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1. Walz J, Chun FK, Klein EA, Reuther A, Saad F, Graefen M, Huland H, Karakiewicz PI: Nomogram predicting the probability of early recurrence after radical prostatectomy for prostate cancer. J Urol; 2009 Feb;181(2):601-7; discussion 607-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Nomogram predicting the probability of early recurrence after radical prostatectomy for prostate cancer.
  • PURPOSE: We developed a nomogram predicting the probability of early biochemical recurrence after radical prostatectomy because early recurrence predisposes to distant metastasis and prostate cancer related mortality.
  • MATERIALS AND METHODS: From January 1992 to December 2005, 2,911 patients underwent radical prostatectomy for localized prostate cancer.
  • Age, prostate specific antigen, pathological Gleason sum, surgical margin, extracapsular extension, seminal vesicle invasion and lymph node invasion were considered.
  • [MeSH-major] Neoplasm Recurrence, Local / pathology. Nomograms. Prostatectomy / methods. Prostatic Neoplasms / pathology. Prostatic Neoplasms / surgery
  • [MeSH-minor] Age Factors. Aged. Aged, 80 and over. Biopsy, Needle. Cohort Studies. Humans. Immunohistochemistry. Kaplan-Meier Estimate. Male. Middle Aged. Neoplasm Staging. Predictive Value of Tests. Probability. Prognosis. Proportional Hazards Models. Retrospective Studies. Risk Assessment. Sensitivity and Specificity. Survival Analysis. Time Factors

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  • [CommentIn] Eur Urol. 2009 Nov;56(5):885-6 [20965035.001]
  • (PMID = 19084864.001).
  • [ISSN] 1527-3792
  • [Journal-full-title] The Journal of urology
  • [ISO-abbreviation] J. Urol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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2. Bolla M, Artignan X, Fourneret P, Brochon D, Ringeisen F, Descotes JL: [Neoadjuvant hormonal treatment combined with external irradiation in the management of prostate cancer]. Bull Cancer; 2006 Nov;93(11):1101-5
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  • [Title] [Neoadjuvant hormonal treatment combined with external irradiation in the management of prostate cancer].
  • [Transliterated title] L'association hormonothérapie néoadjuvante et irradiation externe dans les cancers de la prostate.
  • Very high risk prostate cancers, T3-4 N0 M0 or pelvic lymph node involvement (c or pN1) whatever the UICC T stage, need a long term androgen suppression of 3 years or more.
  • [MeSH-major] Antineoplastic Agents, Hormonal / therapeutic use. Neoadjuvant Therapy / methods. Neoplasms, Hormone-Dependent / drug therapy. Neoplasms, Hormone-Dependent / radiotherapy. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / radiotherapy

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  • (PMID = 17145579.001).
  • [ISSN] 1769-6917
  • [Journal-full-title] Bulletin du cancer
  • [ISO-abbreviation] Bull Cancer
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Antineoplastic Agents, Hormonal
  • [Number-of-references] 23
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3. Elabbady AA, Khedr MM: Free/total PSA ratio can help in the prediction of high gleason score prostate cancer in men with total serum prostate specific antigen (PSA) of 3-10 ng/ml. Int Urol Nephrol; 2006;38(3-4):553-7
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  • [Title] Free/total PSA ratio can help in the prediction of high gleason score prostate cancer in men with total serum prostate specific antigen (PSA) of 3-10 ng/ml.
  • PURPOSE: We evaluate the use of free/total prostate specific antigen (PSA) ratio in improving the prediction of cancers of higher Gleason scores.
  • The mean age for the 62 patients with histologically proven prostate cancer was 62.3+/-5.5 years (49-73).
  • In the 20 patients with free PSA ratio>20%, 1 patient (5%), had prostate cancer of high Gleason score and the remaining 19 (95%) patients had low Gleason scores.
  • CONCLUSIONS: In this study, men with prostate cancer and lower F/T PSA ratio were at a higher risk of having higher Gleason scores (7-10) and those with higher F/T PSA ratio were more likely to have lower Gleason scores.
  • [MeSH-major] Prostate-Specific Antigen / blood. Prostatic Neoplasms / blood. Prostatic Neoplasms / pathology


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4. Grainger EM, Schwartz SJ, Wang S, Unlu NZ, Boileau TW, Ferketich AK, Monk JP, Gong MC, Bahnson RR, DeGroff VL, Clinton SK: A combination of tomato and soy products for men with recurring prostate cancer and rising prostate specific antigen. Nutr Cancer; 2008;60(2):145-54
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  • [Title] A combination of tomato and soy products for men with recurring prostate cancer and rising prostate specific antigen.
  • Tomato and soy products are hypothesized to reduce the risk of prostate cancer or enhance efficacy of therapy.
  • A study was completed to determine if men with active prostate cancer will adhere to a dietary intervention rich in tomato products and a soy protein supplement men (n = 41) with recurrent, asymptomatic prostate cancer were randomized among 2 groups: Group A (n = 20) consumed tomato products (no soy) for Weeks 0 through 4, targeting a minimum of 25 mg of lycopene/day.
  • Serum prostate-specific antigen decreased between Weeks 0 and 8 for 14 / 41 men (34%).
  • In conclusion, prostate cancer patients will consume diets rich in tomato products and soy with excellent compliance and bioavailability of phytochemicals.
  • Further studies combining tomato and soy foods to determine efficacy for prostate cancer prevention or management are encouraged.
  • [MeSH-major] Carotenoids / therapeutic use. Neoplasm Recurrence, Local / prevention & control. Prostate-Specific Antigen / blood. Prostate-Specific Antigen / drug effects. Prostatic Neoplasms / blood. Prostatic Neoplasms / drug therapy. Soybean Proteins / therapeutic use
  • [MeSH-minor] Administration, Oral. Aged. Antineoplastic Agents / administration & dosage. Antineoplastic Agents / therapeutic use. Biological Availability. Biomarkers, Tumor / blood. Cross-Over Studies. Dietary Supplements. Disease Progression. Drug Therapy, Combination. Humans. Lycopersicon esculentum / chemistry. Male. Patient Compliance. Soybeans / chemistry. Treatment Outcome

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  • (PMID = 18444145.001).
  • [ISSN] 0163-5581
  • [Journal-full-title] Nutrition and cancer
  • [ISO-abbreviation] Nutr Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016058; United States / NCI NIH HHS / CA / R01 CA112632
  • [Publication-type] Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / Soybean Proteins; 36-88-4 / Carotenoids; EC 3.4.21.77 / Prostate-Specific Antigen; SB0N2N0WV6 / lycopene
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5. Ryan CJ, Harzstark AH, Rosenberg J, Lin A, Claros C, Goldfine ID, Kerner JF, Small EJ, Youngren JF: A pilot dose-escalation study of the effects of nordihydroguareacetic acid on hormone and prostate specific antigen levels in patients with relapsed prostate cancer. BJU Int; 2008 Feb;101(4):436-9
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  • [Title] A pilot dose-escalation study of the effects of nordihydroguareacetic acid on hormone and prostate specific antigen levels in patients with relapsed prostate cancer.
  • OBJECTIVE: To assess the tolerability of the effects of nordihydroguareacetic acid (NDGA) and its effect on prostate-specific antigen (PSA) kinetics in patients with relapsed prostate cancer, as among the many biological effects of NDGA is the inhibition of the insulin-like growth factor 1 receptor (IGF-1R) tyrosine kinase.
  • PATIENTS AND METHODS: Eligible patients were those with an increasing PSA level after definitive local therapy, in either the non-castrate (androgen-dependent prostate cancer, ADPC) or the castrate state (castration-resistant prostate cancer, CRPC) with no evidence of metastatic disease by bone scan or computed tomography of the abdomen or pelvis.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Masoprocol / therapeutic use. Neoplasm Recurrence, Local / drug therapy. Prostate-Specific Antigen / drug effects. Prostatic Neoplasms / drug therapy


6. Odedina FT, Kumar N: Prostate cancer disparities in Black men of African descent: a comparative literature review of prostate cancer burden among Black men in the United States, Caribbean, United Kingdom, and West Africa. Infect Agent Cancer; 2009 Feb 10;4 Suppl 1:S2
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  • [Title] Prostate cancer disparities in Black men of African descent: a comparative literature review of prostate cancer burden among Black men in the United States, Caribbean, United Kingdom, and West Africa.
  • BACKGROUND: African American men have the highest prostate cancer morbidity and mortality rates than any other racial or ethnic group in the US.
  • Although the overall incidence of and mortality from prostate cancer has been declining in White men since 1991, the decline in African American men lags behind White men.
  • Of particular concern is the growing literature on the disproportionate burden of prostate cancer among other Black men of West African ancestry in the Caribbean Islands, United Kingdom and West Africa.
  • This higher incidence of prostate cancer observed in populations of African descent may be attributed to the fact that these populations share ancestral genetic factors.
  • To better understand the burden of prostate cancer among men of West African Ancestry, we conducted a review of the literature on prostate cancer incidence, prevalence, and mortality in the countries connected by the Transatlantic Slave Trade.
  • RESULTS: Several published studies indicate high prostate cancer burden in Nigeria and Ghana.
  • Prostate cancer morbidity and/or mortality data from the Caribbean Islands and the United Kingdom also provided comparable or worse prostate cancer burden to that of US Blacks.
  • CONCLUSION: The growing literature on the disproportionate burden of prostate cancer among other Black men of West African ancestry follows the path of the Transatlantic Slave Trade.
  • To better understand and address the global prostate cancer disparities seen in Black men of West African ancestry, future studies should explore the genetic and environmental risk factors for prostate cancer among this group.

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  • (PMID = 19208207.001).
  • [ISSN] 1750-9378
  • [Journal-full-title] Infectious agents and cancer
  • [ISO-abbreviation] Infect. Agents Cancer
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / G12 RR003020
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2638461
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7. Kilbridge KL, Fraser G, Krahn M, Nelson EM, Conaway M, Bashore R, Wolf A, Barry MJ, Gong DA, Nease RF Jr, Connors AF: Lack of comprehension of common prostate cancer terms in an underserved population. J Clin Oncol; 2009 Apr 20;27(12):2015-21
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  • [Title] Lack of comprehension of common prostate cancer terms in an underserved population.
  • PURPOSE: To assess the comprehension of common medical terms used in prostate cancer in patient education materials to obtain informed consent, and to measure outcomes after prostate cancer treatment.
  • PATIENTS AND METHODS: We reviewed patient education materials and prostate-specific quality-of-life instruments to identify technical terms describing sexual, urinary, and bowel function.
  • Prostate cancer knowledge was poor.
  • CONCLUSION: Limited comprehension of prostate cancer terms and low literacy create barriers to obtaining informed consent for treatment and to measuring prostate cancer outcomes accurately in our study population.
  • In addition, the level of prostate cancer knowledge was poor.
  • These results highlight the need for prostate cancer education efforts and outcomes measurements that consider literacy and use nonmedical language.

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  • (PMID = 19307512.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / K07 CA085754; United States / NCI NIH HHS / CA / KO7CA085754
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2669763
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8. Pruthi RS, Swords K, Schultz H, Carson CC 3rd, Wallen EM: The impact of obesity on the diagnosis of prostate cancer using a modern extended biopsy scheme. J Urol; 2009 Feb;181(2):574-7; discussion 578
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The impact of obesity on the diagnosis of prostate cancer using a modern extended biopsy scheme.
  • PURPOSE: The effect of obesity on prostate cancer detection and behavior remains uncertain.
  • MATERIALS AND METHODS: We retrospectively reviewed the records of a consecutive series of 500 men who underwent transrectal ultrasound guided prostate biopsy using a 10 to 12 core biopsy scheme.
  • Variables, including patient age, prostate specific antigen, prostate specific antigen density, digital rectal examination findings, transrectal ultrasound prostate volume and biopsy outcome, including grade, were compared to anthropometric measures, including body mass index.
  • Obese men were younger (62.0 vs 63.8 years), had a larger prostate (57.7 vs 47.8 cc) and were less likely to have any abnormality on digital rectal examination (19.6% vs 30.8%).
  • On statistical modeling for the OR in nonobese vs obese men there was a trend toward lower detection based on crude and age adjusted ORs but not on multivariate OR controlling for age, prostate specific antigen and prostate volume.
  • In men with negative biopsies those who were obese vs nonobese had a larger prostate volume and trended toward a higher median prostate specific antigen and age.
  • CONCLUSIONS: Of men undergoing prostate biopsy using a modern extended biopsy scheme obese men were younger, had a larger prostate and were less likely to have abnormal digital rectal examinations.
  • Although some trends toward a lower detection rate in obese men were observed, such differences were not observed on multivariate analysis, nor were any differences observed in the incidence of higher grade tumors, thus questioning the effect of obesity on prostate cancer detection and behavior in our cases series.
  • [MeSH-major] Biopsy, Needle / methods. Obesity / complications. Prostatic Neoplasms / pathology. Ultrasound, High-Intensity Focused, Transrectal
  • [MeSH-minor] Age Factors. Aged. Analysis of Variance. Body Mass Index. Case-Control Studies. Humans. Immunohistochemistry. Logistic Models. Male. Middle Aged. Neoplasm Staging. Odds Ratio. Prostate-Specific Antigen / blood. Reference Values. Retrospective Studies. Risk Assessment. Sensitivity and Specificity. Tumor Burden


9. Loblaw DA, Cheung P: External beam irradiation for localized prostate cancer--the promise of hypofractionation. Can J Urol; 2006 Feb;13 Suppl 1:62-6
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  • [Title] External beam irradiation for localized prostate cancer--the promise of hypofractionation.
  • Within the field of radiation oncology in the last 10 years, there have been two major thematic advances in the understanding and treatment of prostate cancer.
  • The second important discovery was that prostate cancer reacts differently than other tumors to radiation whereby higher doses of radiation per day ("hypofractionated radiation") seem to be more effective in killing prostate cancer cells.
  • The early experience of two hypofractionated trials in intermediate- and high-risk prostate cancer where the equivalent of > 80 Gy (in 2 Gy per day fractions) delivered in 5-6 weeks is reported.
  • In summary, hypofractionated radiation coupled with high-precision techniques may allow for better prostate cancer control rates, shorter treatment times and less toxicity.
  • [MeSH-major] Dose Fractionation. Prostatic Neoplasms / radiotherapy

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  • (PMID = 16526985.001).
  • [ISSN] 1195-9479
  • [Journal-full-title] The Canadian journal of urology
  • [ISO-abbreviation] Can J Urol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Canada
  • [Number-of-references] 11
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10. Cha TL, Qiu L, Chen CT, Wen Y, Hung MC: Emodin down-regulates androgen receptor and inhibits prostate cancer cell growth. Cancer Res; 2005 Mar 15;65(6):2287-95
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  • [Title] Emodin down-regulates androgen receptor and inhibits prostate cancer cell growth.
  • Hormone-refractory relapse is an inevitable and lethal event for advanced prostate cancer patients after hormone deprivation.
  • A growing body of evidence indicates that hormone deprivation may promote this aggressive prostate cancer phenotype.
  • Notably, androgen receptor (AR) not only mediates the effect of androgen on the tumor initiation but also plays the major role in the relapse transition.
  • This provides a strong rationale for searching new effective agents targeting the down-regulation of AR to treat or prevent advanced prostate cancer progression.
  • Here, we show that emodin, a natural compound, can directly target AR to suppress prostate cancer cell growth in vitro and prolong the survival of C3(1)/SV40 transgenic mice in vivo.
  • Our work indicates a new mechanism for the emodin-mediated anticancer effect and justifies further investigation of emodin as a therapeutic and preventive agent for prostate cancer.
  • [MeSH-major] Androgen Receptor Antagonists. Emodin / pharmacology. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / pathology. Receptors, Androgen / metabolism
  • [MeSH-minor] Animals. COS Cells. Cell Growth Processes / drug effects. Cell Line, Tumor. Cell Nucleus / metabolism. Cercopithecus aethiops. Down-Regulation / drug effects. Gene Expression Regulation, Neoplastic / drug effects. HSP90 Heat-Shock Proteins / metabolism. Humans. Male. Mice. Mice, Transgenic. Nuclear Proteins / metabolism. Proto-Oncogene Proteins / metabolism. Proto-Oncogene Proteins c-mdm2. Transcriptional Activation / drug effects. Transfection. Ubiquitin / metabolism. Xenograft Model Antitumor Assays

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  • (PMID = 15781642.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01 CA099031; United States / NCI NIH HHS / CA / R01 CA109311
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgen Receptor Antagonists; 0 / HSP90 Heat-Shock Proteins; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins; 0 / Receptors, Androgen; 0 / Ubiquitin; EC 6.3.2.19 / MDM2 protein, human; EC 6.3.2.19 / Mdm2 protein, mouse; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2; KA46RNI6HN / Emodin
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11. Seitz M, Schlenker B, Gratzke C, Weidlich P, Stief CG, Reich O: [Standards for the punch biopsy of the prostate]. MMW Fortschr Med; 2007 Jan 25;149(4):35-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Standards for the punch biopsy of the prostate].
  • If, within the framework of screening examinations for the early detection of cancer of the prostate, the patient wishes a PSA test, the physician should accommodate him, but only after providing comprehensive information about the possible consequences and complications.
  • If a certain threshold value is exceeded, a punch biopsy of the prostate is recommended.
  • This procedure must be performed in accordance with accepted standards to enable, within the diagnostic chain, the reliable detection of a carcinoma of the prostate
  • [MeSH-major] Biomarkers, Tumor / blood. Patient Education as Topic. Prostate / pathology. Prostate-Specific Antigen / blood. Prostatic Neoplasms / diagnosis
  • [MeSH-minor] Biopsy, Needle. Early Diagnosis. Germany. Humans. Informed Consent. Male. Mass Screening. Postoperative Complications / etiology. Practice Guidelines as Topic


12. Newmark HL, Heaney RP: Dairy products and prostate cancer risk. Nutr Cancer; 2010;62(3):297-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dairy products and prostate cancer risk.
  • Increased calcium intake from dairy products has been suggested as a risk factor for prostate cancer.
  • Several epidemiologic correlations have indicated an increased risk of prostate cancer with long-term, high intake of dairy products in male U.S. physicians and males in Sweden.
  • We propose, however, that the high dietary phosphate of dairy products affects much larger fluctuation in serum phosphate and may be a more likely source of prostate cancer risk from high dietary intake of dairy products.
  • [MeSH-major] Dairy Products / adverse effects. Prostatic Neoplasms / etiology

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  • (PMID = 20358466.001).
  • [ISSN] 1532-7914
  • [Journal-full-title] Nutrition and cancer
  • [ISO-abbreviation] Nutr Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Calcium, Dietary; 0 / Phosphates; SY7Q814VUP / Calcium
  • [Number-of-references] 14
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13. Merrick GS, Butler WM, Wallner KE, Galbreath RW, Adamovich E: Monotherapeutic brachytherapy for clinically organ-confined prostate cancer. W V Med J; 2005 Jul-Aug;101(4):168-71
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  • [Title] Monotherapeutic brachytherapy for clinically organ-confined prostate cancer.
  • Since the mid-1980s, permanent prostate brachytherapy has been utilized increasingly as a potentially curative treatment for patients of all ages with clinically localized prostate cancer To determine the 8-year biochemical progression-free survival rate for patients who had undergone monotherapeutic brachytherapy for clinically organ-confined prostate cancer, we conducted a study of 202 patients at Schiffler Cancer Center at Wheeling Hospital in Wheeling, W.Va.
  • These patients had undergone brachytherapy without supplemental external beam radiation therapy or androgen deprivation therapy for clinical T1b-T2c NxM0 (2002 AJCC) prostate cancer from April 1995 through May 2001.
  • Clinical, treatment and dosimetric parameters evaluated for biochemical progression-free survival included patient age, clinical T-stage, Gleason score, pretreatment PSA, risk group, percent positive biopsies, isotope, prostate volume, brachytherapy planning volume, V100/150/200, D90, tobacco status, hypertension and diabetes.
  • [MeSH-major] Brachytherapy / methods. Prostatic Neoplasms / pathology. Prostatic Neoplasms / radiotherapy. Radiotherapy Planning, Computer-Assisted
  • [MeSH-minor] Aged. Analysis of Variance. Cohort Studies. Dose-Response Relationship, Radiation. Follow-Up Studies. Humans. Male. Middle Aged. Multivariate Analysis. Neoplasm Staging. Proportional Hazards Models. Prostate-Specific Antigen / blood. Radiotherapy Dosage. Retrospective Studies. Risk Assessment. Survival Analysis. Treatment Outcome


14. Perner S, Schmidt FH, Hofer MD, Kuefer R, Rubin M: [TMPRSS2-ETS gene fusion in prostate cancer]. Urologe A; 2007 Jul;46(7):754-60
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  • [Title] [TMPRSS2-ETS gene fusion in prostate cancer].
  • By analogy, fusion status in prostate cancer may determine clinical outcome and secondary genetic alterations as witnessed in Ewing's tumors.
  • MATERIAL: These novel gene fusions occur in the majority of prostate cancers identified by PSA screening and are the driving mechanism for overexpression of the three members of the ETS transcription factor family, either ERG (21q22.3), ETV1 (7p21.2), or ETV4 (17q21).
  • Considering the high incidence of prostate cancer and the high frequency of this gene fusion, the TMPRSS2-ETS gene fusion is the most common genetic aberration so far described in human malignancies.
  • Also similar to the Philadelphia chromosome in chronic myelogenous leukemia (CML), the gene fusion in prostate cancer has potential as an important candidate for the development of targeted therapy.
  • [MeSH-major] Biomarkers, Tumor / genetics. Neoplasm Proteins / genetics. Oncogene Fusion / genetics. Prostatic Neoplasms / epidemiology. Prostatic Neoplasms / genetics. Proto-Oncogene Proteins c-ets / genetics. Serine Endopeptidases / genetics

