), hormone-refractory prostate cancer tissues, and paired untreated primary prostate cancer and normal prostate (including benign prostatic hypertrophy (BPH)) tissues using real-time quantitative PCR.
  • Moreover, to confirm the AGE-RAGE interaction in prostate cancer, DU145 cells stimulated with AGE-bovine serum albumin (AGE-BSA) were examined by in vitro matrigel assay, cell viability assay, MTT assay, reverse transcription-polymerase chain reaction (RT-PCR), and Western blot.
  • RESULTS: DU145 cells, a hormone-independent prostate cancer cell line, showed the highest RAGE mRNA expression.
  • In prostate tissues, untreated prostate cancer tissue and hormone-refractory prostate cancer tissue showed higher RAGE and amphoterin mRNA expression than normal prostate tissue.
  • CONCLUSIONS: The AGE-RAGE interaction is important in prostate cancer development, and inhibition of this interaction has potential as a new molecular target for cancer therapy or prevention.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. HMGB1 Protein / genetics. Prostatic Neoplasms / genetics. Prostatic Neoplasms / physiopathology. Receptors, Immunologic / genetics
  • [MeSH-minor] Advanced Glycosylation End Product-Specific Receptor. Blotting, Western. Cell Line, Tumor. Cell Survival. Formazans. Glycosylation End Products, Advanced / metabolism. Humans. Ligands. Male. Neoplasm Invasiveness. Prostatic Hyperplasia / genetics. Prostatic Hyperplasia / pathology. Prostatic Hyperplasia / physiopathology. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction. Tetrazolium Salts

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  • (PMID = 15666359.001).
  • [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 / Advanced Glycosylation End Product-Specific Receptor; 0 / Formazans; 0 / Glycosylation End Products, Advanced; 0 / HMGB1 Protein; 0 / Ligands; 0 / RNA, Messenger; 0 / Receptors, Immunologic; 0 / Tetrazolium Salts; 23305-68-2 / MTT formazan
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56. 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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  • [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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57. 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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58. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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59. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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60. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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


61. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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62. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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63. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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64. 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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65. 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


66. Gaurav K, Fitch J, Panda M: Increased frequency and nocturia in a middle aged male may not always be due to benign prostatic hypertrophy: a case report. Cases J; 2009;2:9274
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  • [Title] Increased frequency and nocturia in a middle aged male may not always be due to benign prostatic hypertrophy: a case report.
  • Primary signet ring cell carcinoma of urinary bladder is a rare type of bladder tumor and carries a very high mortality rate.
  • It may have a clinical presentation similar to common diseases like benign prostatic hypertrophy and the management options are extremely limited.
  • He was found to have an increased creatinine of 2.8 mg/dl and a prostate specific antigen level of 0.18 ng/ml.
  • Diagnostic work up including abdominal ultrasonography, computed tomography scan, retrograde pyelogram, cystography and cystoscopic biopsies revealed the diagnosis of primary signet ring cell carcinoma of urinary bladder.

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  • [ISSN] 1757-1626
  • [Journal-full-title] Cases journal
  • [ISO-abbreviation] Cases J
  • [Language] eng
  • [Publication-type] Journal Article
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67. Leav I, Plescia J, Goel HL, Li J, Jiang Z, Cohen RJ, Languino LR, Altieri DC: Cytoprotective mitochondrial chaperone TRAP-1 as a novel molecular target in localized and metastatic prostate cancer. Am J Pathol; 2010 Jan;176(1):393-401
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  • [Title] Cytoprotective mitochondrial chaperone TRAP-1 as a novel molecular target in localized and metastatic prostate cancer.
  • Molecular chaperones of the heat shock protein-90 (Hsp90) family promote cell survival, but the molecular requirements of this pathway in tumor progression are not understood.
  • Here, we show that a mitochondria-localized Hsp90 chaperone, tumor necrosis factor receptor-associated protein-1 (TRAP-1), is abundantly and ubiquitously expressed in human high-grade prostatic intraepithelial neoplasia, Gleason grades 3 through 5 prostatic adenocarcinomas, and metastatic prostate cancer, but largely undetectable in normal prostate or benign prostatic hyperplasia in vivo.
  • Prostate lesions formed in genetic models of the disease, including the transgenic adenocarcinoma of the mouse prostate and mice carrying prostate-specific deletion of the phosphatase tensin homolog tumor suppressor (Pten(pc-/-)), also exhibit high levels of TRAP-1.
  • Expression of TRAP-1 in nontransformed prostatic epithelial BPH-1 cells inhibited cell death, whereas silencing of TRAP-1 in androgen-independent PC3 or DU145 prostate cancer cells by small interfering RNA enhanced apoptosis.
  • Targeting TRAP-1 with a novel class of mitochondria-directed Hsp90 inhibitors, ie, Gamitrinibs, caused rapid and complete killing of androgen-dependent or -independent prostate cancer, but not BPH-1 cells, whereas reintroduction of TRAP-1 in BPH-1 cells conferred sensitivity to Gamitrinib-induced cell death.
  • These data identify TRAP-1 as a novel mitochondrial survival factor differentially expressed in localized and metastatic prostate cancer compared with normal prostate.
  • Targeting this pathway with Gamitrinibs could be explored as novel molecular therapy in patients with advanced prostate cancer.