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  • (PMID = 17458530.001).
  • [ISSN] 0340-2592
  • [Journal-full-title] Der Urologe. Ausg. A
  • [ISO-abbreviation] Urologe A
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article; Meta-Analysis; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins; 0 / Proto-Oncogene Proteins c-ets; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.- / TMPRSS2 protein, human
  • [Number-of-references] 24
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15. Lawson DA, Xin L, Lukacs R, Xu Q, Cheng D, Witte ON: Prostate stem cells and prostate cancer. Cold Spring Harb Symp Quant Biol; 2005;70:187-96
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  • [Title] Prostate stem cells and prostate cancer.
  • Understanding prostate stem cells (PSCs) may provide insight for the design of therapeutics for prostate cancer.
  • We have developed a quantitative in vivo colony-forming assay and have demonstrated that the Sca-1 antigen is present on the surface of a prostate cell subpopulation that possesses multiple stem cell properties.
  • Immunofluorescent analysis demonstrates that Sca-1 is expressed by both basal and luminal cells in the proximal region of the adult prostate, but is not expressed by either lineage in more distal regions.
  • Sca-1 is also expressed by nearly all cells within fetal prostate epithelial chords, suggesting Sca-1 may be conserved on PSCs throughout development.
  • Malignant epithelial cells from TRAMP mice, as well as normal prostate cells with lentiviral-mediated alteration of the PTEN/AKT signaling pathway, give rise to PIN lesions and prostate cancer in vivo.
  • Alteration of PTEN/AKT signaling in Sca-1-enriched PSCs also results in PIN lesions, suggesting that PSCs can serve as one target for prostate carcinogenesis.
  • [MeSH-major] Neoplastic Stem Cells / pathology. Prostate / cytology. Prostatic Neoplasms / pathology. Stem Cells / cytology
  • [MeSH-minor] Animals. Antigens, Ly / metabolism. Colony-Forming Units Assay. Male. Membrane Proteins / metabolism. Mice. Mice, Inbred C57BL. Mice, Transgenic. Models, Biological. PTEN Phosphohydrolase / metabolism. Proto-Oncogene Proteins c-akt / metabolism. Signal Transduction. Transforming Growth Factor beta / metabolism. Tumor Stem Cell Assay

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  • (PMID = 16869753.001).
  • [ISSN] 0091-7451
  • [Journal-full-title] Cold Spring Harbor symposia on quantitative biology
  • [ISO-abbreviation] Cold Spring Harb. Symp. Quant. Biol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / T32 CA09056
  • [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 / Antigens, Ly; 0 / Ly6a protein, mouse; 0 / Membrane Proteins; 0 / Transforming Growth Factor beta; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.1.3.48 / Pten protein, mouse; EC 3.1.3.67 / PTEN Phosphohydrolase
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16. Davidson DD, Koch MO, Lin H, Jones TD, Biermann K, Cheng L: Does the size matter?: Prostate weight does not predict PSA recurrence after radical prostatectomy. Am J Clin Pathol; 2010 Apr;133(4):662-8
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  • [Title] Does the size matter?: Prostate weight does not predict PSA recurrence after radical prostatectomy.
  • Previous studies suggest that low prostate weight is a significant negative prognostic factor for prostate cancer.
  • In the current study, the data for 431 men who underwent radical retropubic prostatectomy between 1990 and 1998 were analyzed for association between prostate weight and various clinical and pathologic parameters.
  • These included age, preoperative prostate-specific antigen (PSA) level, PSA recurrence, pathologic stage, Gleason grade, extraprostatic extension, positive surgical margins, tumor volume, associated high-grade prostatic intraepithelial neoplasia, perineural invasion, and lymph node metastasis.
  • A significant positive correlation was found between prostate weight and increasing patient age or increasing preoperative PSA level.
  • There was no significant independent association between prostate weight and any of the other variables examined.
  • No association was found between prostate weight and PSA recurrence.
  • Although increasing prostate weight correlates with increased patient age and higher preoperative PSA level, it does not independently predict postoperative cancer recurrence.
  • [MeSH-major] Prostate / pathology. Prostate-Specific Antigen / blood. Prostatic Neoplasms / pathology
  • [MeSH-minor] Aged. Humans. Male. Middle Aged. Neoplasm Recurrence, Local / pathology. Neoplasm Staging. Organ Size. Postoperative Period. Prognosis. Prostatectomy. Regression Analysis. Treatment Outcome


17. Finne P, Fallah M, Hakama M, Ciatto S, Hugosson J, de Koning H, Moss S, Nelen V, Auvinen A: Lead-time in the European Randomised Study of Screening for Prostate Cancer. Eur J Cancer; 2010 Nov;46(17):3102-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Lead-time in the European Randomised Study of Screening for Prostate Cancer.
  • BACKGROUND: Lead-time is defined as the time by which screening advances the diagnosis compared with absence of screening.
  • MATERIAL AND METHODS: In the first screening round, a total of 56,294 men aged 55-74 years were screened with serum prostate specific antigen (PSA) in five countries of the European Randomised Study of Screening for Prostate Cancer (ERSPC) with an overall detection rate (prevalence) of 2.8% (1972 prostate cancers).
  • Prostate cancer incidence among 92,142 men randomly allocated to the control arm of the trial was also assessed.
  • Lead-time was estimated as the time required to accumulate a similar cumulative risk of prostate cancer in the control arm to the detection rate in the intervention arm, i.e. from the ratio of detection rate (prevalence of screen-detected cases) and expected incidence (cumulative risk).
  • Lead-time based on advanced prostate cancer only was slightly shorter, mean 5.3 years (95% CI 4.6-6.0).
  • CONCLUSION: The lead-time for prostate cancer found in ERSPC substantially exceeded that found for breast, cervical and colorectal cancer screening.
  • One round of prostate cancer screening can advance clinical diagnosis by 4-8 years.
  • [MeSH-major] Prostatic Neoplasms / diagnosis
  • [MeSH-minor] Aged. Clinical Protocols. Early Detection of Cancer / methods. Europe / epidemiology. Humans. Incidence. Male. Middle Aged. Prostate-Specific Antigen / blood. Risk Assessment. Time Factors

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  • [Copyright] Copyright © 2010. Published by Elsevier Ltd.
  • (PMID = 21047593.001).
  • [ISSN] 1879-0852
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 3.4.21.77 / Prostate-Specific Antigen
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18. Butler LM, Wang R, Wong AS, Koh WP, Yu MC: Cigarette smoking and risk of prostate cancer among Singapore Chinese. Cancer Causes Control; 2009 Dec;20(10):1967-74
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cigarette smoking and risk of prostate cancer among Singapore Chinese.
  • Prospective epidemiologic studies conducted in Western populations support an association between current smoking and aggressive subtypes of prostate cancer.
  • In Singapore, where prostate-specific antigen is not used for population-wide screening, prostate cancer incidence has tripled within the past two decades.
  • Using Cox regression methods, we examined the relationship between smoking and prostate cancer established between 1993 and 1998 in a cohort of 27,293 Singapore Chinese men.
  • As of December 2006, 250 incident prostate cancer cases were diagnosed.
  • Smoking was not a major risk factor for prostate cancer in our Singapore Chinese cohort, a traditionally low risk population with parallel increases in incidence and mortality.
  • [MeSH-major] Asian Continental Ancestry Group / ethnology. Carcinoma / etiology. Prostatic Neoplasms / etiology. Smoking / adverse effects

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  • (PMID = 19579052.001).
  • [ISSN] 1573-7225
  • [Journal-full-title] Cancer causes & control : CCC
  • [ISO-abbreviation] Cancer Causes Control
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA55069; United States / NCI NIH HHS / CA / R35 CA53890
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Netherlands
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19. Fowler JF: The radiobiology of prostate cancer including new aspects of fractionated radiotherapy. Acta Oncol; 2005;44(3):265-76
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The radiobiology of prostate cancer including new aspects of fractionated radiotherapy.
  • These differences work the opposite way round for prostate tumors versus late complications compared with most other types of tumor.
  • Using the Linear-Quadratic formula it is aimed to explain these differences, especially for treatments of prostate cancer.
  • The unusually slow growth rate of prostate cancers is associated with their high sensitivity to increased fraction size, so a large number of small fractions, such as 35 or 40 "daily" doses of 2 Gy, is not an optimum treatment.
  • Theoretical modeling shows a stronger enhancement of tumor effect than of late complications for larger (and fewer) fractions, in prostate tumors uniquely.
  • Biologically Effective Doses and Normalized Total Doses (in 2 Gy fraction equivalents) are given for prostate tumor, late rectal reactions, and--a new development--acute rectal mucosa.
  • Tables showing the change of fraction-size sensitivity (the alpha/beta ratio) with proliferation rates of tissues lead to the association of slow cell doubling times in prostate tumors with small alpha/beta ratios.
  • The alpha/beta ratios of prostate tumors appear to be as low as 1.5 Gy (95% confidence interval 1.3-1.8 Gy), in contrast with the value of about 10 Gy for most other types of tumor.
  • From this important difference stems the superior schedules of, for example, 20 fractions of 3 Gy, or 10 fractions of 4.7 Gy, or 5 fractions of 7 Gy, which can all give tumor results equivalent to 80-90 Gy in 2 Gy fractions, while keeping late complications equivalent to only 72 Gy in 2 Gy fractions.
  • Combination treatments of external beam (EBRT) and brachytherapy boost doses (25F x 2 Gy plus 2 x 10 Gy) can give higher biological tumor effects than any EBRT using daily 2 Gy doses, and with acceptable late complications.
  • Monotherapy by brachytherapy for low-risk cancer prostate using two to four fractions in a few days can give even higher biological effects on the tumors.
  • [MeSH-major] Dose Fractionation. Prostatic Neoplasms / radiotherapy

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  • (PMID = 16076699.001).
  • [ISSN] 0284-186X
  • [Journal-full-title] Acta oncologica (Stockholm, Sweden)
  • [ISO-abbreviation] Acta Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Norway
  • [Number-of-references] 31
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20. Surapaneni KM, Venkata GR: Lipid peroxidation and antioxidant status in patients with carcinoma of prostate. Indian J Physiol Pharmacol; 2006 Oct-Dec;50(4):350-4
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  • [Title] Lipid peroxidation and antioxidant status in patients with carcinoma of prostate.
  • Prostate cancer is the most prevalent cancer found in men above the age of fifty years and is frequently diagnosed in men between 45 and 89 years of age with a median age of 72 years.
  • This work was undertaken to assess oxidative stress and anti oxidant status in patients with carcinoma of prostate.
  • Glutathione (GSH), Malondialdehyde (MDA), Super Oxide Dismutase (SOD) levels in Erythrocytes and plasma Glutathione-S-Transferase (GST) levels were estimated in patients with carcinoma of prostate and compared to controls.
  • It was observed that Erythrocyte GSH levels were significantly lower and Erythrocyte MDA & SOD levels were significantly higher in patients with carcinoma of prostate compared to controls.
  • Oxidative stress may be involved in prostate cancer as evidenced by the higher MDA levels and lower GSH levels.
  • [MeSH-major] Antioxidants / metabolism. Lipid Peroxidation / physiology. Prostatic Neoplasms / metabolism

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  • (PMID = 17402264.001).
  • [ISSN] 0019-5499
  • [Journal-full-title] Indian journal of physiology and pharmacology
  • [ISO-abbreviation] Indian J. Physiol. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Chemical-registry-number] 0 / Antioxidants; 0 / Thiobarbituric Acid Reactive Substances; 4Y8F71G49Q / Malondialdehyde; EC 1.15.1.1 / Superoxide Dismutase; EC 2.5.1.18 / Glutathione Transferase; GAN16C9B8O / Glutathione
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21. Lowe JF, Frazee LA: Update on prostate cancer chemoprevention. Pharmacotherapy; 2006 Mar;26(3):353-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Update on prostate cancer chemoprevention.
  • BACKGROUND: Prostate cancer is the most common type of cancer and the second leading cause of cancer-related deaths in American men.
  • Its high rate of occurrence and long lead time to clinically significant disease make prostate cancer an ideal disease for pharmacologic or nutritional chemoprevention.
  • METHODS: To identify the various chemoprevention strategies for prostate cancer, a MEDLINE search (from 1967-2005) and bibliographic search of the English-language literature were conducted.
  • RESULTS: Epidemiologic and retrospective studies have assessed the effect of carotenoids (e.g., lycopene), vitamins, selenium, and nonsteroidal antiinflammatory drugs (NSAIDs) on the rate of occurrence of prostate cancer.
  • The few published prospective trials evaluated prostate cancer as a secondary end point.
  • Lycopene (as beta-carotene) and selenium supplementation have been associated with a reduced risk of prostate cancer in nested case-control studies, but only in subgroups of men with low baseline plasma lycopene (or beta-carotene) and selenium levels respectively.
  • The Prostate Cancer Prevention Trial prospectively evaluated finasteride, a 5-alpha-reductase inhibitor, as chemoprevention.
  • The results showed a 25% relative risk reduction in prostate cancer, albeit at an increased risk of invasive tumors.
  • CONCLUSION: Data regarding lycopene, vitamin E, and selenium as chemoprevention for prostate cancer appear promising.
  • Prospective trials such as the Selenium and Vitamin E Cancer Prevention Trial (SELECT) will clarify the role of these agents in prostate cancer prevention.
  • Although finasteride has decreased overall prostate cancer occurrence, the risk of invasive tumors may outweigh the benefit of this agent.
  • The continuing Reduction by Dutasteride of Prostate Cancer Events (REDUCE) trial may help define a role for the 5-alpha-reductase inhibitors in cancer chemoprevention.
  • At this time, nothing has been proven effective as chemoprevention against clinically significant prostate cancer.
  • [MeSH-major] Prostatic Neoplasms / prevention & control

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  • [CommentIn] Pharmacotherapy. 2006 Oct;26(10):1533; author reply 1533 [16999665.001]
  • (PMID = 16503715.001).
  • [ISSN] 0277-0008
  • [Journal-full-title] Pharmacotherapy
  • [ISO-abbreviation] Pharmacotherapy
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 5-alpha Reductase Inhibitors; 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Azasteroids; 0 / Enzyme Inhibitors; 0 / Vitamins; 1406-18-4 / Vitamin E; 36-88-4 / Carotenoids; 57GNO57U7G / Finasteride; H6241UJ22B / Selenium; O0J6XJN02I / Dutasteride
  • [Number-of-references] 48
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22. Ishkanian AS, Zafarana G, Thoms J, Bristow RG: Array CGH as a potential predictor of radiocurability in intermediate risk prostate cancer. Acta Oncol; 2010 Oct;49(7):888-94
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Array CGH as a potential predictor of radiocurability in intermediate risk prostate cancer.
  • Prostate cancer is the most common male cancer and up to one fifth of diagnosed patients will die of their disease.
  • Current prognostic variables including T-category (of the TNM staging), the absolute or kinetics of prostatic specific antigen (PSA) and the pathologic Gleason score (GS) are utilized to place men in low, intermediate and high-risk prostate cancer risk groupings.
  • Somatic alterations in prostate cancer.
  • Herein, we review the potential for somatic alterations in tumor-associated genes (based on comparative genomic hybridization (CGH) in prostate cancers to be novel prognostic, and possibly predictive, factors for prostate cancer radiotherapy response.
  • Intermediate risk prostate cancers show alterations in a number of genes thought to be involved in radiosensitivity, DNA repair, cell death and stem cell renewal.
  • Conclusions. The use of high-resolution CGH for fine-mapping of deletions and amplifications in pre-radiotherapy prostate cancer biopsies is feasible.
  • Genetic alterations may delineate localized prostate cancer from systemic disease and be used as a predictive factor in that patients would be individually triaged to local (surgery versus radiotherapy) and/or adjuvant (adjuvant androgen ablation or post-operative radiotherapy) therapies in a prospective fashion to improve outcome.
  • [MeSH-major] Carcinoma / diagnosis. Carcinoma / radiotherapy. Comparative Genomic Hybridization / methods. Prostatic Neoplasms / diagnosis. Prostatic Neoplasms / radiotherapy
  • [MeSH-minor] Algorithms. Animals. Humans. Male. Neoplasm Staging. Prognosis. Risk. Treatment Outcome


23. Braeckman J, Autier P, Garbar C, Marichal MP, Soviany C, Nir R, Nir D, Michielsen D, Bleiberg H, Egevad L, Emberton M: Computer-aided ultrasonography (HistoScanning): a novel technology for locating and characterizing prostate cancer. BJU Int; 2008 Feb;101(3):293-8
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  • [Title] Computer-aided ultrasonography (HistoScanning): a novel technology for locating and characterizing prostate cancer.
  • OBJECTIVE: To assess the extent to which prostate HistoScanning (PHS), a new ultrasound-based technology that uses computer-aided analysis to quantify tissue disorganization induced by malignant processes, can identify and characterize foci of prostate cancer compared with step-sectioned radical prostatectomy (RP) specimens.
  • In 13 men the histology was examined on sections of the whole-mount prostate onto which a grid of 5 x 5 mm squares was applied.
  • On a test set of 14 of the 29 patients, PHS analysis was used before knowing the histology results (blinded data), to predict the maximum tumour diameter, focality, laterality and extraprostatic extension (EPE).
  • RESULTS: Identification and characterization by PHS of the index tumour in the 14 patients in the test set correlated closely (r = 0.95, P < 0.001) with the reference test.
  • In the same set of data, EPE was attributed to one prostate cancer that on pathological inspection was deemed to be organ-confined (pT2b).
  • CONCLUSIONS: PHS has the potential to identify and characterize prostate cancer foci noninvasively.
  • The precision appears to be sufficient to suggest that PHS might be useful as a triage test for men deemed to be at risk of prostate cancer and who wish to avoid prostate biopsy.
  • [MeSH-major] Image Interpretation, Computer-Assisted / standards. Prostate / pathology. Prostate-Specific Antigen / blood. Prostatic Neoplasms / ultrasonography


24. Nair TM: On selecting mRNA isoform features for profiling prostate cancer. Comput Biol Chem; 2009 Dec;33(6):421-8
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  • [Title] On selecting mRNA isoform features for profiling prostate cancer.
  • In our earlier study we had used mRNA isoforms expression to identify biomarkers for prostate cancer (Li et. al, 2006.
  • Further, we have rigorously analyzed the isoform expression data to understand the variability and heterogeneity associated with the expression levels between (i) prostate cancer cell lines and non-prostate cancer cell lines and (ii) normal prostate tissue and prostate cancer tissue.
  • [MeSH-major] Gene Expression Profiling. Prostatic Neoplasms / genetics. RNA, Messenger / genetics

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  • (PMID = 19889581.001).
  • [ISSN] 1476-928X
  • [Journal-full-title] Computational biology and chemistry
  • [ISO-abbreviation] Comput Biol Chem
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Protein Isoforms; 0 / RNA, Messenger
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25. Harris AM, Warner BW, Wilson JM, Becker A, Rowland RG, Conner W, Lane M, Kimbler K, Durbin EB, Baron AT, Kyprianou N: Effect of alpha1-adrenoceptor antagonist exposure on prostate cancer incidence: an observational cohort study. J Urol; 2007 Nov;178(5):2176-80
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  • [Title] Effect of alpha1-adrenoceptor antagonist exposure on prostate cancer incidence: an observational cohort study.
  • PURPOSE: The quinazoline based alpha1-adrenoceptor antagonists doxazosin and terazosin suppress prostate tumor growth via the induction of apoptosis and decrease in tissue vascularity.
  • To assess the effect of alpha1-blocker exposure on the incidence of prostate cancer we performed an exploratory, observational cohort study.
  • MATERIALS AND METHODS: The medical records of all male patients enrolled at Lexington Veterans Affairs Medical Center were searched to identify men treated with quinazoline based alpha1-adrenoreceptor antagonists between January 1, 1998 and December 31, 2002 for hypertension and/or benign prostatic enlargement.
  • Medical records were subsequently linked to the Markey Cancer Center Kentucky Cancer Registry, a statewide population based central cancer registry that is part of the National Cancer Institute Surveillance, Epidemiology and End Results Program, to identify all incident prostate cancer cases diagnosed.
  • All newly diagnosed prostate cancer cases unexposed to alpha1-adrenoreceptor antagonists in the total male Veterans Affairs population during this period were also identified from the Kentucky Cancer Registry database.
  • Measures of disease incidence, relative risk and attributable risk were calculated to compare the risk of prostate cancer in alpha1-blocker exposed vs unexposed men.
  • Kaplan-Meier curves and Cox regression models were used to compare overall survival between alpha1-blocker exposed and unexposed prostate cancer cases.
  • These data yielded an unadjusted RR of 0.683 (95% CI 0.532, 0.876) and a risk difference of -0.0076, indicating that 7.6 fewer prostate cancer cases developed per 1,000 exposed men.
  • Thus, exposure to quinazoline alpha1-blockers may have prevented 32 prostate cancer cases among the 4,070 treated men during the study period.
  • Therefore, men exposed to quinazoline alpha1-adrenoceptor antagonists were at 1.46 times lower RR and 31.7% lower attributable risk for prostate cancer than unexposed men.
  • CONCLUSIONS: These data suggest that exposure to quinazoline based alpha1-adrenoceptor antagonists significantly decreases the incidence of prostate cancer.
  • This evidence suggests that the apoptotic and anti-angiogenic effects of these drugs may prevent the development of prostate cancer.