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  • (PMID = 19948822.001).
  • [ISSN] 1525-2191
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA078810; United States / NCI NIH HHS / CA / R01 CA089720; United States / NCI NIH HHS / CA / CA118005; United States / NCI NIH HHS / CA / R01 CA109874-05; United States / NCI NIH HHS / CA / CA78810; United States / NCI NIH HHS / CA / CA109874-05; United States / NCI NIH HHS / CA / R01 CA109874; United States / NCI NIH HHS / CA / R01 CA089720-05; United States / NCI NIH HHS / CA / CA90917; United States / NCI NIH HHS / CA / CA089720-05; United States / NCI NIH HHS / CA / CA109874; United States / NCI NIH HHS / CA / CA89720; United States / NCI NIH HHS / CA / R56 CA089720; United States / NCI NIH HHS / CA / R01 CA118005; United States / NCI NIH HHS / CA / R01 CA090917
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / HSP90 Heat-Shock Proteins; 0 / Molecular Chaperones; 0 / TRAP-1 protein, mouse; 0 / TRAP1 protein, human
  • [Other-IDs] NLM/ PMC2797899
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68. Yocum AK, Khan AP, Zhao R, Chinnaiyan AM: Development of selected reaction monitoring-MS methodology to measure peptide biomarkers in prostate cancer. Proteomics; 2010 Oct;10(19):3506-14
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  • [Title] Development of selected reaction monitoring-MS methodology to measure peptide biomarkers in prostate cancer.
  • Prostate cancer is a leading cause of cancer-related death.
  • The current modality of diagnosis, the measurement of serum PSA, not only suffers from lack of specificity, but does not distinguish clinical cases in which current treatment measures would be most successful, i.e. aggressive, life-threatening tumors.
  • The SID selected reaction monitoring-MS/MS methodology was then transferred to tissue samples, in which the assay shows potential to differentiate benign disease from localized cancer and localized cancer from aggressive metastatic disease.
  • These results establish the preliminary development of a rational targeted MS platform that strives to bridge the gap between discovery and validation of biomarkers for the detection of prostate cancer.
  • [MeSH-major] Biomarkers, Tumor / analysis. Prostate-Specific Antigen / analysis. Prostatic Neoplasms / diagnosis. Tandem Mass Spectrometry / methods
  • [MeSH-minor] Cell Line, Tumor. Humans. Male. Sensitivity and Specificity


69. Chen M, Chen LM, Lin CY, Chai KX: The epidermal growth factor receptor (EGFR) is proteolytically modified by the Matriptase-Prostasin serine protease cascade in cultured epithelial cells. Biochim Biophys Acta; 2008 May;1783(5):896-903
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  • Prostasin re-expression in the PC-3 prostate carcinoma cells down-regulated the epidermal growth factor receptor (EGFR) protein expression and EGF-induced phosphorylation of the extracellular signal-regulated kinases (Erk1/2).
  • The EGFR ECD proteolytic modification by matriptase-prostasin is also observed in the BEAS-2B normal lung epithelial cells, the BPH-1 benign prostate hyperplasia and the MDA-MB-231 breast cancer cell lines; and represents a novel mechanism for epithelial cells to modulate EGF-EGFR signaling.