26. Bradley SV, Oravecz-Wilson KI, Bougeard G, Mizukami I, Li L, Munaco AJ, Sreekumar A, Corradetti MN, Chinnaiyan AM, Sanda MG, Ross TS: Serum antibodies to huntingtin interacting protein-1: a new blood test for prostate cancer. Cancer Res; 2005 May 15;65(10):4126-33
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  • [Title] Serum antibodies to huntingtin interacting protein-1: a new blood test for prostate cancer.
  • Huntingtin-interacting protein 1 (HIP1) is frequently overexpressed in prostate cancer.
  • In addition to human cancers, HIP1 is also overexpressed in prostate tumors from the transgenic adenocarcinoma of the mouse prostate (TRAMP) mouse model.
  • Here we provide evidence that HIP1 plays an important role in mouse tumor development, as tumor formation in the TRAMP mice was impaired in the Hip1null/null background.
  • In addition, we report that autoantibodies to HIP1 developed in the sera of TRAMP mice with prostate cancer as well as in the sera from human prostate cancer patients.
  • This led to the development of an anti-HIP1 serum test in humans that had a similar sensitivity and specificity to the anti-alpha-methylacyl CoA racemase (AMACR) and prostate-specific antigen tests for prostate cancer and when combined with the anti-AMACR test yielded a specificity of 97%.
  • These data suggest that HIP1 plays a functional role in tumorigenesis and that a positive HIP1 autoantibody test may be an important serum marker of prostate cancer.
  • [MeSH-major] Adenocarcinoma / immunology. Autoantibodies / blood. DNA-Binding Proteins / immunology. Prostatic Neoplasms / immunology

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  • (PMID = 15899803.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA098730-02; United States / NCI NIH HHS / CA / R01 CA82419-01; United States / NCI NIH HHS / CA / R01-CA82363-01A1
  • [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 / Autoantibodies; 0 / DNA-Binding Proteins; 0 / HIP1 protein, human
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27. Nam RK, Reeves JR, Toi A, Dulude H, Trachtenberg J, Emami M, Daigneault L, Panchal C, Sugar L, Jewett MA, Narod SA: A novel serum marker, total prostate secretory protein of 94 amino acids, improves prostate cancer detection and helps identify high grade cancers at diagnosis. J Urol; 2006 Apr;175(4):1291-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A novel serum marker, total prostate secretory protein of 94 amino acids, improves prostate cancer detection and helps identify high grade cancers at diagnosis.
  • PURPOSE: New biomarkers for prostate cancer are needed.
  • MATERIALS AND METHODS: We conducted a case-control study of 1,212 men with no previous history of prostate cancer and who underwent a prostate biopsy from 1998 to 2000 because of an increased PSA or an abnormal DRE.
  • Cases were patients with prostate cancer, and controls were patients who had no evidence of cancer.
  • Multivariate logistic regression analysis was used to determine whether or not PSP94 levels improved the predictive value for prostate cancer.
  • The adjusted odds ratios for the presence of prostate cancer for patients with the lowest quartile of PSP94, compared to patients in the highest quartile was 2.70 (95% CI 1.8 - 4.0, p <0.0001).
  • CONCLUSIONS: Patients with low total PSP94 levels had a high probability for having prostate cancer detected at biopsy.
  • [MeSH-major] Biomarkers, Tumor / blood. Follicle Stimulating Hormone / blood. Prostatic Neoplasms / blood. Prostatic Neoplasms / pathology. Prostatic Secretory Proteins / blood


28. Chiang CF, Son EL, Wu GJ: Oral treatment of the TRAMP mice with doxazosin suppresses prostate tumor growth and metastasis. Prostate; 2005 Sep 1;64(4):408-18
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  • [Title] Oral treatment of the TRAMP mice with doxazosin suppresses prostate tumor growth and metastasis.
  • BACKGROUND: We used the TRAMP mouse model for testing the effect of oral doxazosin treatment on the in vivo prostate tumor growth and metastasis.
  • At the end of oral treatment, tumor weight was determined, and metastasis to multiple organs examined.
  • The levels of MUC18, Bcl-2, Bax, caspase-3, poly (ADP-ribose) polymerase (PARP), phospho (Ser473)-AKT, and Ki-67 in the mouse prostate tumors were determined.
  • RESULTS: Oral treatment of the TRAMP mice with doxazosin for 45-81 days did not decrease the size of preexisting prostate tumors, but it limited the metastasis to peri-aortic lymph nodes.
  • A prolonged treatment of TRAMP mice with doxazosin (156-196 days), if administered early, decreased the prostate tumor weight and completely suppressed metastasis.
  • The doxazosin treatment did not further decrease the expression of an already low level of Bcl-2 in all prostate tumors, but it increased the expression of Bax, and the activation of caspase-3, and the cleavage of a downstream substrate, PARP.
  • The treatment in the early phase appeared to promote prostate tumor growth and increased the expression of a proliferative index, Ki-67.
  • CONCLUSIONS: Doxazosin, if administered early, may be useful for preventing the prostate tumor formation, and also for limiting or completely suppressing the metastasis of prostate cancer in the TRAMP model.
  • [MeSH-major] Adrenergic alpha-Antagonists / pharmacology. Doxazosin / pharmacology. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / secondary

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  • [Copyright] Copyright 2005 Wiley-Liss, Inc.
  • (PMID = 15789364.001).
  • [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 / Adrenergic alpha-Antagonists; 0 / Androgen-Binding Protein; 0 / Antigens, CD; 0 / Antigens, CD146; 0 / Bax protein, mouse; 0 / Ki-67 Antigen; 0 / Mcam protein, mouse; 0 / Neural Cell Adhesion Molecules; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / bcl-2-Associated X Protein; 0 / probasin; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.4.22.- / Casp3 protein, mouse; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases; NW1291F1W8 / Doxazosin
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29. Zhang P, Zheng Y, Ran H, Leng Z, Wang Z: Case report: gastric adenocarcinoma metastatic to the prostate gland. J Radiol Case Rep; 2010;4(3):35-8
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  • [Title] Case report: gastric adenocarcinoma metastatic to the prostate gland.
  • Metastasis to the prostate gland from gastric cancer is exceedingly rare.
  • We have presented a rare case of gastric malignancy metastasizing to the prostate diagnosed by transrectal ultrasound guided prostate biopsy.

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  • (PMID = 22470718.001).
  • [ISSN] 1943-0922
  • [Journal-full-title] Journal of radiology case reports
  • [ISO-abbreviation] J Radiol Case Rep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC3303380
  • [Keywords] NOTNLM ; gastric adenocarcinoma / metastases / secondary prostatic cancer / transrectal ultrasound
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30. Tamura K, Furihata M, Chung SY, Uemura M, Yoshioka H, Iiyama T, Ashida S, Nasu Y, Fujioka T, Shuin T, Nakamura Y, Nakagawa H: Stanniocalcin 2 overexpression in castration-resistant prostate cancer and aggressive prostate cancer. Cancer Sci; 2009 May;100(5):914-9
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  • [Title] Stanniocalcin 2 overexpression in castration-resistant prostate cancer and aggressive prostate cancer.
  • Prostate cancer is usually androgen-dependent and responds well to androgen ablation therapy based on castration.
  • However, at a certain stage some prostate cancers eventually acquire a castration-resistant phenotype where they progress aggressively and show very poor response to any anticancer therapies.
  • To characterize the molecular features of these clinical castration-resistant prostate cancers, we previously analyzed gene expression profiles by genome-wide cDNA microarrays combined with microdissection and found dozens of trans-activated genes in clinical castration-resistant prostate cancers.
  • Among them, we report the identification of a new biomarker, stanniocalcin 2, as an overexpressed gene in castration-resistant prostate cancer cells.
  • Real-time polymerase chain reaction and immunohistochemical analysis confirmed overexpression of stanniocalcin 2, a 302-amino-acid glycoprotein hormone, specifically in castration-resistant prostate cancer cells and aggressive castration-naïve prostate cancers with high Gleason scores (8-10).
  • The gene was not expressed in normal prostate, nor in most indolent castration-naïve prostate cancers.
  • Knockdown of stanniocalcin 2 expression by short interfering RNA in a prostate cancer cell line resulted in drastic attenuation of prostate cancer cell growth.
  • Concordantly, stanniocalcin 2 overexpression in a prostate cancer cell line promoted prostate cancer cell growth, indicating its oncogenic property.
  • These findings suggest that stanniocalcin 2 could be involved in aggressive phenotyping of prostate cancers, including castration-resistant prostate cancers, and that it should be a potential molecular target for development of new therapeutics and a diagnostic biomarker for aggressive prostate cancers.
  • [MeSH-major] Castration. Glycoproteins / metabolism. Intercellular Signaling Peptides and Proteins / metabolism. Prostatic Neoplasms / metabolism. Prostatic Neoplasms / pathology
  • [MeSH-minor] Cell Line, Tumor. Disease Progression. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Male. RNA Interference

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  • (PMID = 19298603.001).
  • [ISSN] 1349-7006
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Glycoproteins; 0 / Intercellular Signaling Peptides and Proteins; 0 / STC2 protein, human
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31. Mann MJ, DeCastro GJ, Desai M, Benson MC, McKiernan JM: Predictive significance of surgical margin status after prostatectomy for prostate cancer during PSA era. Urology; 2008 Dec;72(6):1203-7
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  • [Title] Predictive significance of surgical margin status after prostatectomy for prostate cancer during PSA era.
  • OBJECTIVES: The presence of positive surgical margins (PSMs) after prostatectomy for prostate cancer has long been an indicator of poor survival outcomes.
  • However, with the downstaging of cancer occurring in the prostate-specific antigen testing era, we sought to determine whether the risk associated with PSMs retains the same effect on prognosis as before the prostate-specific antigen testing era.
  • RESULTS: The median age, preoperative prostate-specific antigen, and Gleason score was 61.6 years, 6 ng/mL, and 7, respectively, and >50% of patients had pathologic Stage T2 disease.
  • [MeSH-major] Prostate-Specific Antigen / blood. Prostatectomy / methods. Prostatic Neoplasms / diagnosis. Prostatic Neoplasms / surgery
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Humans. Male. Medical Oncology / methods. Middle Aged. Neoplasm Recurrence, Local / diagnosis. Neoplasm Recurrence, Local / pathology. Predictive Value of Tests. Prognosis. Risk Factors. Treatment Outcome


32. Hori J, Okuyama M, Azumi M, Kato Y, Saga Y, Hashimoto H, Tokumitsu M, Kakizaki H: [Indication of repeat prostate biopsy for the diagnosis of prostate cancer]. Hinyokika Kiyo; 2006 Nov;52(11):835-8; discussion 838-9
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  • [Title] [Indication of repeat prostate biopsy for the diagnosis of prostate cancer].
  • There is no standard criterion for repeat prostate biopsy in cases with a negative initial biopsy.
  • We retrospectively analyzed our experience of repeat prostate biopsy to establish its indication for the diagnosis of prostate cancer.
  • From April 1997 to March 2005, 35 consecutive patients underwent repeat prostate biopsy at the department of Urology, Asahikawa Medical College Hospital because of clinically suspicious prostate cancer despite a negative initial biopsy.
  • We compared patients' age, number of cores obtained during repeat biopsy, digital rectal examination findings, total prostate volume, the time from the first to the last biopsy, total prostate specific antigen (PSA) value, free PSA/total PSA ratio, PSA density and PSA velocity between cancer-positive and cancer-negative groups.
  • Prostate cancer was detected in 17 of 35 patients (49%).
  • Fifteen patients with prostate cancer were diagnosed by the first repeat biopsy and other 2 patients were diagnosed by the second repeat biopsy.
  • Persistently elevated total PSA and a higher PSA density in cases with a negative initial biopsy might be a good indication of repeat prostate biopsy for the diagnosis of prostate cancer.
  • [MeSH-major] Biopsy. Prostate / pathology. Prostatic Neoplasms / pathology


33. Wang LG, Chiao JW: Prostate cancer chemopreventive activity of phenethyl isothiocyanate through epigenetic regulation (review). Int J Oncol; 2010 Sep;37(3):533-9
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  • [Title] Prostate cancer chemopreventive activity of phenethyl isothiocyanate through epigenetic regulation (review).
  • Prostate cancer is one of the most commonly diagnosed cancers in men.
  • Therefore, finding strategies for the prevention of prostate cancer initiation and disease progression is a medical challenge.
  • Consumption of cruciferous vegetables has been reported to be associated with reduced incidence of prostate cancer cases.
  • In this review, we summarize the recent findings of PEITC on prostate cancer prevention with an emphasis on epigenetic mechanisms.
  • The gene for detoxifying enzyme pi-class glutathione S-transferase (GSTP1), silenced in the vast majority of prostate tumor cells, could be reactivated and the enzymatic function recovered.
  • The epigenetic regulation may play a critical role, along with interactive mechanisms including the disruption of microtubule polymerization, in prostate cancer prevention by PEITC.
  • [MeSH-major] Anticarcinogenic Agents / pharmacology. Isothiocyanates / pharmacology. Prostatic Neoplasms / genetics. Prostatic Neoplasms / prevention & control


34. Ellinger J, Bastian PJ, Biermann K, Schmidt ME, Textor J, Bollmann D, Zhou H, Müller SC: Prostate cancer tissue is masked by bicalutamide: a case report. Eur J Med Res; 2007 May 29;12(5):212-5
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  • [Title] Prostate cancer tissue is masked by bicalutamide: a case report.
  • Prostate cancer is the most common malignant tumor in men.
  • Recently, a slightly decreased frequency of margin positivity following neoadjuvant bicalutamide treatment due to tumor shrinkage was reported.
  • In this case, local recurrence was confirmed by needle biopsy in a patient five years following radical prostatectomy for prostate adenocarcinoma.
  • After therapy with 50 mg bicalutamide for a month, the tumour was resected.
  • We think that bicalutamide may be capable of masking prostate cancer cells.
  • [MeSH-major] Adenocarcinoma / drug therapy. Androgen Antagonists / adverse effects. Anilides / adverse effects. Neoplasm Recurrence, Local / pathology. Nitriles / adverse effects. Prostatic Neoplasms / drug therapy. Tosyl Compounds / adverse effects
  • [MeSH-minor] Biopsy, Needle. Humans. Immunohistochemistry. Male. Middle Aged. Neoadjuvant Therapy. Prostate / drug effects. Prostate-Specific Antigen / blood. Prostatectomy

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  • (PMID = 17513193.001).
  • [ISSN] 0949-2321
  • [Journal-full-title] European journal of medical research
  • [ISO-abbreviation] Eur. J. Med. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Anilides; 0 / Nitriles; 0 / Tosyl Compounds; A0Z3NAU9DP / bicalutamide; EC 3.4.21.77 / Prostate-Specific Antigen
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35. Drott JB, Alexeyev O, Bergström P, Elgh F, Olsson J: Propionibacterium acnes infection induces upregulation of inflammatory genes and cytokine secretion in prostate epithelial cells. BMC Microbiol; 2010;10:126
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  • [Title] Propionibacterium acnes infection induces upregulation of inflammatory genes and cytokine secretion in prostate epithelial cells.
  • BACKGROUND: The immune stimulating bacterium Propionibacterium acnes is a frequent colonizer of benign and malignant prostate tissue.
  • To understand the pathogenesis of the earliest phase of this infection, we examined the P. acnes triggered immune response in cultivated prostate epithelial cells.
  • RESULTS: Prostate epithelial cells are triggered to secrete IL-6, IL-8 and GM-CSF when infected with P. acnes.
  • CONCLUSIONS: P. acnes has potential to trigger a strong immune reaction in the prostate glandular epithelium.
  • Upon infection of prostate via the retrograde urethral route, the induced inflammatory reaction might facilitate bacterial colonization deeper in the prostate tissue where persistent inflammation may impact the development of prostate diseases as hyperplasia and/or malignancy.
  • [MeSH-major] Cytokines / secretion. Epithelial Cells / immunology. Epithelial Cells / microbiology. Gram-Positive Bacterial Infections / immunology. Propionibacterium acnes / immunology. Prostate / microbiology

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  • (PMID = 20420679.001).
  • [ISSN] 1471-2180
  • [Journal-full-title] BMC microbiology
  • [ISO-abbreviation] BMC Microbiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytokines
  • [Other-IDs] NLM/ PMC2867951
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36. Loeb S, Yu X, Nadler RB, Roehl KA, Han M, Hawkins SA, Catalona WJ: Does body mass index affect preoperative prostate specific antigen velocity or pathological outcomes after radical prostatectomy? J Urol; 2007 Jan;177(1):102-6; discussion 106
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Does body mass index affect preoperative prostate specific antigen velocity or pathological outcomes after radical prostatectomy?
  • PURPOSE: Several studies suggest that obesity may be associated with more aggressive prostate cancer.
  • Similarly the rate of serum prostate specific antigen change is associated with adverse tumor features and prostate cancer specific mortality rates after radical prostatectomy and radiation therapy.
  • We examined the associations among obesity, prostate specific antigen velocity and adverse tumor features in men treated with radical prostatectomy.
  • Prostate specific antigen velocity and other clinicopathological features were compared among men with a body mass index of less than 25, 25 to 29.9 and 30 or greater.
  • RESULTS: Although Gleason score and prostate volume were similar among groups, there was a significantly lower proportion with organ confined disease and fewer low volume tumors as body mass index increased.
  • Of patients with a body mass index of 30 or greater 52% had a preoperative prostate specific antigen velocity of more than 2 ng/ml yearly compared to 34% with a body mass index of 25 to 29.9 and 26% with a body mass index of less than 25 (p = 0.04).
  • Although on univariate analysis body mass index was associated with adverse clinical and pathological tumor features, on multivariate analysis with other preoperative variables body mass index did not add significant independent predictive information concerning pathological stage (OR 1.02, 95% CI 0.96-1.08).
  • However, it did not provide independent predictive information concerning final pathological tumor stage.
  • Nevertheless, obesity was significantly associated with increased preoperative prostate specific antigen velocity.
  • Additional studies are needed to further clarify the links between body mass index, prostate specific antigen velocity and prostate cancer progression, and determine whether weight reduction could lead to improved outcomes.
  • [MeSH-major] Body Mass Index. Prostate-Specific Antigen / blood. Prostatectomy. Prostatic Neoplasms / blood. Prostatic Neoplasms / pathology

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  • (PMID = 17162013.001).
  • [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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37. Begley LA, Kasina S, MacDonald J, Macoska JA: The inflammatory microenvironment of the aging prostate facilitates cellular proliferation and hypertrophy. Cytokine; 2008 Aug;43(2):194-9
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  • [Title] The inflammatory microenvironment of the aging prostate facilitates cellular proliferation and hypertrophy.
  • Benign Prostatic Hypertrophy (BPH, also known as benign prostatic hyperplasia or benign prostatic enlargement), is one of the most common benign proliferative conditions associated with aging in men and is pathologically characterized by the proliferation of fibroblast/myofibroblast and epithelial cell types in the prostate.
  • Previous studies from our laboratory have shown that the CXC-type chemokines, CXCL5 and CXCL12, are secreted by aging prostate stroma and promote both proliferative and transcriptional responses from prostate epithelial cells.
  • Using array-based gene expression profiling and quantitative reverse-transcriptase polymerase chain reaction, we now show that the transcriptome of the aging prostate stroma is characterized by the up-regulation of several genes that encode secreted inflammatory mediators, including secreted CXC-type chemokines (CXCL1, CXCL2, CXCL5, CXCL6, CXCL12), interleukins (IL11, IL33), and transcripts with cytokine homology (CYTL1).
  • At the protein level, ELISA experiments demonstrated that CXCL1, CXCL5, and CXCL6 were secreted by primary prostate stromal fibroblasts explanted from aging prostate stroma.
  • Dose-response assays confirmed that, like CXCL5 and CXCL12, CXCL1 and CXCL6 promote low-level proliferative responses from both prostate stromal fibroblasts and epithelial cells.
  • Taken together, these data suggest that inflammatory mediators are secreted by prostatic stroma consequent to aging, that the levels of these mediators are sufficient to promote low-level increases in the proliferative rate of both epithelial and stromal fibroblast cell types.
  • Moreover, these processes may account for the low-level, but cumulative, proliferation of both epithelial and fibroblastic/myofibroblastic cell types that characterizes the aging-associated development of benign prostatic hypertophy.

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  • (PMID = 18572414.001).
  • [ISSN] 1096-0023
  • [Journal-full-title] Cytokine
  • [ISO-abbreviation] Cytokine
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK065313-010001; United States / NIDDK NIH HHS / DK / R01 DK081841; United States / NCI NIH HHS / CA / P30 CA046592; United States / NIDDK NIH HHS / DK / P50 DK065313; United States / NIDDK NIH HHS / DK / P50 DK065313-010001; United States / NCI NIH HHS / CA / 5 P30 CA46592; United States / NCI NIH HHS / CA / P30 CA046592-159017; United States / NIDDK NIH HHS / DK / 1 P50 DK065313; United States / NCI NIH HHS / CA / CA046592-159017; United States / NIDDK NIH HHS / DK / R01 DK081841-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Other-IDs] NLM/ NIHMS66226; NLM/ PMC2538565
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38. Vikram A, Jena GB, Ramarao P: Increased cell proliferation and contractility of prostate in insulin resistant rats: linking hyperinsulinemia with benign prostate hyperplasia. Prostate; 2010 Jan 1;70(1):79-89
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  • [Title] Increased cell proliferation and contractility of prostate in insulin resistant rats: linking hyperinsulinemia with benign prostate hyperplasia.
  • BACKGROUND: Obesity, dyslipidemia, Hyperinsulinemia, and insulin resistance (IR) are key features of metabolic syndrome and are considered as risk factors for benign prostatic hyperplasia (BPH) as well as type 2 diabetes.
  • Effect of HFD feeding on the testosterone-induced prostatic growth was evaluated.
  • Pioglitazone (PG, 20 mg/kg) was used for the reversal of compensatory hyperinsulinemia and to examine the subsequent effect on the prostatic growth.
  • RESULTS: Prostatic enlargement was observed in the HFD-fed rats.
  • Significant increase in the cell proliferation markers confirmed the occurrence of cellular hyperplasia in the prostate of hyperinsulinemic rat.
  • Enhanced alpha-adrenoceptor mediated contraction in the prostate of HFD-fed rats indicates augmented contractility of the gland.
  • However, testosterone treatment further augmented the prostatic growth in HFD-fed rats.
  • PG treatment led to improved insulin sensitivity, decreased plasma insulin level and prostate weight, indicating the role of compensatory hyperinsulinemia in the prostate growth.
  • CONCLUSIONS: The present investigation reports that HFD-feeding induced hyperinsulinemic condition leads to increased cellular proliferation, enhanced alpha-adrenoceptor mediated contraction, and enlargement of the prostate in rats.
  • [MeSH-major] Cell Proliferation. Hyperinsulinism / complications. Hyperinsulinism / pathology. Insulin Resistance. Prostate / pathology. Prostatic Hyperplasia / etiology. Prostatic Hyperplasia / pathology

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  • [Copyright] (c) 2009 Wiley-Liss, Inc.
  • (PMID = 19790233.001).
  • [ISSN] 1097-0045
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Dietary Fats
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39. Yazici S, Inci K, Yuksel S, Bilen CY, Ozen H: Radical prostatectomy after previous prostate surgery: effects on surgical difficulty and pathologic outcomes. Urology; 2009 Apr;73(4):856-9
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  • [Title] Radical prostatectomy after previous prostate surgery: effects on surgical difficulty and pathologic outcomes.
  • OBJECTIVES: To evaluate the surgical difficulty and pathologic outcomes of patients who had undergone radical prostatectomy after previous prostate surgery.
  • METHODS: A total of 45 patients with previous prostate surgery underwent radical retropubic prostatectomy for prostate cancer.
  • The surgical difficulty and pathologic outcomes for this group of patients (group 1) were compared with those for 50 consecutive patients who had undergone radical retropubic prostatectomy as their only prostatic surgery (group 2).
  • RESULTS: Radical prostatectomy was technically more challenging in the patients after previous prostate surgery compared with surgery-naive patients, with significantly more estimated blood loss (P <.05) and a longer operative time (P <.001).
  • CONCLUSIONS: Although radical retropubic prostatectomy is technically more difficult after previous prostate surgery, it can be performed safely with no difference in pathologic outcomes from those seen in patients with no history of prostate surgery.
  • [MeSH-major] Prostate / surgery. Prostatectomy. Prostatic Neoplasms / surgery

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  • (PMID = 19022487.001).
  • [ISSN] 1527-9995
  • [Journal-full-title] Urology
  • [ISO-abbreviation] Urology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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40. Osunkoya AO, Hansel DE, Sun X, Netto GJ, Epstein JI: Aberrant diffuse expression of p63 in adenocarcinoma of the prostate on needle biopsy and radical prostatectomy: report of 21 cases. Am J Surg Pathol; 2008 Mar;32(3):461-7
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  • [Title] Aberrant diffuse expression of p63 in adenocarcinoma of the prostate on needle biopsy and radical prostatectomy: report of 21 cases.
  • Aberrant diffuse expression of p63 in prostate carcinoma cells is a rare and poorly understood phenomenon.
  • We studied 19 cases of prostate cancer with aberrant diffuse expression of p63 on needle biopsy and reviewed the subsequent radical prostatectomies in 6 cases.
  • Needle biopsy cases ranged from Gleason patterns 3 to 5 with tumor identified on one or more cores, ranging from a minute focus to 80% of the core.
  • In all 8 radical prostatectomies p63 positive cancer was present, with in 2/8 cases both p63 positive cancer and usual p63 negative acinar prostate cancer.
  • The presence of p63 positive atypical glands with an infiltrative pattern and perineural invasion on radical prostatectomy confirmed the needle biopsy diagnosis of carcinoma.
  • Rarely, prostate cancer can aberrantly express diffuse p63 staining in a nonbasal cell distribution leading to the erroneous diagnosis of atrophy or atypical basal cell proliferation.
  • The diagnosis of prostate cancer is based on the morphology and confirmed by the absence of high molecular weight cytokeratin staining and positivity for alpha-methylacyl-CoA racemase in the atypical glands.
  • Pathologists need to be aware of this rare and unusual phenomenon, which is a potential pitfall in prostate cancer diagnosis.
  • [MeSH-major] Adenocarcinoma / chemistry. Biopsy, Needle. Membrane Proteins / analysis. Prostatectomy. Prostatic Neoplasms / chemistry

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  • (PMID = 18300803.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CKAP4 protein, human; 0 / Membrane Proteins
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41. Cooper CS, Foster CS: Concepts of epigenetics in prostate cancer development. Br J Cancer; 2009 Jan 27;100(2):240-5
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  • [Title] Concepts of epigenetics in prostate cancer development.
  • Substantial evidence now supports the view that epigenetic changes have a role in the development of human prostate cancer.
  • Examination of cancer methylation patterns supports a stem cell origin of prostate cancer.
  • It is well established that methylation of GSTpi is a marker of prostate cancer, and global patterns of histone marking appear to be linked to cancer prognosis with levels of acetylated histones H3K9, H3K18, and H4K12, and of dimethylated H4R3 and H3K4, dividing low-grade prostate cancer (Gleason 6 or less) into two prognostically separate groups.
  • [MeSH-major] Epigenesis, Genetic. Prostatic Neoplasms / genetics

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  • (PMID = 19002169.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0501019
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Number-of-references] 31
  • [Other-IDs] NLM/ PMC2634711
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42. Dos Reis ST, Pontes J Jr, Villanova FE, Borra PM, Antunes AA, Dall'oglio MF, Srougi M, Leite KR: Genetic polymorphisms of matrix metalloproteinases: susceptibility and prognostic implications for prostate cancer. J Urol; 2009 May;181(5):2320-5
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  • [Title] Genetic polymorphisms of matrix metalloproteinases: susceptibility and prognostic implications for prostate cancer.
  • PURPOSE: Prostate cancer is the most common tumor in males in Brazil.
  • We investigated the correlation between MMP1, 2, 7 and 9 polymorphisms with susceptibility to prostate cancer, and classic prognostic parameters of prostate cancer.
  • RESULTS: For the MMP1 gene the polymorphic allele was more common in the control group than in the prostate cancer group (p <0.001).
  • For the MMP9 gene the incidence of the polymorphic homozygote genotype was higher in the prostate cancer group (p <0.001).
  • CONCLUSIONS: MMP1 and MMP2 may protect against prostate cancer development and MMP9 may be related to higher risk.
  • [MeSH-major] Genetic Predisposition to Disease / epidemiology. Matrix Metalloproteinases / genetics. Polymorphism, Genetic. Prostatic Neoplasms / genetics
  • [MeSH-minor] Aged. Biomarkers, Tumor / genetics. Case-Control Studies. Chi-Square Distribution. Confidence Intervals. DNA, Neoplasm / analysis. Gene Expression Regulation, Neoplastic. Humans. Male. Matrix Metalloproteinase 1 / genetics. Matrix Metalloproteinase 2 / genetics. Matrix Metalloproteinase 9 / genetics. Middle Aged. Odds Ratio. Polymerase Chain Reaction. Probability. Prognosis. Sensitivity and Specificity

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  • [CommentIn] J Urol. 2010 Mar;183(3):1258 [20097381.001]
  • [ErratumIn] J Urol. 2009 Jul;182(1):400
  • (PMID = 19303106.001).
  • [ISSN] 1527-3792
  • [Journal-full-title] The Journal of urology
  • [ISO-abbreviation] J. Urol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DNA, Neoplasm; EC 3.4.24.- / Matrix Metalloproteinases; EC 3.4.24.24 / Matrix Metalloproteinase 2; EC 3.4.24.35 / Matrix Metalloproteinase 9; EC 3.4.24.7 / Matrix Metalloproteinase 1
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43. Li TH, Zhao H, Peng Y, Beliakoff J, Brooks JD, Sun Z: A promoting role of androgen receptor in androgen-sensitive and -insensitive prostate cancer cells. Nucleic Acids Res; 2007;35(8):2767-76
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  • [Title] A promoting role of androgen receptor in androgen-sensitive and -insensitive prostate cancer cells.
  • Although the vital role of the androgen receptor (AR) has been well demonstrated in primary prostate cancers, its role in the androgen-insensitive prostate cancers still remains unclear.
  • Here, we used a small hairpin RNA approach to directly assess AR activity in prostate cancer cells.
  • Reduction of AR expression in the two androgen-sensitive prostate cancer cell lines, LNCaP and LAPC4, significantly decreased AR-mediated transcription and cell growth.
  • Intriguingly, in two androgen-insensitive prostate cell lines, LNCaP-C42B4 and CWR22Rv1, knockdown of AR expression showed a more pronounced effect on AR-induced transcription and cell growth than androgen depletion.
  • Finally, we demonstrated a direct role for AR in promoting tumor formation and growth in a xenograft model.
  • Taken together, our results elucidate an important role for the AR in androgen-insensitive prostate cancer cells, and suggest that AR can be used as a therapeutic target for androgen-insensitive prostate cancers.

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  • (PMID = 17426117.001).
  • [ISSN] 1362-4962
  • [Journal-full-title] Nucleic acids research
  • [ISO-abbreviation] Nucleic Acids Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA070297-11A2; United States / NCI NIH HHS / CA / R01 CA070297-10; United States / NCI NIH HHS / CA / CA70297; United States / NCI NIH HHS / CA / R01 CA070297; United States / NCI NIH HHS / CA / K01 CA123532; United States / NIDDK NIH HHS / DK / R01 DK061002-05; United States / NCI NIH HHS / CA / CA070297-10; United States / NCI NIH HHS / CA / CA087767-05; United States / NCI NIH HHS / CA / R01 CA070297-11A2; United States / NCI NIH HHS / CA / CA087767-04; United States / NCI NIH HHS / CA / R01 CA070297-12; United States / NIDDK NIH HHS / DK / R01 DK061002-04; United States / NCI NIH HHS / CA / CA070297-12; United States / NCI NIH HHS / CA / R01 CA087767-05; United States / NIDDK NIH HHS / DK / DK061002-04; United States / NCI NIH HHS / CA / R29 CA070297; United States / NIDDK NIH HHS / DK / Z01 DK061002; United States / NCI NIH HHS / CA / CA123532-01; United States / NIDDK NIH HHS / DK / R56 DK061002; United States / NCI NIH HHS / CA / R01 CA087767; United States / NIDDK NIH HHS / DK / R01 DK061002; United States / NIDDK NIH HHS / DK / DK061002-05; United States / NIDDK NIH HHS / DK / DK61002; United States / NCI NIH HHS / CA / R01 CA087767-04; United States / NCI NIH HHS / CA / CA87767
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Androgen Receptor Antagonists; 0 / Androgens; 0 / Receptors, Androgen; 08J2K08A3Y / Dihydrotestosterone
  • [Other-IDs] NLM/ PMC1885678
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44. Thomas LN, Douglas RC, Lazier CB, Too CK, Rittmaster RS, Tindall DJ: Type 1 and type 2 5alpha-reductase expression in the development and progression of prostate cancer. Eur Urol; 2008 Feb;53(2):244-52
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Type 1 and type 2 5alpha-reductase expression in the development and progression of prostate cancer.
  • OBJECTIVES: Both normal and pathological growth of the prostate is dependent on dihydrotestosterone (DHT) synthesis, which is catalysed by two 5alpha-reductase (5alphaR) isoenzymes, 5alphaR1 and 5alphaR2, of which only 5alphaR2 has traditionally been viewed as important in the prostate.
  • The objective of this study was to evaluate the role of both isoenzymes during development/progression of prostate cancer.
  • METHODS: A thorough literature search was performed with the MEDLINE database to identify studies that have assessed expression of 5alphaR1/2 in prostate tissue.
  • RESULTS: DHT suppression data for the 5alphaR2-specific inhibitor, finasteride, and the dual 5alphaR1/2 inhibitor, dutasteride, show that both isoenzymes are active in benign prostate.
  • Furthermore, immunostaining studies have shown that 5alphaR1 expression increases and 5alphaR2 expression decreases in prostatic intraepithelial neoplasia (PIN) and prostate cancer, compared with nonmalignant prostate tissue.
  • Dual inhibition of both isoenzymes with dutasteride may, therefore, be effective in preventing or delaying the growth of prostate cancer.
  • The 4-yr REduction by DUtasteride of prostate Cancer Events (REDUCE) trial is underway to test this hypothesis.
  • Androgen-withdrawal therapy can reverse prostate tumour growth by reducing circulating testosterone.
  • However, 5alphaR-catalysed DHT synthesis within the prostate can continue and most tumours eventually develop resistance to androgen-deprivation therapy.
  • CONCLUSIONS: The consensus of evidence to date shows that 5alphaR1 is present in the prostate, and that levels are higher in malignant compared with benign prostate hyperplasia tissue.
  • [MeSH-major] 3-Oxo-5-alpha-Steroid 4-Dehydrogenase / metabolism. Prostatic Neoplasms / enzymology

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  • (PMID = 18006217.001).
  • [ISSN] 0302-2838
  • [Journal-full-title] European urology
  • [ISO-abbreviation] Eur. Urol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Azasteroids; 0 / Enzyme Inhibitors; 0 / Isoenzymes; 57GNO57U7G / Finasteride; EC 1.3.99.5 / 3-Oxo-5-alpha-Steroid 4-Dehydrogenase; O0J6XJN02I / Dutasteride
  • [Number-of-references] 59
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45. Benchikh El Fegoun A, Villers A, Moreau JL, Richaud P, Rebillard X, Beuzeboc P: [PSA and follow-up after treatment of prostate cancer]. Prog Urol; 2008 Mar;18(3):137-44
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [PSA and follow-up after treatment of prostate cancer].
  • [Transliterated title] PSA et suivi après traitement du cancer de la prostate.
  • [MeSH-major] Continuity of Patient Care. Prostate-Specific Antigen / blood. Prostatic Neoplasms / blood. Prostatic Neoplasms / therapy
  • [MeSH-minor] Biomarkers, Tumor / blood. Chemotherapy, Adjuvant. Humans. Male. Neoplasm Metastasis. Neoplasm Recurrence, Local / blood. Neoplasm Recurrence, Local / diagnosis. Prostatectomy. Radiotherapy, Adjuvant


46. Bastian PJ, Carter BH, Bjartell A, Seitz M, Stanislaus P, Montorsi F, Stief CG, Schröder F: Insignificant prostate cancer and active surveillance: from definition to clinical implications. Eur Urol; 2009 Jun;55(6):1321-30
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Insignificant prostate cancer and active surveillance: from definition to clinical implications.
  • CONTEXT: Due to early detection strategies, prostate cancer is diagnosed early in its natural history.
  • It remains unclear whether all patients diagnosed with prostate cancer warrant radical treatment or may benefit from delayed intervention following active surveillance.
  • EVIDENCE ACQUISITION: Medline was searched using the following terms: prostate cancer, active surveillance and expectant management for dates up to October 2008.
  • Once a patients requires active treatment, most patients still present with curable prostate cancer.
  • Furthermore, only few deaths due to prostate cancer have occurred.
  • CONCLUSIONS: Active surveillance is an alternative option to immediate treatment of men with presumed insignificant prostate cancer.
  • It seems that criteria used to identify men with low-risk prostate cancer are rather similar, and immediate treatment of men meeting these criteria may result in an unnecessary number of treatments in these highly selected patients.
  • [MeSH-major] Monitoring, Physiologic / methods. Prostate-Specific Antigen / blood. Prostatic Neoplasms / diagnosis. Prostatic Neoplasms / therapy
  • [MeSH-minor] Aged. Disease Progression. Early Detection of Cancer. Evidence-Based Medicine. Follow-Up Studies. Humans. Male. Middle Aged. Neoplasm Invasiveness / pathology. Neoplasm Staging. Observation / methods. Patient Selection. Risk Assessment. Sensitivity and Specificity. Time Factors


47. Haworth A, Ebert M, St Clair S, Carey BM, Flynn A, Bottomley DM, Duchesne GM, Joseph D, Ash D: Impact of selection of post-implant technique on dosimetry parameters for permanent prostate implants. Brachytherapy; 2005;4(2):146-53
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Impact of selection of post-implant technique on dosimetry parameters for permanent prostate implants.
  • PURPOSE: To investigate the variability of prostate implant quality indices between three different methods of calculating the post-implant dose distribution.
  • METHODS AND MATERIALS: In a study of 9 permanent prostate implant patients, post-implant dosimetry was carried out using three methods of identifying seed positions within the prostate volume:.
  • (1) prostate volumes defined by transrectal ultrasound (TRUS) immediately following implant were registered with shift-film defined seed positions, (2) seeds were identified directly from the post-implant TRUS images, and (3) CT was used to define seed positions and prostate volumes from images acquired at 41-65 days post-implant.
  • For each method, the volume of prostate receiving 90%, 100%, and 150% of the prescribed dose (V90, V100, V150) and the dose delivered to 90% of the prostate volume (D90) were calculated.
  • CONCLUSIONS: There are many uncertainties in the calculation of parameters that are commonly used to describe the quality of a permanent prostate implant.
  • Differences in the parameters calculated were most likely a result of a combination of factors including uncertainties in delineating the prostate with different imaging modalities, differences in source identification techniques, and intraobserver variability.
  • [MeSH-major] Brachytherapy / instrumentation. Prostatic Neoplasms / radiotherapy. Prostheses and Implants

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  • (PMID = 15893269.001).
  • [ISSN] 1538-4721
  • [Journal-full-title] Brachytherapy
  • [ISO-abbreviation] Brachytherapy
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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48. Sekine Y, Demosky SJ, Stonik JA, Furuya Y, Koike H, Suzuki K, Remaley AT: High-density lipoprotein induces proliferation and migration of human prostate androgen-independent cancer cells by an ABCA1-dependent mechanism. Mol Cancer Res; 2010 Sep;8(9):1284-94
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High-density lipoprotein induces proliferation and migration of human prostate androgen-independent cancer cells by an ABCA1-dependent mechanism.
  • Androgen deprivation therapy for prostate cancer leads to a significant increase of high-density lipoprotein (HDL), which is generally viewed as beneficial, particularly for cardiovascular disease, but the effect of HDL on prostate cancer is unknown.
  • In this study, we investigated the effect of HDL on prostate cancer cell proliferation, migration, intracellular cholesterol levels, and the role of cholesterol transporters, namely ABCA1, ABCG1, and SR-BI in these processes.
  • In human prostate biopsy samples, ABCA1 mRNA expression was ∼2-fold higher in the androgen deprivation therapy group than in subjects with benign prostatic hyperplasia or pretreatment prostate cancer groups.
  • In summary, these results suggest that HDL by an ABCA1-dependent mechanism can mediate signal transduction, leading to increased proliferation and migration of prostate cancer cells.
  • [MeSH-major] ATP-Binding Cassette Transporters / metabolism. Cell Movement / drug effects. Lipoproteins, HDL / pharmacology. Prostatic Neoplasms / metabolism. Prostatic Neoplasms / pathology
  • [MeSH-minor] ATP Binding Cassette Transporter 1. Androgens / metabolism. Cell Line, Tumor. Cell Proliferation / drug effects. Cholesterol / metabolism. Enzyme Activation / drug effects. Extracellular Signal-Regulated MAP Kinases / metabolism. Gene Expression Regulation, Neoplastic / drug effects. Humans. Intracellular Space / drug effects. Intracellular Space / metabolism. Male. Proto-Oncogene Proteins c-akt / metabolism. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Small Interfering / metabolism. Simvastatin / pharmacology