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  • (PMID = 18054338.001).
  • [ISSN] 0006-3002
  • [Journal-full-title] Biochimica et biophysica acta
  • [ISO-abbreviation] Biochim. Biophys. Acta
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA 096854; United States / NCI NIH HHS / CA / CA104944-04; United States / NCI NIH HHS / CA / R01 CA096851-05; United States / NCI NIH HHS / CA / R01 CA096851; United States / NCI NIH HHS / CA / CA096851-05; United States / NCI NIH HHS / CA / R01 CA 104944; United States / NCI NIH HHS / CA / R01 CA104944; United States / NCI NIH HHS / CA / R01 CA104944-04
  • [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] Netherlands
  • [Chemical-registry-number] 42HK56048U / Tyrosine; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.- / matriptase; EC 3.4.21.- / prostasin
  • [Other-IDs] NLM/ NIHMS48494; NLM/ PMC3214967
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70. 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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71. Sartor O: Prostate cancer. Saturation biopsy does not accurately localize tumors. Nat Rev Urol; 2010 Sep;7(9):479-80
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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72. 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


73. 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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74. 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


75. 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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76. 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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77. 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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78. 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


79. 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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80. 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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  • [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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81. 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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  • [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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82. 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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  • [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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83. 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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  • [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

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  • (PMID = 19213608.001).
  • [ISSN] 1538-4721
  • [Journal-full-title] Brachytherapy
  • [ISO-abbreviation] Brachytherapy
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Iodine Radioisotopes; 0 / Radioisotopes; 5TWQ1V240M / Palladium; EC 3.4.21.77 / Prostate-Specific Antigen
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84. Szymanski KM, Wei JT, Dunn RL, Sanda MG: Development and validation of an abbreviated version of the expanded prostate cancer index composite instrument for measuring health-related quality of life among prostate cancer survivors. Urology; 2010 Nov;76(5):1245-50
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  • [Title] Development and validation of an abbreviated version of the expanded prostate cancer index composite instrument for measuring health-related quality of life among prostate cancer survivors.
  • OBJECTIVES: Widespread implementation of health-related quality-of-life (HRQOL) measurement in prostate cancer practice and research requires concise instruments.
  • With 50 questions, the full-length Expanded Prostate Cancer Index Composite (EPIC) is cumbersome to administer outside of studies focusing exclusively on HRQOL.
  • To facilitate HRQOL measurement in a broad range of prostate cancer research and practice settings, we developed and validated an abbreviated version of the EPIC.
  • METHODS: The 50 questions that constitute the full-length EPIC-50 were evaluated to identify the items suitable for elimination while retaining the ability to measure the 5 prostate cancer-specific HRQOL domains of the EPIC-50.
  • The resulting abbreviated version (EPIC-26) was validated using question responses from 252 subjects who had undergone brachytherapy, external beam radiotherapy, or prostatectomy for prostate cancer.
  • CONCLUSIONS: EPIC-26 is a brief, valid, and reliable subjective measure of health quality among patients with prostate cancer and is suitable for measuring the HRQOL among patients undergoing treatment of early-stage prostate cancer.

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  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
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  • (PMID = 20350762.001).
  • [ISSN] 1527-9995
  • [Journal-full-title] Urology
  • [ISO-abbreviation] Urology
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA095662; United States / NCI NIH HHS / CA / RC1 CA146596; United States / NCI NIH HHS / CA / R01-CA95662
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Validation Studies
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS192642; NLM/ PMC3152317
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85. Suzuki H, Komiya A, Kamiya N, Imamoto T, Kawamura K, Miura J, Suzuki N, Nakatsu H, Hata A, Ichikawa T: Development of a nomogram to predict probability of positive initial prostate biopsy among Japanese patients. Urology; 2006 Jan;67(1):131-6
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  • [Title] Development of a nomogram to predict probability of positive initial prostate biopsy among Japanese patients.
  • OBJECTIVES: Several nomograms for prostate cancer detection have recently been developed.
  • Because the incidence of prostate cancer is lower among Asian men, nomograms based on Western populations cannot be directly applied to Japanese men.
  • We, therefore, developed a model for predicting the probability of a positive initial prostate biopsy using clinical and laboratory data from a Japanese male population.
  • METHODS: Data were collected from 834 Japanese male referrals who underwent initial prostate biopsies as individual screening.
  • We analyzed age, total prostate-specific antigen (PSA) level, free/total PSA (f/t PSA) ratio, prostate volume, and digital rectal examination findings.
  • RESULTS: Independent predictors of a positive biopsy result included elevated PSA levels, decreased f/T PSA ratio, advanced age, small prostate volume, and abnormal digital rectal examination findings.
  • If externally validated, applying this model could reduce unnecessary biopsy procedures by 32% and reduce the overall need for prostate biopsies by 26%.
  • CONCLUSIONS: In this study of a Japanese population, incorporating clinical and laboratory data into a prebiopsy nomogram significantly improved the prediction of prostate cancer compared with predictions based solely on the individual factors.
  • [MeSH-major] Nomograms. Prostate / pathology. Prostatic Neoplasms / pathology