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  • [Copyright] © 2010 AACR.
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  • (PMID = 20671065.001).
  • [ISSN] 1557-3125
  • [Journal-full-title] Molecular cancer research : MCR
  • [ISO-abbreviation] Mol. Cancer Res.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / NIH0013975756; United States / PHS HHS / / NIH0013975756; United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ABCA1 protein, human; 0 / ATP Binding Cassette Transporter 1; 0 / ATP-Binding Cassette Transporters; 0 / Androgens; 0 / Lipoproteins, HDL; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 97C5T2UQ7J / Cholesterol; AGG2FN16EV / Simvastatin; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases
  • [Other-IDs] NLM/ NIHMS222887; NLM/ PMC2941551
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49. Bettendorf O, Schmidt H, Staebler A, Grobholz R, Heinecke A, Boecker W, Hertle L, Semjonow A: Chromosomal imbalances, loss of heterozygosity, and immunohistochemical expression of TP53, RB1, and PTEN in intraductal cancer, intraepithelial neoplasia, and invasive adenocarcinoma of the prostate. Genes Chromosomes Cancer; 2008 Jul;47(7):565-72
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chromosomal imbalances, loss of heterozygosity, and immunohistochemical expression of TP53, RB1, and PTEN in intraductal cancer, intraepithelial neoplasia, and invasive adenocarcinoma of the prostate.
  • Recent studies have shown that intraductal prostate carcinoma (IDC-P) should be considered as a separate lesion distinct from prostatic intraepithelial neoplasia (PIN).
  • The purpose of the present study was to analyze the genetic relationship between benign prostatic tissue, PIN, invasive cancer, IDC-P, and extracapsular tumor tissue to get further information about the role of IDC-P in the development of prostate cancer.
  • One hundred five radical prostatectomy specimens were investigated immunohistochemically, 77 cases were analyzed by PCR for LOH of the tumor suppressor genes TP53 and RB1, and 11 cases of IDC-P and 10 cases of PIN were investigated using comparative genomic hybridization (CGH).
  • We could demonstrate a significant increase of LOH for TP53 or RB1 from benign tissue to PIN.
  • LOH of both TP53 and RB1 were frequently found in IDC-P (52%), followed by extracapsular tumor tissue (44%), invasive cancer (24%), PIN (19%), and benign prostatic tissue (17%).
  • Decreased expression could be demonstrated in extracapsular tumor tissue and in IDC-P.
  • IDC-P represents a separate prostatic lesion and should be graded as a poorly differentiated carcinoma.
  • [MeSH-major] Chromosomal Instability. Loss of Heterozygosity. PTEN Phosphohydrolase / metabolism. Prostatic Neoplasms / genetics. Prostatic Neoplasms / metabolism. Retinoblastoma Protein / metabolism. Tumor Suppressor Protein p53 / metabolism
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Aged. Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. Carcinoma, Intraductal, Noninfiltrating / genetics. Carcinoma, Intraductal, Noninfiltrating / metabolism. Carcinoma, Intraductal, Noninfiltrating / pathology. Humans. Immunoenzyme Techniques. Male. Middle Aged. Neoplasm Invasiveness. Prognosis. Prostatic Intraepithelial Neoplasia / genetics. Prostatic Intraepithelial Neoplasia / metabolism. Prostatic Intraepithelial Neoplasia / pathology


50. Morikawa T, Nagata M, Tomita K, Kitamura T, Goto A, Chong JM, Fukayama M: Phyllodes tumor of the prostate with exuberant glandular hyperplasia. Pathol Int; 2006 Mar;56(3):158-61
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  • [Title] Phyllodes tumor of the prostate with exuberant glandular hyperplasia.
  • Reported herein is an unusual case of prostatic phyllodes tumor with exuberant glandular hyperplasia that led to misdiagnosis of adenocarcinoma.
  • The tumor was detected in a 52-year-old man who had a 1 year history of dysuria.
  • Adenocarcinoma of the prostate was diagnosed from a needle biopsy specimen.
  • Histologically, the tumor had an atypical stromal cell proliferation and elongated slit-like glands characteristic of a phyllodes tumor.
  • The tumor was also accompanied by a florid proliferation of small acini, most of which lacked basal cells, a common manifestation of adenocarcinoma in the overall tumor area.
  • The following features of the resected tumor were helpful for concluding that these acini were benign: lack of cytological anaplasia in spite of structural atypia, presence of scattered basal cells confirmed by immunohistochemistry (high-molecular-weight cytokeratin), and histological transition from these acini to apparently benign slit-like glands.
  • The final diagnosis was then made as 'phyllodes tumor of the prostate with exuberant glandular hyperplasia'.
  • Atypical stromal cells might provide a clue for the recognition of this rare tumor at initial diagnosis by needle biopsy.
  • [MeSH-major] Biopsy, Needle. Diagnostic Errors. Phyllodes Tumor / pathology. Prostatic Neoplasms / pathology

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  • (PMID = 16497250.001).
  • [ISSN] 1320-5463
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Australia
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51. Hazzaa SM, Elashry OM, Afifi IK: Clusterin as a diagnostic and prognostic marker for transitional cell carcinoma of the bladder. Pathol Oncol Res; 2010 Mar;16(1):101-9
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  • Blood and urine samples were used from 68 patients with TCC of the bladder and from 61 patients with benign urological diseases.
  • Quantitation of clusterin mRNA was carried out in 68 bladder tumor specimens from radical cystectomy or transurethral resection and 26 normal bladder specimens from BPH patients by using RT-PCR method.
  • Sensitivity and specificity of serum and urine clusterin as a tumor marker for TCC of the bladder was found to be 80%, 91%, 87.1% and 96.7% respectively.
  • Overexpression of clusterin mRNA was significantly associated with tumor recurrence and overall survival (p < 0.001).
  • [MeSH-major] Biomarkers, Tumor / analysis. Carcinoma, Transitional Cell / diagnosis. Clusterin / biosynthesis. Urinary Bladder Neoplasms / diagnosis
  • [MeSH-minor] Adult. Enzyme-Linked Immunosorbent Assay. Female. Humans. Male. Middle Aged. Neoplasm Staging. Prognosis. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 19757199.001).
  • [ISSN] 1532-2807
  • [Journal-full-title] Pathology oncology research : POR
  • [ISO-abbreviation] Pathol. Oncol. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Clusterin
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52. Thompson IM, Ankerst DP, Chi C, Goodman PJ, Tangen CM, Lucia MS, Feng Z, Parnes HL, Coltman CA Jr: Assessing prostate cancer risk: results from the Prostate Cancer Prevention Trial. J Natl Cancer Inst; 2006 Apr 19;98(8):529-34
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  • [Title] Assessing prostate cancer risk: results from the Prostate Cancer Prevention Trial.
  • BACKGROUND: Prostate-specific antigen (PSA) testing is the primary method used to diagnose prostate cancer in the United States.
  • Methods to integrate other risk factors associated with prostate cancer into individualized risk prediction are needed.
  • We used prostate biopsy data from men who participated in the Prostate Cancer Prevention Trial (PCPT) to develop a predictive model of prostate cancer.
  • METHODS: We included 5519 men from the placebo group of the PCPT who underwent prostate biopsy, had at least one PSA measurement and a digital rectal examination (DRE) performed during the year before the biopsy, and had at least two PSA measurements performed during the 3 years before the prostate biopsy.
  • Logistic regression was used to model the risk of prostate cancer and high-grade disease associated with age at biopsy, race, family history of prostate cancer, PSA level, PSA velocity, DRE result, and previous prostate biopsy.
  • RESULTS: A total of 1211 (21.9%) men were diagnosed with prostate cancer by prostate biopsy.
  • Variables that predicted prostate cancer included higher PSA level, positive family history of prostate cancer, and abnormal DRE result, whereas a previous negative prostate biopsy was associated with reduced risk.
  • Higher PSA level, abnormal DRE result, older age at biopsy, and African American race were predictive for high-grade disease (Gleason score > or =7) whereas a previous negative prostate biopsy reduced this risk.
  • CONCLUSIONS: This predictive model allows an individualized assessment of prostate cancer risk and risk of high-grade disease for men who undergo a prostate biopsy.
  • [MeSH-major] Biopsy, Needle. Prostatic Neoplasms / epidemiology. Prostatic Neoplasms / pathology
  • [MeSH-minor] African Americans / statistics & numerical data. Age Factors. Aged. Confounding Factors (Epidemiology). Digital Rectal Examination. Genetic Predisposition to Disease. Humans. Logistic Models. Male. Predictive Value of Tests. Prognosis. Prostate-Specific Antigen / blood. Randomized Controlled Trials as Topic. Research Design. Risk Assessment. Risk Factors. Time Factors. United States / epidemiology

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  • [CommentIn] J Natl Cancer Inst. 2006 Apr 19;98(8):506-7 [16622114.001]
  • (PMID = 16622122.001).
  • [ISSN] 1460-2105
  • [Journal-full-title] Journal of the National Cancer Institute
  • [ISO-abbreviation] J. Natl. Cancer Inst.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 5UO1CA86402-04; United States / NCI NIH HHS / CA / CA35178; United States / NCI NIH HHS / CA / CA37429; United States / NCI NIH HHS / CA / CA45808
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] EC 3.4.21.77 / Prostate-Specific Antigen
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53. Halpin M, Phillips M, Oliffe JL: Prostate cancer stories in the Canadian print media: representations of illness, disease and masculinities. Sociol Health Illn; 2009 Mar;31(2):155-69
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  • [Title] Prostate cancer stories in the Canadian print media: representations of illness, disease and masculinities.
  • Despite the popularity of print media as an information source for men with prostate cancer, the representation of prostate cancer within this medium remains relatively understudied.
  • This article details the findings from an analysis of prostate cancer articles published in two Canadian national newspapers, The Globe and Mail and the National Post, from January 2001 through to December 2006.
  • The 817 prostate cancer articles published during this period were retrieved and reviewed using manifest and latent analyses.
  • The latent analysis was guided by the connections between masculinities and prostate cancer in the newspapers' stories.
  • Findings indicated a low frequency of articles that substantively discussed prostate cancer and that the descriptive content reproduced hegemonic masculine ideals, such as competition and stoicism.
  • These findings support how representations of prostate cancer in Canadian newspapers predominately replicate detrimental ideologies and perspectives of men's health.
  • [MeSH-major] Gender Identity. Health Knowledge, Attitudes, Practice. Men's Health. Newspapers as Topic / statistics & numerical data. Prostatic Neoplasms. Social Perception

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  • (PMID = 18983423.001).
  • [ISSN] 1467-9566
  • [Journal-full-title] Sociology of health & illness
  • [ISO-abbreviation] Sociol Health Illn
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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54. Casciani E, Gualdi GF: Prostate cancer: value of magnetic resonance spectroscopy 3D chemical shift imaging. Abdom Imaging; 2006 Jul-Aug;31(4):490-9
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  • [Title] Prostate cancer: value of magnetic resonance spectroscopy 3D chemical shift imaging.
  • The results of recent studies of magnetic resonance imaging (MRI) combined with three-dimensional magnetic resonance spectroscopic imaging (3D-MRSI) demonstrate that the MRI/3D-MRSI exam is a unique method by which to noninvasively study the cellular metabolism and anatomy of the prostate.
  • 3D-MRSI is emerging as the most specificity tool for non-invasive evaluation of the prostate cancer.
  • Assessment of cancer spread outside the prostate can be significantly improved by combining MRI findings with estimates of metabolic abnormalities provided by 3D-MRSI.
  • Clinically, combined MRI/3D-MRSI has already demonstrated a potential for improved diagnosis, staging, and treatment planning for patients with prostate cancer.
  • This article reviewed the value of 3D-MRS imaging for the diagnosis, localization, staging, aggressiveness, and treatment planning of prostate cancer.
  • [MeSH-major] Imaging, Three-Dimensional. Magnetic Resonance Spectroscopy. Prostatic Neoplasms / diagnosis. Prostatitis / diagnosis
  • [MeSH-minor] Biopsy, Needle. Humans. Male. Neoplasm Staging

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  • (PMID = 16955379.001).
  • [ISSN] 0942-8925
  • [Journal-full-title] Abdominal imaging
  • [ISO-abbreviation] Abdom Imaging
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 51
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55. Gallus S, Foschi R, Negri E, Talamini R, Franceschi S, Montella M, Ramazzotti V, Tavani A, Dal Maso L, La Vecchia C: Dietary zinc and prostate cancer risk: a case-control study from Italy. Eur Urol; 2007 Oct;52(4):1052-6
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  • [Title] Dietary zinc and prostate cancer risk: a case-control study from Italy.
  • OBJECTIVES: Zinc concentration is higher in the prostate than in most other tissues.
  • Since information on the role of zinc on prostate carcinogenesis is controversial, we analysed the issue in a case-control study.
  • METHODS: Between 1991 and 2002, we conducted a multicentre hospital-based case-control study on prostate cancer in Italy.
  • Cases included 1294 men with incident, histologically confirmed prostate cancer.
  • The trend in risk was significant for advanced cancers only, the OR being 2.02 (95% CI, 1.14-3.59) for prostate cancers with a high Gleason score.
  • CONCLUSIONS: In this large study we found a direct association between high zinc intake and prostate cancer risk, particularly for advanced cancers.
  • Our findings allow one to exclude a favourable effect of zinc on prostate carcinogenesis.
  • [MeSH-major] Diet. Prostatic Neoplasms / epidemiology. Zinc / adverse effects

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  • [CommentIn] Eur Urol. 2007 Oct;52(4):1056-7 [17292534.001]
  • [CommentIn] Eur Urol. 2007 Oct;52(4):1262-3; author reply 1263-4 [17445972.001]
  • (PMID = 17292532.001).
  • [ISSN] 0302-2838
  • [Journal-full-title] European urology
  • [ISO-abbreviation] Eur. Urol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] J41CSQ7QDS / Zinc
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56. Gunes S, Bagci H, Sarikaya S, Bilen CY, Kara N: Prostate-specific antigen and 17-hydroxylase polymorphic genotypes in patients with prostate cancer and benign prostatic hyperplasia. DNA Cell Biol; 2007 Dec;26(12):873-8
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  • [Title] Prostate-specific antigen and 17-hydroxylase polymorphic genotypes in patients with prostate cancer and benign prostatic hyperplasia.
  • We investigated the association of prostate cancer (PCa) and benign prostatic hyperplasia (BPH) with genetic polymorphisms in prostate-specific antigen (PSA) (-158 G/A) and 17-hydroxylase (CYP17) (-34 T/C) genes in a Turkish population.
  • [MeSH-major] Polymorphism, Genetic. Prostate-Specific Antigen / genetics. Prostatic Hyperplasia / genetics. Prostatic Neoplasms / genetics. Steroid 17-alpha-Hydroxylase / genetics


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

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  • [Copyright] Copyright 2006 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
  • (PMID = 17167821.001).
  • [ISSN] 0022-3417
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / DNA-Binding Proteins; 0 / LIM Domain Proteins; 0 / LMO2 protein, human; 0 / Metalloproteins; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger
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58. Meyer P, Zuern C, Hermanns N, Haak T: The association between paternal prostate cancer and type 2 diabetes. J Carcinog; 2007;6:14
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  • [Title] The association between paternal prostate cancer and type 2 diabetes.
  • However, diabetes mellitus may be a protective factor for prostate cancer since both were found to be negatively associated.
  • Most notably, a lower number of prostate cancers was observed in fathers of diabetic patients (OR 0.47; 95% CI 0.22 to 0.94; p = 0.032).
  • Thus, the observed lower level of history of prostate cancer can be regarded as highly reliable.The analysis of 801 type 2 diabetics and 1267 controls showed that cancer of stomach was elevated among mothers of controls (OR 2.67; p = 0.0106).
  • In accordance with the previous investigation, we again obseved a lower number of prostate cancers in fathers of diabetic patients (OR 0.49; p = 0.0279).However, the application of the statistical method of Mantel-Haenszel showed no significant result concerning any of the cancer histories.
  • CONCLUSION: Fathers of patients suffering from type 2 diabetes were diagnosed less frequently with prostate cancer compared to fathers of non-diabetic controls.
  • As first-degree relatives, e.g. diabetic patients and their fathers, share 50% of their genes, it appears plausible that genetic factors may play an important role in the negative association between diabetes and prostate cancer.
  • However, different statistic analyses showed controversial results concerning the effect of type 2 diabetes on prostate cancers.

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  • (PMID = 17897447.001).
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59. Kuo YF, Goodwin JS, Shahinian VB: Gonadotropin-releasing hormone agonist use in men without a cancer registry diagnosis of prostate cancer. BMC Health Serv Res; 2008 Jul 14;8:146
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  • [Title] Gonadotropin-releasing hormone agonist use in men without a cancer registry diagnosis of prostate cancer.
  • BACKGROUND: Use of gonadotropin-releasing hormone (GnRH) agonists has become popular for virtually all stages of prostate cancer.
  • Such cases may be missed by tumor registries, leading to underestimates of the total extent of GnRH agonist use.
  • METHODS: We used linked Surveillance, Epidemiology and End-Results (SEER)-Medicare data from 1993 through 2001 to identify GnRH agonist use in men with either a diagnosis of prostate cancer registered in SEER, or with a diagnosis of prostate cancer based only on Medicare claims (from the 5% control sample of Medicare beneficiaries residing in SEER areas without a registered diagnosis of cancer).
  • The proportion of incident GnRH agonist users without a registry diagnosis of prostate cancer was calculated.
  • Factors associated with lack of a registry diagnosis were examined in multivariable analyses.
  • RESULTS: Of incident GnRH agonist users, 8.9% had no diagnosis of prostate cancer registered in SEER.
  • In a multivariable logistic regression model, lack of a registry diagnosis of prostate cancer in GnRH agonist users was significantly more likely with increasing comorbidity, whereas it was less likely in men who had undergone either inpatient admission or procedures such as radical prostatectomy, prostate biopsy, or transurethral resection of the prostate.
  • CONCLUSION: Reliance solely on tumor registry data may underestimate the rate of GnRH agonist use in men with prostate cancer.

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  • (PMID = 18620606.001).
  • [ISSN] 1472-6963
  • [Journal-full-title] BMC health services research
  • [ISO-abbreviation] BMC Health Serv Res
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA116758-03; United States / NCI NIH HHS / CA / CA116758-04; United States / NCI NIH HHS / CA / CA116758-01; United States / NCI NIH HHS / CA / R01CA116758; United States / NCI NIH HHS / CA / R01 CA116758-04; United States / NCI NIH HHS / CA / R01 CA116758-01; United States / NCI NIH HHS / CA / R01 CA116758; United States / NCI NIH HHS / CA / CA116758-02; United States / NCI NIH HHS / CA / R01 CA116758-02; United States / NCI NIH HHS / CA / P50CA105631; United States / NCI NIH HHS / CA / P50 CA105631; United States / NCI NIH HHS / CA / CA116758-03
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 33515-09-2 / Gonadotropin-Releasing Hormone
  • [Other-IDs] NLM/ PMC2483971
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60. Gitenay D, Baron VT: Is EGR1 a potential target for prostate cancer therapy? Future Oncol; 2009 Sep;5(7):993-1003
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  • [Title] Is EGR1 a potential target for prostate cancer therapy?
  • Prostate cancer is a major cause of cancer-related death in American men, for which finding new therapeutic strategies remains a challenge.
  • Although it has long been considered a tumor suppressor, a wealth of new evidence shows that EGR1 promotes the progression of prostate cancer.
  • While EGR1 mediates apoptosis in response to stress and DNA damage by regulating a tumor suppressor network, it also promotes the proliferation of prostate cancer cells by a mechanism that is not fully understood.
  • Thus, EGR1 might be targeted for prostate cancer therapy either by ectopic expression in combination with radiotherapy or chemotherapy, or by direct inhibition for systemic treatment.