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  • (PMID = 16413348.001).
  • [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
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86. Haiman CA, Patterson N, Freedman ML, Myers SR, Pike MC, Waliszewska A, Neubauer J, Tandon A, Schirmer C, McDonald GJ, Greenway SC, Stram DO, Le Marchand L, Kolonel LN, Frasco M, Wong D, Pooler LC, Ardlie K, Oakley-Girvan I, Whittemore AS, Cooney KA, John EM, Ingles SA, Altshuler D, Henderson BE, Reich D: Multiple regions within 8q24 independently affect risk for prostate cancer. Nat Genet; 2007 May;39(5):638-44
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  • [Title] Multiple regions within 8q24 independently affect risk for prostate cancer.
  • After the recent discovery that common genetic variation in 8q24 influences inherited risk of prostate cancer, we genotyped 2,973 SNPs in up to 7,518 men with and without prostate cancer from five populations.
  • We identified seven risk variants, five of them previously undescribed, spanning 430 kb and each independently predicting risk for prostate cancer (P = 7.9 x 10(-19) for the strongest association, and P < 1.5 x 10(-4) for five of the variants, after controlling for each of the others).
  • None of the prostate cancer risk variants aligns to a known gene or alters the coding sequence of an encoded protein.

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  • (PMID = 17401364.001).
  • [ISSN] 1061-4036
  • [Journal-full-title] Nature genetics
  • [ISO-abbreviation] Nat. Genet.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA54281; United States / NCI NIH HHS / CA / CA063464-09S1; United States / NCI NIH HHS / CA / CA79596; United States / NCI NIH HHS / CA / R01 CA084979; United States / NCI NIH HHS / CA / CA84979; United States / NHGRI NIH HHS / HG / HG02758; United States / NCI NIH HHS / CA / CA69568; United States / NCI NIH HHS / CA / R01 CA063464-09S1; United States / NCI NIH HHS / CA / U01 CA067044; United States / NCI NIH HHS / CA / CA63464; United States / NICHD NIH HHS / HD / K12 HD000850; United States / NCI NIH HHS / CA / R01 CA063464; United States / NCI NIH HHS / CA / CA67044; United States / NCI NIH HHS / CA / R01 CA054281; United States / NCI NIH HHS / CA / U01 CA063464; United States / NCI NIH HHS / CA / R01 CA079596; United States / NHGRI NIH HHS / HG / K01 HG002758; United States / NCI NIH HHS / CA / P50 CA069568; United States / NCI NIH HHS / CA / R37 CA054281; United States / NICHD NIH HHS / HD / HD00850; United States / NCI NIH HHS / CA / R01 CA067044
  • [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/ NIHMS50020; NLM/ PMC2638766
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87. Meinbach DS, Lokeshwar BL: Insulin-like growth factors and their binding proteins in prostate cancer: cause or consequence? Urol Oncol; 2006 Jul-Aug;24(4):294-306
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  • [Title] Insulin-like growth factors and their binding proteins in prostate cancer: cause or consequence?
  • Insulin-like growth factors (IGFs) promote growth and survival of many types of tumor cells.
  • The levels of IGF binding proteins (IGFBPs) have been associated with reduced risk for prostate and other cancers.
  • Experimental studies have implicated high levels of IGF-I directly and IGFBP-3 inversely in prostate cancer growth, survival, and progression.
  • However, recent evidence suggests a much weaker association of IGF-I with prostate cancer development and a stronger antagonistic association of IGFBP-3 with prostate cancer progression.
  • Considering the clonal heterogeneity and unpredictable progression pattern of prostate cancer, the role of any single growth factor or its regulator (IGFBP) as a single determining factor is limited.
  • This review is a critical appraisal of the role of IGFs, IGFBP, and IGF-I receptor (the IGF axis) in both experimental and clinical prostate cancer genesis and progression.
  • [MeSH-major] Insulin-Like Growth Factor Binding Proteins / physiology. Insulin-Like Growth Factor I / physiology. Insulin-Like Growth Factor II / physiology. Prostatic Neoplasms / etiology

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  • (PMID = 16818181.001).
  • [ISSN] 1078-1439
  • [Journal-full-title] Urologic oncology
  • [ISO-abbreviation] Urol. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA 061038
  • [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 Proteins; 67763-96-6 / Insulin-Like Growth Factor I; 67763-97-7 / Insulin-Like Growth Factor II; EC 2.7.10.1 / Receptor, IGF Type 1
  • [Number-of-references] 175
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88. Risbridger GP, Davis ID, Birrell SN, Tilley WD: Breast and prostate cancer: more similar than different. Nat Rev Cancer; 2010 Mar;10(3):205-12
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  • [Title] Breast and prostate cancer: more similar than different.
  • Breast cancer and prostate cancer are the two most common invasive cancers in women and men, respectively.
  • Many of the recent advances in understanding the pathophysiology of breast and prostate cancers have paved the way for new treatment strategies.
  • In this Opinion article we discuss some key issues common to breast and prostate cancer and how new insights into these cancers could improve patient outcomes.
  • [MeSH-major] Breast Neoplasms. Prostatic Neoplasms

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  • [CommentIn] Nat Rev Cancer. 2010 Jul;10(7):523 [20574451.001]
  • (PMID = 20147902.001).
  • [ISSN] 1474-1768
  • [Journal-full-title] Nature reviews. Cancer
  • [ISO-abbreviation] Nat. Rev. Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Hormones
  • [Number-of-references] 127
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89. Stopiglia RM, Ferreira U, Silva MM Jr, Matheus WE, Denardi F, Reis LO: Prostate specific antigen decrease and prostate cancer diagnosis: antibiotic versus placebo prospective randomized clinical trial. J Urol; 2010 Mar;183(3):940-4
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  • [Title] Prostate specific antigen decrease and prostate cancer diagnosis: antibiotic versus placebo prospective randomized clinical trial.
  • PURPOSE: Prostate inflammation can lead to an increase in serum prostate specific antigen concentration and confound the use of prostate specific antigen kinetics.
  • Repeat prostate specific antigen measurements after a period of observation or a course of empirical antibiotics are controversial in terms of the optimal approach to reduce the confounding impact on prostate cancer screening.
  • This issue was analyzed in patients with a diagnosis of type IV or asymptomatic prostatitis (National Institutes of Health classification) and high prostate specific antigen.
  • MATERIALS AND METHODS: We studied 200 men between 50 and 75 years old with a high prostate specific antigen (between 2.5 and 10 ng/dl).
  • Of these patients 98 (49%) had a diagnosis of type IV prostatitis.
  • Prostate specific antigen was determined after treatment and all patients underwent transrectal ultrasound guided biopsy of the prostate.
  • RESULTS: In group 1, 29 (59.18%) patients presented with a decrease in prostate specific antigen and 9 (31%) had cancer on biopsy, while in group 2 there were 26 (53.06%) patients with a decrease in prostate specific antigen and 7 (26.9%) with prostate cancer.
  • There was no statistical difference in either group in relation to prostate specific antigen decrease after treatment or the presence of tumor.
  • CONCLUSIONS: A considerable number of patients (49%) were diagnosed with type IV prostatitis and high prostate specific antigen in agreement with the current literature.
  • Of the patients 26.9% to 31% presented with a decrease in prostate specific antigen after the use of antibiotic or placebo and harbor cancer as demonstrated on prostate biopsy.
  • Prostate specific antigen decreases do not indicate the absence of prostate cancer.
  • [MeSH-major] Prostate-Specific Antigen / blood. Prostatic Neoplasms / blood. Prostatic Neoplasms / diagnosis. Prostatitis / blood
  • [MeSH-minor] Aged. Anti-Bacterial Agents / therapeutic use. Diagnosis, Differential. Double-Blind Method. Humans. Male. Middle Aged. Prospective Studies