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  • (PMID = 19792968.001).
  • [ISSN] 1744-8301
  • [Journal-full-title] Future oncology (London, England)
  • [ISO-abbreviation] Future Oncol
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA102688-05; United States / NCI NIH HHS / CA / R01 CA102688; United States / NCI NIH HHS / CA / R01 CA102688-05; United States / NCI NIH HHS / CA / R01-CA102688
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Early Growth Response Protein 1
  • [Number-of-references] 98
  • [Other-IDs] NLM/ NIHMS155263; NLM/ PMC2776080
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61. Briganti A, Chun FK, Suardi N, Gallina A, Walz J, Graefen M, Shariat S, Ebersdobler A, Rigatti P, Perrotte P, Saad F, Montorsi F, Huland H, Karakiewicz PI: Prostate volume and adverse prostate cancer features: fact not artifact. Eur J Cancer; 2007 Dec;43(18):2669-77
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  • [Title] Prostate volume and adverse prostate cancer features: fact not artifact.
  • PURPOSE: A recent prostate cancer finasteride chemoprevention trial showed a higher rate of sextant biopsy-detected high grade prostate cancer (HGPCa) in finasteride exposed men, whose prostates were significantly smaller than those of controls.
  • We investigated the association between prostate size and prostate cancer grade and stage in a large (n=3412) single center radical prostatectomy cohort, which was unexposed to any form of hormonal manipulation.
  • RESULTS: Small prostates were associated with higher rate of HGPCa at biopsy and at radical prostatectomy (both p<0.001), with higher rate of extracapsular extension (p<0.001), seminal vesicle invasion (p<0.001) and with tumor volume >3.4 cc, after accounting for age, PSA, clinical stage and year of surgery.
  • CONCLUSIONS: Our findings demonstrate that prostate cancers located in small glands are fundamentally more aggressive than those located within larger glands.
  • In consequence, prostate cancer detection and treatment strategies should account for prostate volume.
  • [MeSH-major] Prostate / pathology. Prostatectomy / statistics & numerical data. Prostatic Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Biopsy. Humans. Male. Middle Aged. Neoplasm Invasiveness / pathology. Organ Size. Regression Analysis. Seminal Vesicles / pathology


62. Rostad K, Mannelqvist M, Halvorsen OJ, Oyan AM, Bø TH, Stordrange L, Olsen S, Haukaas SA, Lin B, Hood L, Jonassen I, Akslen LA, Kalland KH: ERG upregulation and related ETS transcription factors in prostate cancer. Int J Oncol; 2007 Jan;30(1):19-32
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  • [Title] ERG upregulation and related ETS transcription factors in prostate cancer.
  • The aim of this study was to identify and validate differentially expressed genes in matched pairs of benign and malignant prostate tissue.
  • Samples included 29 histologically verified primary tumors and 23 benign controls.
  • Among the genes most consistently and highly upregulated in prostate cancer was the ETS family transcription factor ERG (ETS related gene).
  • This finding was validated in an expanded patient series (37 tumors and 38 benign samples) using DNA oligonucleotide microarray and real-time quantitative PCR assays.
  • ERG was 20- to more than 100-fold overexpressed in prostate cancer compared with benign prostate tissue in more than 50% of patients according to quantitative PCR.
  • Surprisingly, ERG mRNA levels were found to be significantly higher in the endothelial cell line, HUVEC, than in the prostate cell lines PC3, DU145 and LNCaP.
  • In situ hybridization of prostate cancer tissue revealed that ERG was abundantly expressed in both prostate cancer cells and associated endothelial cells.
  • The consistency and magnitude of ERG overexpression in prostate cancer appeared unique, but several related ETS transcription factors were also overexpressed in matched pairs of tumor and benign samples, whereas ETS2 was significantly underexpressed.
  • Our findings support the hypothesis that ERG overexpression and related ETS transcription factors are important for early prostate carcinogenesis.
  • [MeSH-major] DNA-Binding Proteins / genetics. Gene Expression Regulation, Neoplastic. Prostatic Neoplasms / genetics. Proto-Oncogene Proteins c-ets / genetics. Trans-Activators / genetics
  • [MeSH-minor] DNA Primers. Humans. In Situ Hybridization. Male. Oligonucleotide Array Sequence Analysis. Polymerase Chain Reaction. Prostate / physiology. Prostatectomy

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  • (PMID = 17143509.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / DNA Primers; 0 / DNA-Binding Proteins; 0 / ERG protein, human; 0 / Proto-Oncogene Proteins c-ets; 0 / Trans-Activators
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63. Zhang P, Wang ZM, Chong T, Zhao LH: [Analysis of reference range responsible to normal percent value of free prostate specific antigen from men without prostate disease]. Sichuan Da Xue Xue Bao Yi Xue Ban; 2007 Sep;38(5):871-3, 903
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  • [Title] [Analysis of reference range responsible to normal percent value of free prostate specific antigen from men without prostate disease].
  • OBJECTIVE: To study the effect of age on the percent value for free prostate specific antigen (fPSA) from men, and the relationships between the percent fPSA and the pathological grade or the clinical stage of prostate cancer (PCa), and also to determine appropriate reference value range for Chinese men.
  • Out of 713, 679 men without prostate disease were divided into 5 groups by age, and then the relationships were studied between man age and PSA, fPSA or percent fPSA, respectively.
  • With the help of the related data of men without prostate disease, the appropriate reference value range was established for Chinese men.
  • According to the data of our early studies and the reference value range of percent fPSA given by the test kit and the previously reported medical references, the data of 10%, 15% and 20% were selected as the percent fPSA threshold values to distinguish PCa or health men without prostate disease.
  • CONCLUSION: The percent fPSA may be more useful than PSA in the detection of prostate cancer.
  • The reference range of > or = 15% percent fPSA is more appropriate threshold value for diagnosing the prostate cancer in Chinese man population.
  • [MeSH-major] Prostate-Specific Antigen / blood
  • [MeSH-minor] Adult. Age Factors. Aged. Biomarkers, Tumor / blood. Humans. Male. Middle Aged. Neoplasm Staging. Prostatic Neoplasms / blood. Prostatic Neoplasms / diagnosis. Prostatic Neoplasms / pathology. Reference Values. Sensitivity and Specificity

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  • (PMID = 17953381.001).
  • [ISSN] 1672-173X
  • [Journal-full-title] Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition
  • [ISO-abbreviation] Sichuan Da Xue Xue Bao Yi Xue Ban
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 3.4.21.77 / Prostate-Specific Antigen
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64. Yang WB, Cai F, Cheng CT, Cao G, Qing ZY: [Role of prostate stem cell antigen in human pancreatic carcinoma: a tissue microarray-based study]. Nan Fang Yi Ke Da Xue Xue Bao; 2009 Oct;29(10):2135-7
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  • [Title] [Role of prostate stem cell antigen in human pancreatic carcinoma: a tissue microarray-based study].
  • OBJECTIVE: To investigate the expression of prostate stem cell antigen (PSCA) in human pancreatic carcinoma and explore its role in the oncogenesis of pancreatic cancer.
  • RESULTS: The positivity rate of PSCA in pancreatic carcinoma was 79.5% (62/78), and PSCA staining was more intense in the malignant cells than in the benign cells (chi2=15.81, P<0.005) and chronic pancreatitis tissues (chi2=11.33, P<0.005).
  • No obvious association was found between PSCA expression and the other variables of pancreatic carcinoma (including gender, age at surgery, tumor grade, and TNM stages).
  • CONCLUSION: The expression of PSCA can be related to the development of pancreatic cancer, but not to the clinicopathological factors of the tumor.
  • [MeSH-major] Antigens, Neoplasm / metabolism. Carcinoma, Ductal / metabolism. Neoplasm Proteins / metabolism. Pancreatic Neoplasms / metabolism. Tissue Array Analysis / methods

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  • (PMID = 19861285.001).
  • [ISSN] 1673-4254
  • [Journal-full-title] Nan fang yi ke da xue xue bao = Journal of Southern Medical University
  • [ISO-abbreviation] Nan Fang Yi Ke Da Xue Xue Bao
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / GPI-Linked Proteins; 0 / Neoplasm Proteins; 0 / PSCA protein, human
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65. Davis JW, Nakanishi H, Kumar VS, Bhadkamkar VA, McCormack R, Fritsche HA, Handy B, Gornet T, Babaian RJ: Circulating tumor cells in peripheral blood samples from patients with increased serum prostate specific antigen: initial results in early prostate cancer. J Urol; 2008 Jun;179(6):2187-91; discussion 2191
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  • [Title] Circulating tumor cells in peripheral blood samples from patients with increased serum prostate specific antigen: initial results in early prostate cancer.
  • PURPOSE: We evaluated the hypothesis that circulating tumor cells as determined using the CellSearch System would correlate with tumor volume, pathological stage and Gleason score in men with localized prostate cancer.
  • MATERIALS AND METHODS: Samples of blood (30 ml) were drawn from 97 men with localized prostate cancer before radical prostatectomy, on postoperative days 2 to 3 and at 6 weeks.
  • A control group consisted of 25 men with an increased prostate specific antigen and no tumor detected on extended prostate biopsy.
  • Samples were analyzed for circulating tumor cells using the CellSearch System.
  • RESULTS: Circulating tumor cells were detected in 21% of patients with cancer and 20% of controls (p = 0.946).
  • At 6 weeks after prostatectomy circulating tumor cells were detected in 16% and 11% (p = 0.51) of the men positive and negative for circulating tumor cells at baseline, respectively.
  • Of the 20 patients with cancer who had circulating tumor cells at baseline 18 showed no circulating tumor cells after surgery.
  • Circulating tumor cell values did not correlate with tumor volume, pathological stage or Gleason score.
  • Only 3.1% of the men with cancer and 8% of the control group had 3 or more circulating tumor cells per 22.5 ml blood at baseline.
  • CONCLUSIONS: In metastatic breast, prostate and other cancers more than 5 circulating tumor cells are often detected using the CellSearch System, and may correlate with prognosis.
  • However, in the setting of localized prostate cancer the number of detectable circulating tumor cells was low, with findings comparable to those in men who were biopsy negative for cancer.
  • We found no correlation between the number of circulating tumor cells and known prognostic factors in this population.
  • [MeSH-major] Neoplastic Cells, Circulating. Prostate-Specific Antigen / blood. Prostatic Neoplasms / blood. Prostatic Neoplasms / pathology


66. Toles CA: Black men are dying from prostate cancer. ABNF J; 2008;19(3):92-5
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  • [Title] Black men are dying from prostate cancer.
  • Prostate cancer is the most frequently diagnosed cancer in the United States, accounting for 33% of all cancer cases among men (American Cancer Society, 2004).
  • In the United States the number of new cases of prostate cancer was estimated at 230,110 and 29,900 will die (American Cancer Society, 2004).
  • Black men (African-American) are 2.5 times more likely to die of prostate cancer than White men (Peters, 2005).
  • [MeSH-major] African Americans / ethnology. African Americans / statistics & numerical data. Prostatic Neoplasms / ethnology. Prostatic Neoplasms / mortality
  • [MeSH-minor] Attitude to Health / ethnology. Cause of Death. Digital Rectal Examination. European Continental Ancestry Group / ethnology. Food Habits / ethnology. Health Education. Health Knowledge, Attitudes, Practice. Health Planning Guidelines. Health Services Needs and Demand. Health Status Disparities. Healthcare Disparities. Humans. Male. Mass Screening. Primary Prevention. Prostate-Specific Antigen. Risk Factors. Social Class. United States / epidemiology

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  • (PMID = 18717207.001).
  • [ISSN] 1046-7041
  • [Journal-full-title] The ABNF journal : official journal of the Association of Black Nursing Faculty in Higher Education, Inc
  • [ISO-abbreviation] ABNF J
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] EC 3.4.21.77 / Prostate-Specific Antigen
  • [Number-of-references] 32
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67. Hooker S, Bonilla C, Akereyeni F, Ahaghotu C, Kittles RA: NAT2 and NER genetic variants and sporadic prostate cancer susceptibility in African Americans. Prostate Cancer Prostatic Dis; 2008;11(4):349-56
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  • [Title] NAT2 and NER genetic variants and sporadic prostate cancer susceptibility in African Americans.
  • Prostate cancer is a common malignancy that disproportionately affects African-American men.
  • Fourteen single nucleotide polymorphisms in NAT2 and four NER genes (ERCC1, XPF/ERCC4, XPG/ERCC5 and CSB/ERCC6) were genotyped in a case-control study of 254 African-American prostate cancer cases and 301 healthy controls from Washington, DC.
  • We found that individuals homozygous for the XPG/ERCC5 -72C/T promoter polymorphism had a significant reduction in risk, for prostate cancer (OR=0.12; 95% CI=0.03-0.48).
  • The protective effect of the promoter SNP on risk for prostate cancer was independent of smoking.
  • We note that there may be other factors, such as dietary exposures, which may modulate prostate cancer risk in combination with genetic variation within the NAT2 and NER genes.
  • Our results, in combination with previous observations of LOH for ERCC5 in prostate tumors, provide further evidence for a role of XPG/ERCC5 in the etiology of prostate cancer.
  • [MeSH-major] African Americans / ethnology. African Americans / genetics. Arylamine N-Acetyltransferase / genetics. Polymorphism, Single Nucleotide / genetics. Prostatic Neoplasms / ethnology. Prostatic Neoplasms / genetics. Receptors, Cytoplasmic and Nuclear / genetics

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  • (PMID = 18026184.001).
  • [ISSN] 1476-5608
  • [Journal-full-title] Prostate cancer and prostatic diseases
  • [ISO-abbreviation] Prostate Cancer Prostatic Dis.
  • [Language] eng
  • [Grant] United States / NIGMS NIH HHS / GM / S06GM08016
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Genetic Markers; 0 / Orphan Nuclear Receptors; 0 / Receptors, Cytoplasmic and Nuclear; 0 / liver X receptor; EC 2.3.1.5 / Arylamine N-Acetyltransferase; EC 2.3.1.5 / NAT2 protein, human
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68. Fernando HS, Sanders AJ, Kynaston HG, Jiang WG: WAVE3 is associated with invasiveness in prostate cancer cells. Urol Oncol; 2010 May-Jun;28(3):320-7
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  • [Title] WAVE3 is associated with invasiveness in prostate cancer cells.
  • We investigated the expression pattern and the effects of manipulating endogenous WAVE3 expression in prostate cancer cells.
  • MATERIALS AND METHODS: Reverse transcriptase-polymerase chain reaction (RT-PCR) of prostate cell lines and immunohistochemical staining of normal and cancer specimens for WAVE3 proteins were done.
  • Immunohistochemistry of prostate tissue specimens showed that the cytoplasm of cancer cells had stronger staining than normal epithelium.
  • CONCLUSIONS: This is the first report on the expression patterns and the functions of WAVE3 in prostate cancer cell lines.
  • This study shows that WAVE3 is pivotal in controlling the invasiveness of prostate cancer cells.
  • Further work is needed to assess WAVE3 as a potential marker for predicting tumor aggressiveness.
  • [MeSH-major] Neoplasm Invasiveness / genetics. Prostatic Neoplasms / genetics. Prostatic Neoplasms / pathology. Wiskott-Aldrich Syndrome Protein Family / biosynthesis
  • [MeSH-minor] Blotting, Western. Cell Adhesion / genetics. Cell Line, Tumor. Cell Proliferation. Gene Expression. Gene Knockdown Techniques. Humans. Immunohistochemistry. Male. Reverse Transcriptase Polymerase Chain Reaction. Transfection

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  • [Copyright] Copyright (c) 2010 Elsevier Inc. All rights reserved.
  • (PMID = 19395286.001).
  • [ISSN] 1873-2496
  • [Journal-full-title] Urologic oncology
  • [ISO-abbreviation] Urol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / WASF3 protein, human; 0 / Wiskott-Aldrich Syndrome Protein Family
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69. Kogan I, Goldfinger N, Milyavsky M, Cohen M, Shats I, Dobler G, Klocker H, Wasylyk B, Voller M, Aalders T, Schalken JA, Oren M, Rotter V: hTERT-immortalized prostate epithelial and stromal-derived cells: an authentic in vitro model for differentiation and carcinogenesis. Cancer Res; 2006 Apr 1;66(7):3531-40
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  • [Title] hTERT-immortalized prostate epithelial and stromal-derived cells: an authentic in vitro model for differentiation and carcinogenesis.
  • Prostate cancer is the most commonly diagnosed type of cancer in men, and there is no available cure for patients with advanced disease.
  • In vitro model systems are urgently required to permit the study of human prostate cell differentiation and malignant transformation.
  • Unfortunately, human prostate cells are particularly difficult to convert into continuously growing cultures.
  • We report here the successful immortalization without viral oncogenes of prostate epithelial cells and, for the first time, prostate stromal cells.
  • These cells exhibit a significant pattern of authentic prostate-specific features.
  • In particular, the epithelial cell culture is able to differentiate into glandular buds that closely resemble the structures formed by primary prostate epithelial cells.
  • The stromal cells have typical characteristics of prostate smooth muscle cells.
  • These immortalized cultures may serve as a unique experimental platform to permit several research directions, including the study of cell-cell interactions in an authentic prostate microenvironment, prostate cell differentiation, and most significantly, the complex multistep process leading to prostate cell transformation.
  • [MeSH-major] Cell Transformation, Neoplastic / metabolism. Cell Transformation, Neoplastic / pathology. DNA-Binding Proteins / physiology. Prostate / cytology. Prostate / metabolism. Prostatic Neoplasms / metabolism. Prostatic Neoplasms / pathology. Telomerase / physiology
  • [MeSH-minor] Aged. Cell Differentiation / physiology. Cell Line, Tumor. Cells, Cultured. Cyclin-Dependent Kinase Inhibitor p16 / biosynthesis. Cyclin-Dependent Kinase Inhibitor p16 / genetics. Epithelial Cells / cytology. Epithelial Cells / metabolism. Epithelial Cells / physiology. Humans. Male. Stromal Cells / cytology. Stromal Cells / metabolism. Stromal Cells / physiology. Transfection. Tumor Suppressor Protein p53 / biosynthesis. Tumor Suppressor Protein p53 / genetics

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  • (PMID = 16585177.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / DNA-Binding Proteins; 0 / TP53 protein, human; 0 / Tumor Suppressor Protein p53; EC 2.7.7.49 / Telomerase
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70. Ross LE, Powe BD, Taylor YJ, Howard DL: Physician-patient discussions with african american men about prostate cancer screening. Am J Mens Health; 2008 Jun;2(2):156-64
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  • [Title] Physician-patient discussions with african american men about prostate cancer screening.
  • Prostate cancer is the second leading cancer killer in men.
  • Men in general and African American men in particular face crucial decisions regarding prostate cancer screening and perhaps treatment for this disease.
  • Major health organizations agree that men should discuss prostate cancer screening with their physicians or other health care professionals.
  • The purpose of the study was to examine sociodemographic and other correlates of physician-patient discussions regarding the advantages and disadvantages of the prostate-specific antigen (PSA) test among African American men aged 40 or older.
  • A majority of African American men reported having discussed the advantages and disadvantages of prostate cancer screening and/or testing with their physicians before ordering it, and physician-patient discussions about the PSA test were associated with increased screening in African American men.
  • Inasmuch as African American men have greater prostate cancer incidence and mortality over other groups, future attempts should be made to find meaningful correlates of PSA screening and test use to help reduce the burden of this disease.
  • [MeSH-major] African Americans / statistics & numerical data. Health Knowledge, Attitudes, Practice. Mass Screening / standards. Prostatic Neoplasms / ethnology. Prostatic Neoplasms / prevention & control
  • [MeSH-minor] Adult. Age Factors. Aged. Communication. Confidence Intervals. Cross-Sectional Studies. Educational Status. Health Education / organization & administration. Humans. Male. Men's Health. Middle Aged. Multivariate Analysis. Odds Ratio. Physician-Patient Relations. Prostate-Specific Antigen / blood. Risk Assessment. Socioeconomic Factors. Survival Analysis. United States / epidemiology


71. Chavarro JE, Stampfer MJ, Hall MN, Sesso HD, Ma J: A 22-y prospective study of fish intake in relation to prostate cancer incidence and mortality. Am J Clin Nutr; 2008 Nov;88(5):1297-303
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  • [Title] A 22-y prospective study of fish intake in relation to prostate cancer incidence and mortality.
  • BACKGROUND: Fish and seafood n-3 fatty acids may prevent or delay the progression of prostate cancer, but epidemiologic studies do not uniformly support this hypothesis.
  • OBJECTIVE: We examined the relation of fish and seafood n-3 fatty acid intakes with prostate cancer incidence and mortality.
  • RESULTS: During 382 144 person-years of follow-up, 2161 men were diagnosed with prostate cancer and 230 died of prostate cancer.
  • Fish intake was unrelated to prostate cancer incidence.
  • Survival analysis among the men diagnosed with prostate cancer revealed that those consuming fish >or=5 times/wk had a 48% lower risk of prostate cancer death than did men consuming fish less than once weekly [relative risk (RR) = 0.52; 95% CI: 0.30, 0.91; P for trend = 0.05].
  • A similar association was found between seafood n-3 fatty acid intake and prostate cancer mortality (RR(Q5 versus Q1) = 0.64; 95% CI: 0.42, 0.99; P for trend = 0.02).
  • CONCLUSION: These results suggest that fish intake is unrelated to prostate cancer incidence but may improve prostate cancer survival.