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  • [Copyright] 2010 American Urological Association Education and Research, Inc. Published by Elsevier Inc. All rights reserved.
  • [CommentIn] J Urol. 2010 Mar;183(3):944-5; discussion 945 [20089278.001]
  • [CommentIn] J Urol. 2010 Nov;184(5):2214-5; author reply 2215 [20864135.001]
  • [CommentIn] J Urol. 2010 Mar;183(3):944; discussion 945 [20089266.001]
  • (PMID = 20089269.001).
  • [ISSN] 1527-3792
  • [Journal-full-title] The Journal of urology
  • [ISO-abbreviation] J. Urol.
  • [Language] eng
  • [Publication-type] Journal Article; Randomized Controlled Trial
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; EC 3.4.21.77 / Prostate-Specific Antigen
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90. Alonzi R, Padhani AR, Maxwell RJ, Taylor NJ, Stirling JJ, Wilson JI, d'Arcy JA, Collins DJ, Saunders MI, Hoskin PJ: Carbogen breathing increases prostate cancer oxygenation: a translational MRI study in murine xenografts and humans. Br J Cancer; 2009 Feb 24;100(4):644-8
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  • [Title] Carbogen breathing increases prostate cancer oxygenation: a translational MRI study in murine xenografts and humans.
  • Hypoxia has been associated with poor local tumour control and relapse in many cancer sites, including carcinoma of the prostate.
  • This translational study tests whether breathing carbogen gas improves the oxygenation of human prostate carcinoma xenografts in mice and in human patients with prostate cancer.
  • A total of 23 DU145 tumour-bearing mice, 17 PC3 tumour-bearing mice and 17 human patients with prostate cancer were investigated.
  • Quantitative R(2)* pixel maps were produced for each tumour and at each time point and changes in R(2)* induced by carbogen were determined.
  • In all, 14 human subjects were evaluable; 64% had reductions in tumour R(2)* during carbogen inhalation with a mean reduction of 21.6% (P=0.0005).
  • Decreases in prostate tumour R(2)* in both animal models and human patients as a result of carbogen inhalation suggests the presence of significant hypoxia.
  • The finding that carbogen gas breathing improves prostate tumour oxygenation provides a rationale for testing the radiosensitising effects of combining carbogen gas breathing with radiotherapy in prostate cancer patients.
  • [MeSH-major] Carbon Dioxide / metabolism. Oxygen / metabolism. Oxygen Inhalation Therapy. Prostatic Neoplasms / metabolism. Prostatic Neoplasms / therapy
  • [MeSH-minor] Aged. Animals. Cell Hypoxia. Cell Line, Tumor. Humans. Magnetic Resonance Imaging. Male. Mice. Middle Aged. Neoplasm Transplantation / diagnostic imaging. Radiography. Transplantation, Heterologous

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  • (PMID = 19190629.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0701945; United Kingdom / Cancer Research UK / / C39/A3987
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 142M471B3J / Carbon Dioxide; 8063-77-2 / carbogen; S88TT14065 / Oxygen
  • [Other-IDs] NLM/ PMC2653742
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91. Hubosky SG, Davis JW, Given RW, Fabrizio MD: Robotically assisted radical laparoscopic prostatectomy in a patient with ectopic ureteral insertion into the prostate. J Robot Surg; 2007;1(1):85-8
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  • [Title] Robotically assisted radical laparoscopic prostatectomy in a patient with ectopic ureteral insertion into the prostate.
  • Robotically assisted laparoscopic radical prostatectomy (RaLRP) has become an alternative surgical treatment option for patients with localized prostate cancer.
  • We describe the first successful completion of RaLRP for localized prostate cancer in a patient with coexisting complete left ureteral duplication and ectopic insertion of the upper pole moiety ureter into the prostatic urethra.
  • After standard radical prostate excision and vesicourethral anastomosis, the unique anatomy in this case required additional reconstructive maneuvers including construction of a Y-type conjoined ureteral anastomosis and ureteroneocystotomy.