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  • (PMID = 18996866.001).
  • [ISSN] 1938-3207
  • [Journal-full-title] The American journal of clinical nutrition
  • [ISO-abbreviation] Am. J. Clin. Nutr.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA042182-20; United States / NCI NIH HHS / CA / CA042182-20; United States / NCI NIH HHS / CA / CA058684-13; United States / NCI NIH HHS / CA / R01 CA090598; United States / NCI NIH HHS / CA / R01 CA058684-13; United States / NCI NIH HHS / CA / CA090598-05S1; United States / NCI NIH HHS / CA / R01 CA058684; United States / NCI NIH HHS / CA / R01 CA042182; United States / NCI NIH HHS / CA / R01 CA090598-05S1
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Fatty Acids, Omega-3
  • [Other-IDs] NLM/ NIHMS180899; NLM/ PMC2843087
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72. Albertsen PC: Treatment of localized prostate cancer: when is active surveillance appropriate? Nat Rev Clin Oncol; 2010 Jul;7(7):394-400
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Treatment of localized prostate cancer: when is active surveillance appropriate?
  • Testing for prostate-specific antigen (PSA) has caused a dramatic increase in the incidence of prostate cancer during the past two decades.
  • Data from a recently reported randomized trial indicate that as many as 48 men must undergo treatment to prevent one prostate cancer-related death.
  • To date, prostate cancer-specific survival is over 99%.
  • For men harboring tumors with a Gleason score >7, data from two recently reported Swedish trials suggest lower prostate cancer-related mortality for those men receiving either surgery or radiation.
  • [MeSH-major] Prostatic Neoplasms / diagnosis. Prostatic Neoplasms / therapy
  • [MeSH-minor] Digital Rectal Examination. Disease Progression. Humans. Male. Prognosis. Prostate-Specific Antigen / blood. Risk Assessment. Survival Rate


73. Pace G, Pomante R, Vicentini C: Sarcoma of prostate: case report and review of the literature. Arch Ital Urol Androl; 2010 Jun;82(2):105-8
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  • [Title] Sarcoma of prostate: case report and review of the literature.
  • OBJECTIVES: Prostate sarcomas are rare entity, the most common is leiomyosarcoma which account for 0.1% of all prostate malignancies.
  • The overall survival rate remains poor regardless of initial tumour size, grade or histological subtype.
  • Immunohistochemistry reveals tumour cells diffusely positive for vimentin, smooth muscle actin, focally positive for progesterone receptor, whilst keratins are usually negative.
  • MATERIALS AND METHODS: We describe a case of a patient affected by sarcoma of prostate.
  • Furthermore, we reviewed the cases of prostate sarcomas available in literature to clarify the best therapeutic options to be applied.
  • CONCLUSIONS: Prostate sarcomas are highly aggressive, with limited therapeutic options.
  • An early diagnosis and complete surgical excision with negative margins offer patients the long-term disease free survival.

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  • (PMID = 20812534.001).
  • [ISSN] 1124-3562
  • [Journal-full-title] Archivio italiano di urologia, andrologia : organo ufficiale [di] Societa italiana di ecografia urologica e nefrologica
  • [ISO-abbreviation] Arch Ital Urol Androl
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Italy
  • [Number-of-references] 27
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74. Skaudickas D, Kondrotas AJ, Kevelaitis E, Venskutonis PR: The effect of Echinacea purpurea (L.) Moench extract on experimental prostate hyperplasia. Phytother Res; 2009 Oct;23(10):1474-8
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  • [Title] The effect of Echinacea purpurea (L.) Moench extract on experimental prostate hyperplasia.
  • Moench) on the prostate gland of rats using an experimental model of benign prostate hyperplasia (BPH).
  • The animals were administered 50 mg/kg of extract preparation for 4 and 8 weeks and the prostate mass and structural degenerative changes were evaluated in the course of the experiment.
  • The administration of E. purpurea extract to rats with hyperplasia for 4 and 8 weeks gradually and significantly reduced the prostate mass and reversed the degenerative changes in the structure of the prostate gland.
  • [MeSH-major] Echinacea. Phytotherapy. Plant Extracts / therapeutic use. Prostate / drug effects. Prostatic Hyperplasia / drug therapy

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  • [Copyright] (c) 2009 John Wiley & Sons, Ltd.
  • (PMID = 19288499.001).
  • [ISSN] 1099-1573
  • [Journal-full-title] Phytotherapy research : PTR
  • [ISO-abbreviation] Phytother Res
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Plant Extracts
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75. Knight SJ, Latini DM: Sexual side effects and prostate cancer treatment decisions: patient information needs and preferences. Cancer J; 2009 Jan-Feb;15(1):41-4
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  • [Title] Sexual side effects and prostate cancer treatment decisions: patient information needs and preferences.
  • Prostate cancer treatment decision making requires complex trade-offs among treatment outcomes, and sexual function is a central consideration for most men.
  • Although sexual function is included in prostate cancer decision models, survival and fear of recurrence and cancer progression weigh more heavily in these decisions for many men than concerns about treatment impact on sexuality.
  • In this article, we discuss the importance of sexuality in men's treatment decisions for prostate cancer.
  • We focus on men's preferences for maintaining sexual function and their needs for information about the risk of sexual side effects with prostate cancer treatment.
  • Our review suggests that among men diagnosed with prostate cancer sexual function is less important to men than concerns about survival, but is more highly valued than other side effects and treatment characteristics.
  • However, there is evidence that concerns about sexuality are not in proportion with the associated risk for sexual problems with prostate cancer treatment and men acknowledge unmet needs for information about sexuality in making prostate cancer treatment decisions.
  • [MeSH-major] Needs Assessment. Patient Education as Topic. Prostatic Neoplasms / therapy. Sexual Dysfunction, Physiological / etiology


76. Ruhayel Y, Giwercman A, Ulmert D, Rylander L, Bjartell A, Manjer J, Berglund G, Giwercman YL: Male infertility and prostate cancer risk: a nested case-control study. Cancer Causes Control; 2010 Oct;21(10):1635-43
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  • [Title] Male infertility and prostate cancer risk: a nested case-control study.
  • The pathogenesis of prostate cancer is unclear, although experimental evidence implicates androgens as playing an important role.
  • Infertile men frequently suffer from some degree of hypogonadism and may hence be hypothesized to be at lower risk of developing prostate cancer than fertile men.
  • To test this hypothesis, we conducted a case-control study nested within "the Malmö Diet and Cancer Study" cohort in Sweden, inviting 661 prostate cancer cases and 661 age-matched controls to participate.
  • Thus, 891 men were included, providing 445 prostate cancer cases and 446 controls.
  • Logistic regression showed that the infertile men were at significantly lower risk of being diagnosed with prostate cancer than the fertile men (odds ratio, 0.45; 95% confidence interval, 0.25-0.83).
  • We conclude that enduring male infertility is associated with a reduced prostate cancer risk, thus corroborating the theory that normal testicular function, and hence most probably sufficient steroidogenesis, is an important contributing factor to the later development of this malignancy.
  • [MeSH-major] Fertility. Infertility, Male. Prostatic Neoplasms / epidemiology


77. Cai J, Kandagatla P, Singareddy R, Kropinski A, Sheng S, Cher ML, Chinni SR: Androgens Induce Functional CXCR4 through ERG Factor Expression in TMPRSS2-ERG Fusion-Positive Prostate Cancer Cells. Transl Oncol; 2010 Jun 01;3(3):195-203
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  • [Title] Androgens Induce Functional CXCR4 through ERG Factor Expression in TMPRSS2-ERG Fusion-Positive Prostate Cancer Cells.
  • TMPRSS2-ERG fusion transcripts have been shown to be expressed in a majority of prostate cancer (PC) patients because of chromosomal translocations or deletions involving the TMPRSS2 gene promoter and the ERG gene coding sequence.
  • We and others have shown that chemokine receptor CXCR4 expression is upregulated in PC tumor cells, and its ligand, CXCL12, is expressed in bone stromal cells.
  • Results of the current study show that 1) prostate tumor cells coexpress higher ERG and CXCR4 compared with benign tissue, 2) CXCR4 expression is increased in the TMPRSS2-ERG fusion-positive cell line, 3) ERG transcription factor binds to the CXCR4 gene promoter, 4) synthetic androgen (R1881) upregulates both ERG and CXCR4 in TMPRSS2-ERG fusion-positive VCaP cells, 5) small interfering RNA-mediated down-regulation of ERG resulted in the loss of androgen-dependent regulation of CXCR4 expression in VCaP cells, and 6) R1881-activated TMPRSS2-ERG expression functionally activates CXCR4 in VCaP cells.
  • These findings provide a link between TMPRSS2-ERG translocations and enhanced metastasis of tumor cells through CXCR4 function in PC cells.

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  • [Cites] Mol Endocrinol. 1996 Dec;10(12):1582-94 [8961268.001]
  • (PMID = 20563261.001).
  • [ISSN] 1936-5233
  • [Journal-full-title] Translational oncology
  • [ISO-abbreviation] Transl Oncol
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA151557
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2887649
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78. Rouvière O: [MRI of the prostate: optimization of imaging protocols]. J Radiol; 2006 Feb;87(2 Pt 2):210-21
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  • [Title] [MRI of the prostate: optimization of imaging protocols].
  • [Transliterated title] IRM de la prostate: optimisation des protocoles techniques.
  • This article details the imaging protocols for prostate MRI and the influence on image quality of each particular setting: type of coils to be used (endorectal or external phased-array coils?
  • [MeSH-major] Adenocarcinoma / diagnosis. Magnetic Resonance Imaging / methods. Neoplasm Recurrence, Local / diagnosis. Prostatic Neoplasms / diagnosis
  • [MeSH-minor] Aged. Artifacts. Biopsy. Clinical Protocols. Contrast Media. Follow-Up Studies. Humans. Image Enhancement. Lymphatic Metastasis / diagnosis. Male. Positron-Emission Tomography. Prostate / pathology. Prostatectomy. Time Factors. Treatment Outcome. Ultrasonic Therapy

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  • (PMID = 16484946.001).
  • [ISSN] 0221-0363
  • [Journal-full-title] Journal de radiologie
  • [ISO-abbreviation] J Radiol
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Contrast Media
  • [Number-of-references] 42
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79. Schostak M, Christoph F, Schrader M, Panick M, Lingnau A, Miller K: [Prostate biopsy -- practical examination of the adequacy of Chen's virtual strategy]. Aktuelle Urol; 2005 Apr;36(2):149-53
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  • [Title] [Prostate biopsy -- practical examination of the adequacy of Chen's virtual strategy].
  • [Transliterated title] Prostatabiopsie -- Chens virtuelles Schema in der Praxis.
  • INTRODUCTION: Prostate sextant biopsy is considered the gold standard of invasive prostate cancer diagnostics.
  • MATERIAL AND METHOD: Ultrasound-guided ten-core prostate biopsies are performed in our department.
  • Following the model of Chen, three prostate biopsies instead of on are taken from the middle plane.
  • RESULTS: Between July 2003 and February 2004, 191 patients scheduled for a 10-core prostate biopsy were included in the study.
  • Altogether, the prostate carcinoma was detected only by the additional biopsies in 6 patients (9.8 %).
  • [MeSH-major] Biopsy, Needle / methods. Computer Simulation. Endosonography. Imaging, Three-Dimensional. Prostate / pathology. Prostatic Neoplasms / pathology. User-Computer Interface
  • [MeSH-minor] Aged. Humans. Male. Middle Aged. Neoplasm Staging. Sensitivity and Specificity

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  • (PMID = 15902576.001).
  • [ISSN] 0001-7868
  • [Journal-full-title] Aktuelle Urologie
  • [ISO-abbreviation] Aktuelle Urol
  • [Language] ger
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] Germany
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80. Tomlins SA, Rhodes DR, Perner S, Dhanasekaran SM, Mehra R, Sun XW, Varambally S, Cao X, Tchinda J, Kuefer R, Lee C, Montie JE, Shah RB, Pienta KJ, Rubin MA, Chinnaiyan AM: Recurrent fusion of TMPRSS2 and ETS transcription factor genes in prostate cancer. Science; 2005 Oct 28;310(5748):644-8
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  • [Title] Recurrent fusion of TMPRSS2 and ETS transcription factor genes in prostate cancer.
  • Two ETS transcription factors, ERG and ETV1, were identified as outliers in prostate cancer.
  • We identified recurrent gene fusions of the 5' untranslated region of TMPRSS2 to ERG or ETV1 in prostate cancer tissues with outlier expression.
  • By using fluorescence in situ hybridization, we demonstrated that 23 of 29 prostate cancer samples harbor rearrangements in ERG or ETV1.
  • Cell line experiments suggest that the androgen-responsive promoter elements of TMPRSS2 mediate the overexpression of ETS family members in prostate cancer.
  • These results have implications in the development of carcinomas and the molecular diagnosis and treatment of prostate cancer.
  • [MeSH-major] DNA-Binding Proteins / genetics. Membrane Proteins / genetics. Neoplasm Proteins / genetics. Oncogene Proteins, Fusion / genetics. Prostatic Neoplasms / genetics. Serine Endopeptidases / genetics. Trans-Activators / genetics. Transcription Factors / genetics
  • [MeSH-minor] Androgens / metabolism. Cell Line, Tumor. Gene Expression Regulation, Neoplastic. Gene Rearrangement. Humans. In Situ Hybridization, Fluorescence. Male. Molecular Sequence Data. Polymerase Chain Reaction. Translocation, Genetic


81. Yamashita S, Takahashi S, McDonell N, Watanabe N, Niwa T, Hosoya K, Tsujino Y, Shirai T, Ushijima T: Methylation silencing of transforming growth factor-beta receptor type II in rat prostate cancers. Cancer Res; 2008 Apr 1;68(7):2112-21
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  • [Title] Methylation silencing of transforming growth factor-beta receptor type II in rat prostate cancers.
  • To identify methylation-silenced genes in prostate cancers, a microarray analysis for genes up-regulated by treatment with a demethylating agent, 5-aza-2'-deoxycytidine, was performed using three rat prostate cancer cell lines.
  • From the eight genes, Tgfbr2, a key mediator of transforming growth factor-beta (TGF-beta) signaling that has been strongly implicated in human and rat prostate carcinogenesis, was selected, and its silencing in primary samples was analyzed further.
  • Tgfbr2 was methylated and markedly down-regulated in three of seven 3,2'-dimethyl-4-aminobiphenyl-induced invasive adenocarcinomas in the dorsolateral lobe of the rat prostate.
  • In humans, marked down-regulation of TGFBR2 protein was observed in 12 of 20 high-grade prostatic intraepithelial neoplasia and 36 of 60 prostate cancers.
  • DNA methylation of the human TGFBR2 promoter CpG islands repressed transcription, if present, but neither methylation nor mutation were detected in 27 human prostate cancers analyzed.
  • The identification of methylation silencing of Tgfbr2 in rat prostate cancers, in accordance with TGFBR2 down-regulation in human prostate cancers, will enable us to analyze how aberrant methylation is induced in vivo and identify factors that promote and suppress the induction of aberrant methylation.
  • [MeSH-major] Adenocarcinoma / genetics. DNA Methylation. Gene Silencing. Prostatic Neoplasms / genetics. Protein-Serine-Threonine Kinases / genetics. Receptors, Transforming Growth Factor beta / genetics
  • [MeSH-minor] Animals. Azacitidine / analogs & derivatives. Azacitidine / pharmacology. Cell Line, Tumor. Gene Expression Regulation, Enzymologic / drug effects. Gene Expression Regulation, Neoplastic / drug effects. Histones / genetics. Humans. Male. Oligonucleotide Array Sequence Analysis. Rats. Rats, Inbred F344. Up-Regulation / drug effects

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  • (PMID = 18381416.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Histones; 0 / Receptors, Transforming Growth Factor beta; 776B62CQ27 / decitabine; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.30 / transforming growth factor-beta type II receptor; M801H13NRU / Azacitidine
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82. Bahn DK, Silverman P, Lee F Sr, Badalament R, Bahn ED, Rewcastle JC: Focal prostate cryoablation: initial results show cancer control and potency preservation. J Endourol; 2006 Sep;20(9):688-92
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  • [Title] Focal prostate cryoablation: initial results show cancer control and potency preservation.
  • BACKGROUND: Focal prostate cryoablation is the less-than-complete ablation of the gland with ice.
  • Known tumor is ablated aggressively, whereas contralateral prostate tissue and surrounding structures are spared.
  • This method offers targeted local cancer control aiming at sexual potency and urinary continence preservation in patients whose prostate cancer is believed to be unilateral.
  • PATIENTS AND METHODS: Patients who had a strong desire for preservation of sexual function and continence were informed of focal prostate cryoablation as an investigational treatment option for clinically organ-confined, unilateral tumor identified by color Doppler ultrasonography and confirmed by targeted and systematic biopsy.
  • Only stage, not preoperative serum prostate specific antigen concentration (PSA) or tumor differentiation, was considered a potential contraindication.
  • The one biopsy-positive patient was subsequently treated with full-gland cryoablation and remains disease free.
  • CONCLUSION: Focal cryoablation can provide biochemical and local control of prostate cancer while preserving potency and continence.


83. Loeb S, Sutherland DE, D'Amico AV, Roehl KA, Catalona WJ: PSA velocity is associated with gleason score in radical prostatectomy specimen: marker for prostate cancer aggressiveness. Urology; 2008 Nov;72(5):1116-20; discussion 1120
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  • [Title] PSA velocity is associated with gleason score in radical prostatectomy specimen: marker for prostate cancer aggressiveness.
  • OBJECTIVES: Conflicting evidence has been reported on the association of prostate-specific antigen velocity (PSAV) with Gleason score in prostate needle biopsy specimens.
  • The Gleason score is an important prognostic indicator for men with prostate cancer, and, in modern practice, it frequently affects treatment decisions.
  • Statistical analysis was performed to examine the relationship between the preoperative PSAV and the prostatectomy Gleason score and other adverse tumor features.
  • CONCLUSIONS: Our results have further validated PSAV as a marker for prostate cancer aggressiveness.
  • Thus, PSAV could be useful in treatment decision-making and in assessing the likelihood of long-term cancer control in men with prostate cancer.
  • [MeSH-major] Prostate-Specific Antigen / blood. Prostatectomy. Prostatic Neoplasms / blood. Prostatic Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cohort Studies. Humans. Male. Middle Aged. Neoplasm Invasiveness. Neoplasm Staging. Predictive Value of Tests. Reproducibility of Results. Retrospective Studies. Treatment Outcome


84. Helgeson BE, Tomlins SA, Shah N, Laxman B, Cao Q, Prensner JR, Cao X, Singla N, Montie JE, Varambally S, Mehra R, Chinnaiyan AM: Characterization of TMPRSS2:ETV5 and SLC45A3:ETV5 gene fusions in prostate cancer. Cancer Res; 2008 Jan 1;68(1):73-80
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  • [Title] Characterization of TMPRSS2:ETV5 and SLC45A3:ETV5 gene fusions in prostate cancer.
  • Recurrent gene fusions involving oncogenic ETS transcription factors (including ERG, ETV1, and ETV4) have been identified in a large fraction of prostate cancers.
  • Here, we identify ETV5 as the fourth ETS family member involved in recurrent gene rearrangements in prostate cancer.
  • In vitro recapitulation of ETV5 overexpression induced invasion in RWPE cells, a benign immortalized prostatic epithelial cell line.
  • Together, our results suggest that the family of 5' partners previously identified in ETV1 gene fusions can fuse with other ETS family members, suggesting numerous rare gene fusion permutations in prostate cancer.
  • [MeSH-major] Oncogene Fusion. Oncogene Proteins, Fusion / genetics. Prostatic Neoplasms / genetics
  • [MeSH-minor] Cell Line, Tumor. Gene Expression Profiling. Humans. Male. Tumor Cells, Cultured

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  • (PMID = 18172298.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P50CA69568; United States / NCI NIH HHS / CA / R01 CA102872; 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 / Oncogene Proteins, Fusion; 0 / Slc45A3-ETV5 fusion protein, human; 0 / TMPRSS2-ETV5 fusion protein, human
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85. Ueda Y, Higuchii Y, Hashimoto T, Mitsui Y, Maruyamai T, Kondou N, Nojima M, Yamamoto S, Shincho M, Hirota S, Shima H: [Prostate cancer diagnosed through the biopsy of the bone metastatic lesion; a case report]. Hinyokika Kiyo; 2007 May;53(5):327-30
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  • [Title] [Prostate cancer diagnosed through the biopsy of the bone metastatic lesion; a case report].
  • Although digital rectal examination was normal, a high serum prostate specific antigen (PSA) level (85.9 ng/ml) led us to perform sextant prostate biopsy, resulting in negative for cancer.
  • Twelve-core prostate biopsy was performed again, but the result was negative.
  • Pelvic magnetic resonance imaging (MRI) showed a metastatic lesion on the right pubic bone, which was biopsied, and turned out to be poorly differentiated prostate cancer in histology.
  • To our knowledge, there were only two case reports diagnosed as prostate cancer by biopsies of the metastatic lesions in Japanese literature, but none in the English literature.
  • These findings suggest that high serum levels of CEA and CA19-9 in patients with prostate cancer are indications of hormone-refractory prostate cancer resulting in poor prognosis.
  • [MeSH-major] Bone Neoplasms / secondary. Bone and Bones / pathology. Prostatic Neoplasms / diagnosis. Prostatic Neoplasms / pathology
  • [MeSH-minor] Aged, 80 and over. Biopsy. CA-19-9 Antigen / blood. Carcinoembryonic Antigen / blood. Humans. Male. Prostate / pathology. Prostate-Specific Antigen / blood