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  • (PMID = 25484941.001).
  • [ISSN] 1863-2483
  • [Journal-full-title] Journal of robotic surgery
  • [ISO-abbreviation] J Robot Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC4247429
  • [Keywords] NOTNLM ; Ectopic ureter / Laparoscopy / Prostatectomy / Robotic surgery / Ureteral duplication / Ureteroneocystotomy
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92. Soucek K, Kamaid A, Phung AD, Kubala L, Bulinski JC, Harper RW, Eiserich JP: Normal and prostate cancer cells display distinct molecular profiles of alpha-tubulin posttranslational modifications. Prostate; 2006 Jun 15;66(9):954-65
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  • [Title] Normal and prostate cancer cells display distinct molecular profiles of alpha-tubulin posttranslational modifications.
  • METHODS: Herein, we characterized the molecular profile of alpha-tubulin posttranslational modifications in normal human prostate epithelial cells (PrEC), immortalized normal prostate epithelial cells (PZ-HPV-7), androgen-dependent prostate cancer cells (LNCaP), transitional androgen-independent prostate cancer cells (LNCaP-cds and CWR22Rv1), and androgen-independent prostate cancer cells (PC3).
  • CONCLUSION: These data may reveal novel biomarkers of prostate cancer and new therapeutic targets.
  • [MeSH-major] Prostate / chemistry. Prostatic Neoplasms / chemistry. Protein Processing, Post-Translational. Tubulin / analysis. Tubulin / metabolism
  • [MeSH-minor] Acetylation. Androgens / physiology. Blotting, Western. Cell Line. Cell Line, Tumor. Disease Progression. Electrophoresis, Polyacrylamide Gel. Epithelium / chemistry. Epithelium / metabolism. Epithelium / pathology. Humans. Male. Microscopy, Fluorescence. Peptide Synthases / analysis. Peptide Synthases / metabolism. Polyglutamic Acid / analysis. Receptors, Androgen / analysis. Tyrosine / analysis

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  • [Copyright] Copyright 2006 Wiley-Liss, Inc.
  • (PMID = 16541425.001).
  • [ISSN] 0270-4137
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Receptors, Androgen; 0 / Tubulin; 25513-46-6 / Polyglutamic Acid; 42HK56048U / Tyrosine; EC 6.3.2.- / Peptide Synthases; EC 6.3.2.- / tyrosyltubulin ligase
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93. Aggarwal S, Ricklis RM, Williams SA, Denmeade SR: Comparative study of PSMA expression in the prostate of mouse, dog, monkey, and human. Prostate; 2006 Jun 15;66(9):903-10
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  • [Title] Comparative study of PSMA expression in the prostate of mouse, dog, monkey, and human.
  • Future toxicologic studies of these therapies require identification of animal models that express PSMA within the prostate.
  • RESULTS: No substrate hydrolysis was observed in dog or monkey prostate homogenates.
  • Monkey prostate was negative for PSMA protein expression.
  • No significant PSMA mRNA levels were detected by real time PCR in mouse, dog, or monkey prostate tissue compared to PSMA negative tissues.
  • CONCLUSIONS: PSMA is not expressed in any significant amount in the prostates of mouse, beagle dog, or macaque monkeys in this study but is expressed in high levels by human prostate.
  • These non-human species, therefore, are not suitable toxicologic models to assess prostate damage from PSMA-activated intraprostatic prodrug/protoxin therapies.
  • [MeSH-major] Antigens, Surface / analysis. Antigens, Surface / genetics. Gene Expression Regulation, Enzymologic / physiology. Glutamate Carboxypeptidase II / analysis. Glutamate Carboxypeptidase II / genetics. Prostate / chemistry

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  • [Copyright] Copyright 2006 Wiley-Liss, Inc.
  • (PMID = 16496413.001).
  • [ISSN] 0270-4137
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Surface; 0 / RNA, Messenger; EC 3.4.17.21 / Glutamate Carboxypeptidase II; EC 3.4.17.21 / glutamate carboxypeptidase II, human
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94. Danforth KN, Hayes RB, Rodriguez C, Yu K, Sakoda LC, Huang WY, Chen BE, Chen J, Andriole GL, Calle EE, Jacobs EJ, Chu LW, Figueroa JD, Yeager M, Platz EA, Michaud DS, Chanock SJ, Thun MJ, Hsing AW: Polymorphic variants in PTGS2 and prostate cancer risk: results from two large nested case-control studies. Carcinogenesis; 2008 Mar;29(3):568-72
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  • [Title] Polymorphic variants in PTGS2 and prostate cancer risk: results from two large nested case-control studies.
  • Chronic inflammation has been hypothesized to increase