86. Drewa T, Styczynski J: Progenitor cells are responsible for formation primary epithelial cultures in the prostate epithelial model. Int Urol Nephrol; 2007;39(3):851-7
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  • [Title] Progenitor cells are responsible for formation primary epithelial cultures in the prostate epithelial model.
  • We hypothesized prostate epithelial CD133-positive ASC to be responsible for establishing the primary cell culture.
  • The prostate epithelial stem cells were isolated using anti-CD133 microbeads in order to form different cell populations.
  • The morphology of cultures developed from CD133(+) and CD133(-) prostate epithelial cells were compared with prostate epithelium cell culture obtained after simple isolation procedure.
  • Double CD133(+) and CD133(-) cultures from two rats were established after enzymatic digestion and positive selection by SuperMACS device, and two non-selected CD133(+)/CD133(-) cultures were developed by simple prostate epithelial cell isolation from two other rats.
  • It was observed that growth of the CD133(+)/CD133(-) and CD133(+)culture resembled epithelial-like prostate cell culture.
  • We concluded that the epithelial progenitor cells are responsible for establishing primary prostate epithelial cultures in vitro.
  • [MeSH-major] Neoplastic Stem Cells / metabolism. Prostatic Neoplasms / metabolism
  • [MeSH-minor] AC133 Antigen. Animals. Antigens, CD / metabolism. Cell Differentiation. Cells, Cultured. Epithelial Cells / metabolism. Glycoproteins / metabolism. Male. Microspheres. Models, Animal. Peptides / metabolism. Rats. Tumor Cells, Cultured

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  • (PMID = 17318344.001).
  • [ISSN] 0301-1623
  • [Journal-full-title] International urology and nephrology
  • [ISO-abbreviation] Int Urol Nephrol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / AC133 Antigen; 0 / Antigens, CD; 0 / Glycoproteins; 0 / Peptides; 0 / Prom1 protein, rat
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87. Maresca KP, Hillier SM, Femia FJ, Keith D, Barone C, Joyal JL, Zimmerman CN, Kozikowski AP, Barrett JA, Eckelman WC, Babich JW: A series of halogenated heterodimeric inhibitors of prostate specific membrane antigen (PSMA) as radiolabeled probes for targeting prostate cancer. J Med Chem; 2009 Jan 22;52(2):347-57
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  • [Title] A series of halogenated heterodimeric inhibitors of prostate specific membrane antigen (PSMA) as radiolabeled probes for targeting prostate cancer.
  • Prostate specific membrane antigen (PSMA) is a validated molecular marker for prostate cancer.
  • Two lead iodine compounds were radiolabeled with (123)I and (131)I and demonstrated specific PSMA binding on human prostate cancer cells, warranting evaluation as radioligands for the detection, staging, and monitoring of prostate cancer.
  • [MeSH-major] Glutamate Carboxypeptidase II / antagonists & inhibitors. Halogens / chemistry. Prostatic Neoplasms / drug therapy

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  • (PMID = 19111054.001).
  • [ISSN] 1520-4804
  • [Journal-full-title] Journal of medicinal chemistry
  • [ISO-abbreviation] J. Med. Chem.
  • [Language] eng
  • [Grant] United States / NIBIB NIH HHS / EB / 1R43EB004253
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Surface; 0 / Halogens; EC 3.4.17.21 / Glutamate Carboxypeptidase II; EC 3.4.17.21 / glutamate carboxypeptidase II, human
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88. Spahn M, Kneitz S, Scholz CJ, Stenger N, Rüdiger T, Ströbel P, Riedmiller H, Kneitz B: Expression of microRNA-221 is progressively reduced in aggressive prostate cancer and metastasis and predicts clinical recurrence. Int J Cancer; 2010 Jul 15;127(2):394-403
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  • [Title] Expression of microRNA-221 is progressively reduced in aggressive prostate cancer and metastasis and predicts clinical recurrence.
  • Emerging evidence shows that microRNAs (miR) are involved in the pathogenesis of a variety of cancers, including prostate carcinoma (PCa).
  • Little information is available regarding miR expression levels in lymph node metastasis of prostate cancer or the potential of miRs as prognostic markers in this disease.
  • Therefore, we analyzed the global expression of miRs in benign, hyperplastic prostate tissue (BPH), primary PCa of a high risk group of PCa patients, and corresponding metastatic tissues by microarray analysis.
  • In a large study cohort, the prostate-specific oncomir miR-221 was progressively downregulated in aggressive forms of PCa.
  • Kaplan-Meier estimates and Cox proportional hazard models showed that miR-221 downregulation was linked to tumor progression and recurrence in a high risk prostate cancer cohort.
  • [MeSH-major] Biomarkers, Tumor / genetics. MicroRNAs / physiology. Neoplasm Recurrence, Local / diagnosis. Prostatic Neoplasms / genetics. Prostatic Neoplasms / pathology
  • [MeSH-minor] Aged. Cohort Studies. Computational Biology. Disease Progression. Humans. Lymphatic Metastasis. Male. Middle Aged. Oligonucleotide Array Sequence Analysis. Prostatic Hyperplasia / genetics. Prostatic Hyperplasia / metabolism. Prostatic Hyperplasia / pathology. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 19585579.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / MIRN221 microRNA, human; 0 / MicroRNAs; 0 / RNA, Messenger
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89. Denis LJ: Europa Uomo: The European Prostate Cancer Coalition. Arch Ital Urol Androl; 2006 Dec;78(4):157-60
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  • [Title] Europa Uomo: The European Prostate Cancer Coalition.
  • The European Prostate Cancer Coalition is an independent, international, non-profit association of patient led prostate cancer support groups.
  • The European survivors of prostate cancer, now about one million strong, have taken up their responsibility to get involved in the support the control of the disease and focus on prevention, optimal treatment and quality of life.

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  • (PMID = 17269623.001).
  • [ISSN] 1124-3562
  • [Journal-full-title] Archivio italiano di urologia, andrologia : organo ufficiale [di] Societa italiana di ecografia urologica e nefrologica
  • [ISO-abbreviation] Arch Ital Urol Androl
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] Italy
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90. Stock D, Groome PA, Siemens DR: Inflammation and prostate cancer: a future target for prevention and therapy? Urol Clin North Am; 2008 Feb;35(1):117-30; vii
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  • [Title] Inflammation and prostate cancer: a future target for prevention and therapy?
  • Given its long natural history, prostate cancer has become an ideal model for the clinical and basic science study of neoplastic disease in distinct pathologic phases: tumor initiation, progression, invasion, and metastasis.
  • Nonsteroidal anti-inflammatory drugs (NSAIDs), because of their ability to attenuate inflammation, as well as possibly direct anti-cancer properties associated with the inhibition of stromal cyclooxygenase-2, are potential candidates for clinical use in prostate cancer.
  • Though epidemiologic evidence indicating a reduced risk of prostate cancer for NSAID users supports a chemoprotective benefit, observational assessment and clinical trials of these agents among large cohorts of prostate cancer patients are needed to determine their value in prostate cancer management.
  • [MeSH-major] Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Inflammation / drug therapy. Inflammation / pathology. Prostatic Neoplasms / pathology. Prostatic Neoplasms / prevention & control

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  • (PMID = 18061030.001).
  • [ISSN] 0094-0143
  • [Journal-full-title] The Urologic clinics of North America
  • [ISO-abbreviation] Urol. Clin. North Am.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal
  • [Number-of-references] 117
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91. Fang J, Zhou Q, Shi XL, Jiang BH: Luteolin inhibits insulin-like growth factor 1 receptor signaling in prostate cancer cells. Carcinogenesis; 2007 Mar;28(3):713-23
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Luteolin inhibits insulin-like growth factor 1 receptor signaling in prostate cancer cells.
  • Insulin-like growth factor 1 receptor (IGF-1R) activation is required for prostate cell proliferation.
  • Prostate cancer is one of the most commonly diagnosed malignant tumors in Western countries.
  • Overexpression of IGF-1R in prostate cancer is associated with tumor growth.
  • With evidence accumulating for a chemopreventive role of flavonoids, the effects of luteolin, a bioactive flavonoid, on IGF-1R signaling in prostate cancer cells were examined.
  • Luteolin inhibited insulin-like growth factor 1 (IGF-1) induced activation of IGF-1R and AKT in prostate cancer PC-3 and DU145 cells.
  • As a result, luteolin suppressed proliferation and induced apoptosis of prostate cancer cells.
  • Knockdown of IGF-1R by siRNA led to inhibition of proliferation of prostate cancer cells.
  • Results of in vivo tumor growth assay indicated that luteolin inhibited PC-3 tumor growth.
  • Immunoblotting of the extracts of tumor tissues showed that luteolin inhibited IGF-1R/AKT signaling.
  • [MeSH-major] Anticarcinogenic Agents / pharmacology. Cell Cycle / drug effects. Luteolin / pharmacology. Prostatic Neoplasms / pathology. Receptor, IGF Type 1 / antagonists & inhibitors
  • [MeSH-minor] Animals. Cell Line, Tumor. Cyclin D1 / metabolism. Humans. Male. Mice. Mice, Inbred BALB C. Proto-Oncogene Proteins c-akt / metabolism. RNA, Small Interfering / genetics. Signal Transduction / drug effects. Transfection


92. Brouwer IA: Omega-3 PUFA: good or bad for prostate cancer? Prostaglandins Leukot Essent Fatty Acids; 2008 Sep-Nov;79(3-5):97-9
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  • [Title] Omega-3 PUFA: good or bad for prostate cancer?
  • INTRODUCTION: The objective of this meta-analysis was to estimate quantitatively the associations between intake or status of omega-3 polyunsaturated (omega-3 PUFA) fatty acids and occurrence of prostate cancer in observational studies in humans.
  • RESULTS: The combined estimate showed an increased risk of prostate cancer in men with a high intake or blood level of alpha-linolenic acid (ALA) (combined relative risk (RR) 1.36; 95% CI 1.08-1.70).
  • Ecosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) were not significantly associated with prostate cancer.
  • DISCUSSION: The association between high intake of ALA and prostate cancer is of concern and needs further study.
  • However, the fact that the prospective studies do not show a clear association makes a true effect of intake of ALA on prostate cancer less likely.
  • [MeSH-major] Fatty Acids, Omega-3 / blood. Prostatic Neoplasms / epidemiology

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  • (PMID = 18951003.001).
  • [ISSN] 0952-3278
  • [Journal-full-title] Prostaglandins, leukotrienes, and essential fatty acids
  • [ISO-abbreviation] Prostaglandins Leukot. Essent. Fatty Acids
  • [Language] eng
  • [Publication-type] Journal Article; Meta-Analysis; Review
  • [Publication-country] Scotland
  • [Chemical-registry-number] 0 / Fatty Acids, Omega-3; 0RBV727H71 / alpha-Linolenic Acid; 25167-62-8 / Docosahexaenoic Acids
  • [Number-of-references] 20
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93. Marrari A, Iero M, Pilla L, Villa S, Salvioni R, Valdagni R, Parmiani G, Rivoltini L: Vaccination therapy in prostate cancer. Cancer Immunol Immunother; 2007 Apr;56(4):429-45
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  • [Title] Vaccination therapy in prostate cancer.
  • Radical prostatectomy and radiation therapy provide excellent localized prostate cancer (PC) control.
  • Although the majority of prostate carcinoma is nowadays diagnosed at early stages with favourable risk features, in patients up to 30-40% it recurs within 10 years.
  • Furthermore, the lack of effective therapies, once prostate carcinoma becomes refractory to androgen deprivation, mandates the development of alternative therapeutic options.
  • There is a growing interest in harnessing the potency and specificity of anti-tumour immunity through the generation of fully competent dendritic cells and tumour reactive effector lymphocytes.
  • In some cases clinical responses were achieved showing that vaccine-primed T cells induced anti-tumour activity in vivo.
  • [MeSH-major] Cancer Vaccines / therapeutic use. Prostatic Neoplasms / immunology. Prostatic Neoplasms / therapy

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  • (PMID = 17031640.001).
  • [ISSN] 0340-7004
  • [Journal-full-title] Cancer immunology, immunotherapy : CII
  • [ISO-abbreviation] Cancer Immunol. Immunother.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Cancer Vaccines
  • [Number-of-references] 143
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94. Korkes F, Gasperini R, Korkes KL, Silva Neto DC, Castro MG: Testicular metastases: a poor prognostic factor in patients with advanced prostate cancer. World J Urol; 2009 Feb;27(1):113-5
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  • [Title] Testicular metastases: a poor prognostic factor in patients with advanced prostate cancer.
  • PURPOSE: Prostate cancer is the most frequently diagnosed neoplasm in men.
  • Testicular metastases from prostate cancer are rare events that have been previously reported; however, its frequency and clinical meaning are not well established.
  • PATIENTS AND METHODS: A review of patients who underwent androgen deprivation orchidectomy for prostate cancer between 1995 and 2007 was undertaken.
  • In such context, evaluation of testicular parenchyma of patients with advanced prostate cancer could be assessed.
  • RESULTS: Of the 1,693 orchidectomies performed during the period analysed, three cases of testicular metastases of prostate cancer (range 58-76 years) were diagnosed (0.18%).
  • All patients had very atypical neoplasm's behaviour and poor prognosis, dying within the first year.
  • CONCLUSION: In conclusion, testicular metastases from prostate cancer are a rare event, observed in 1.8 per 1,000 cases.
  • [MeSH-major] Prostatic Neoplasms / pathology. Testicular Neoplasms / secondary


95. Wu YJ, Liang CH, Zhou FJ, Gao X, Chen LW, Liu Q: [A case-control study of environmental and genetic factors and prostate cancer in Guangdong]. Zhonghua Yu Fang Yi Xue Za Zhi; 2009 Jul;43(7):581-5
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  • [Title] [A case-control study of environmental and genetic factors and prostate cancer in Guangdong].
  • OBJECTIVE: To explore the etiologic relationship of prostate cancer and environmental and genetic polymorphism in southern China METHODS: A hospital-based and 1:1 matched case-control study was conducted.
  • The blood samples were collected from 85 cases of prostate cancer and 82 controls of other diseases after informing consent.
  • RESULTS: An increased risk of prostate cancer development was observed with the early first spermatorrhea (age < 18) (OR = 2.90, 95% CI: 1.76 - 4.80), early first sexual intercourse (age < or = 24) (OR = 2.38, 95% CI: 1.14 - 4.96), frequent sexual intercourse before 35 year old (OR = 1.80, 95% CI: 1.19 - 2.70), family history of cancer (OR = 2.70, 95% CI: 1.31 - 5.58), more intake of pork (OR =2.27, 95% CI: 1.38 - 3.70).
  • CYP17 A1/A2 and CYP17 A2/A2 genotypes were related with a high risk of prostate cancer and OR values of 1.78 (95% CI: 0.70 - 4.53) and 2.57 (95% CI: 0.91 - 7.25) respectively.
  • Study also showed that there was an interaction between CYP17 polymorphisms and early first spermatorrhea and family cancer history related to the risk of prostate cancer with OR value at 13.35 (95% CI: 1.58 - 113.00) and 4.01 (95% CI: 1.22 - 13.17) respectively.
  • CONCLUSION: Sexual intercourse, dietary intake and family cancer history should be related to prostate cancer occurrence.
  • CYP17 polymorphism might be associated with a high risk of prostate cancer.
  • It suggests that there are multiple environmental and genetic factors to the prostate cancer.
  • [MeSH-major] Environmental Exposure. Prostatic Neoplasms / epidemiology. Prostatic Neoplasms / genetics. Steroid 17-alpha-Hydroxylase / genetics

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  • (PMID = 19954068.001).
  • [ISSN] 0253-9624
  • [Journal-full-title] Zhonghua yu fang yi xue za zhi [Chinese journal of preventive medicine]
  • [ISO-abbreviation] Zhonghua Yu Fang Yi Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] EC 1.14.99.9 / CYP17A1 protein, human; EC 1.14.99.9 / Steroid 17-alpha-Hydroxylase
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96. Salinas CA, Koopmeiners JS, Kwon EM, FitzGerald L, Lin DW, Ostrander EA, Feng Z, Stanford JL: Clinical utility of five genetic variants for predicting prostate cancer risk and mortality. Prostate; 2009 Mar 1;69(4):363-72
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  • [Title] Clinical utility of five genetic variants for predicting prostate cancer risk and mortality.
  • BACKGROUND: A recent report suggests that the combination of five single-nucleotide polymorphisms (SNPs) at 8q24, 17q12, 17q24.3 and a family history of the disease may predict risk of prostate cancer.
  • The present study tests the performance of these factors in prediction models for prostate cancer risk and prostate cancer-specific mortality.
  • Cox proportional hazards models estimated hazard ratios for prostate cancer-specific mortality according to genotypes.
  • RESULTS: The combination of SNP genotypes and family history was significantly associated with prostate cancer risk (p(trend) = 1.5 x 10(-20)).
  • Neither the individual nor combined risk factors was associated with prostate cancer-specific mortality.
  • CONCLUSION: Genotypes for five SNPs plus family history are associated with a significant elevation in risk for prostate cancer and may explain up to 45% of prostate cancer in our population.

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  • [Copyright] 2008 Wiley-Liss, Inc.
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  • (PMID = 19058137.001).
  • [ISSN] 1097-0045
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA097186; United States / NCI NIH HHS / CA / R01 CA056678; United States / NCI NIH HHS / CA / R01 CA56678; United States / NCI NIH HHS / CA / R01 CA082664; United States / NCI NIH HHS / CA / R01 CA092579; United States / NCI NIH HHS / CA / R01 CA056678-05
  • [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
  • [Other-IDs] NLM/ NIHMS105496; NLM/ PMC2788301
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97. Rentsch CA, Cecchini MG, Schwaninger R, Germann M, Markwalder R, Heller M, van der Pluijm G, Thalmann GN, Wetterwald A: Differential expression of TGFbeta-stimulated clone 22 in normal prostate and prostate cancer. Int J Cancer; 2006 Feb 15;118(4):899-906
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  • [Title] Differential expression of TGFbeta-stimulated clone 22 in normal prostate and prostate cancer.
  • Altered expression of these genes may be associated with malignant transformation of the prostate gland.
  • The cDNA array analysis of differential expression of the TGFbeta superfamily and functionally related genes between patient-matched noncancerous prostate (NP) and prostate cancer (PC) bulk tissue specimens highlighted two genes, namely TGFbeta-stimulated clone-22 (TSC-22) and Id4.
  • TSC-22 should be considered as a novel basal cell marker, potentially useful for studying lineage determination within the epithelial compartment of the prostate.
  • Conversely, lack of TSC-22 seems to be a hallmark of malignant transformation of the prostate epithelium.
  • Accordingly, TSC-22 immunohistochemistry may prove to be a diagnostic tool for discriminating benign lesions from malignant ones of the prostate.
  • The suggested tumour suppressor function of TSC-22 warrants further investigation on its role in prostate carcinogenesis and on the TSC-22 pathway as a candidate therapeutic target in PC.
  • [MeSH-major] Inhibitor of Differentiation Proteins / biosynthesis. Prostate / physiology. Prostatic Neoplasms / genetics. Repressor Proteins / biosynthesis. Transforming Growth Factor beta / physiology
  • [MeSH-minor] Aged. Cell Transformation, Neoplastic. Gene Expression Profiling. Humans. Immunohistochemistry. Male. Oligonucleotide Array Sequence Analysis. Polymerase Chain Reaction. RNA, Messenger / biosynthesis. Tumor Cells, Cultured

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  • (PMID = 16106424.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ID4 protein, human; 0 / Inhibitor of Differentiation Proteins; 0 / RNA, Messenger; 0 / Repressor Proteins; 0 / TSC22D1 protein, human; 0 / Transforming Growth Factor beta
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98. Xie D, Gore C, Liu J, Pong RC, Mason R, Hao G, Long M, Kabbani W, Yu L, Zhang H, Chen H, Sun X, Boothman DA, Min W, Hsieh JT: Role of DAB2IP in modulating epithelial-to-mesenchymal transition and prostate cancer metastasis. Proc Natl Acad Sci U S A; 2010 Feb 09;107(6):2485-90
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  • [Title] Role of DAB2IP in modulating epithelial-to-mesenchymal transition and prostate cancer metastasis.
  • A single nucleotide polymorphism in the DAB2IP gene is associated with risk of aggressive prostate cancer (PCa), and loss of DAB2IP expression is frequently detected in metastatic PCa.
  • Here, we show that the loss of DAB2IP expression initiates epithelial-to-mesenchymal transition (EMT), which is visualized by repression of E-cadherin and up-regulation of vimentin in both human normal prostate epithelial and prostate carcinoma cells as well as in clinical prostate-cancer specimens.
  • In DAB2IP knockout mice, prostate epithelial cells exhibited elevated mesenchymal markers, which is characteristic of EMT.
  • Using a human prostate xenograft-mouse model, we observed that knocking down endogenous DAB2IP in human carcinoma cells led to the development of multiple lymph node and distant organ metastases.
  • [MeSH-major] Epithelial Cells / pathology. Mesoderm / pathology. Prostatic Neoplasms / pathology. ras GTPase-Activating Proteins / physiology
  • [MeSH-minor] Animals. Blotting, Western. Cadherins / genetics. Cadherins / metabolism. Cell Line. Cell Line, Tumor. Cell Movement. Gene Expression. Humans. Immunohistochemistry. Male. Mice. Mice, Nude. Neoplasm Metastasis. Neoplasms, Experimental / genetics. Neoplasms, Experimental / metabolism. Neoplasms, Experimental / pathology. RNA, Small Interfering / genetics. Reverse Transcriptase Polymerase Chain Reaction. TCF Transcription Factors / metabolism. Transfection. Transplantation, Heterologous. Vimentin / genetics. Vimentin / metabolism. beta Catenin / metabolism