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[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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[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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[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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[Cites] CA Cancer J Clin. 1999 Jan-Feb;49(1):8-31, 1 [10200775.001]

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(PMID = 17171424.001).

[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] EC 3.4.21.77 / Prostate-Specific Antigen

   

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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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[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

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[ErratumIn] BJU Int. 2008 Jun;101(11):1483. Youngren, Jack F [added]

(PMID = 18234062.001).

[ISSN] 1464-410X

[Journal-full-title] BJU international

[ISO-abbreviation] BJU Int.

[Language] eng

[Grant] United States / NCI NIH HHS / CA / K23 CA115775-01

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

[Publication-country] England

[Chemical-registry-number] 0 / Antineoplastic Agents; 7BO8G1BYQU / Masoprocol; EC 2.7.10.1 / Receptor, IGF Type 1; EC 3.4.21.77 / Prostate-Specific Antigen

   

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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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[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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[CommentIn] J Clin Oncol. 2009 Apr 20;27(12):1938-40 [19307497.001]

(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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[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

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(PMID = 19084847.001).

[ISSN] 1527-3792

[Journal-full-title] The Journal of urology

[ISO-abbreviation] J. Urol.

[Language] eng

[Publication-type] Comparative Study; Journal Article

[Publication-country] United States

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

   

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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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[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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[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

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(PMID = 17615715.001).

[ISSN] 1438-3276

[Journal-full-title] MMW Fortschritte der Medizin

[ISO-abbreviation] MMW Fortschr Med

[Language] ger

[Publication-type] English Abstract; Journal Article

[Publication-country] Germany

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

   

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[Title] 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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[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

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(PMID = 16296198.001).

[ISSN] 0043-3284

[Journal-full-title] The West Virginia medical journal

[ISO-abbreviation] W V Med J

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

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

   

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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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[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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[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

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(PMID = 20231620.001).

[ISSN] 1943-7722

[Journal-full-title] American journal of clinical pathology

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

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

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

   

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[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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[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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[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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Although the presence of CD166 at the tumor cell surface has been correlated with shortened survival, little is known about its function and expression in normal intestinal epithelia.

CD166-positive cells were also detected in benign adenomas in mice; rare cells coexpressed CD166 and CD44 or epithelial-specific antigen.

CD166-positive cells appear at multiple stages of intestinal carcinoma progression, including benign and metastatic tumors.

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[Copyright] Copyright © 2010 AGA Institute. Published by Elsevier Inc. All rights reserved.

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(PMID = 20826154.001).

[ISSN] 1528-0012

[Journal-full-title] Gastroenterology

[ISO-abbreviation] Gastroenterology

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / R01 CA118235; United States / NIDDK NIH HHS / DK / U01 DK085525-02; United States / NHLBI NIH HHS / HL / T32 HL007781; United States / NCI NIH HHS / CA / CA106195-06A1; United States / NCI NIH HHS / CA / CA118235-05; United States / NICHD NIH HHS / HD / T32 HD049309-05; United States / NCI NIH HHS / CA / CA106195; United States / NCI NIH HHS / CA / T32 CA106195; United States / NICHD NIH HHS / HD / HD049309; United States / NICHD NIH HHS / HD / T32 HD049309; United States / NCI NIH HHS / CA / T32 CA106195-06A1; United States / NHLBI NIH HHS / HL / T32 HL007781-14; United States / NIDDK NIH HHS / DK / R01 DK068326; United States / NCI NIH HHS / CA / CA118235; United States / NIDDK NIH HHS / DK / R01 DK068326-05; United States / NIDDK NIH HHS / DK / DK068326; United States / NIDDK NIH HHS / DK / DK085525-02; United States / NICHD NIH HHS / HD / HD049309-05; United States / NHLBI NIH HHS / HL / HL007781-14; United States / NHLBI NIH HHS / HL / HL007781; United States / NIDDK NIH HHS / DK / U01 DK085525; United States / NIDDK NIH HHS / DK / DK085525; United States / NIDDK NIH HHS / DK / DK068326-05; United States / NCI NIH HHS / CA / R01 CA118235-05

[Publication-type] Journal Article; Research Support, N.I.H., Extramural

[Publication-country] United States

[Chemical-registry-number] 0 / ALCAM protein, human; 0 / Antigens, CD; 0 / Biomarkers, Tumor; 0 / Cell Adhesion Molecules, Neuronal; 0 / Fetal Proteins

[Other-IDs] NLM/ NIHMS234467; NLM/ PMC2997177

   

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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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[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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[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

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(PMID = 20590366.001).

[ISSN] 1651-226X

[Journal-full-title] Acta oncologica (Stockholm, Sweden)

[ISO-abbreviation] Acta Oncol

[Language] eng

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

[Publication-country] England

   

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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

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[CommentIn] BJU Int. 2009 Jan;103(1):115; author reply 115-6 [19076972.001]

(PMID = 17922870.001).

[ISSN] 1464-410X

[Journal-full-title] BJU international

[ISO-abbreviation] BJU Int.

[Language] eng

[Publication-type] Evaluation Studies; Journal Article

[Publication-country] England

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

   

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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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[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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[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

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[CommentIn] J Urol. 2006 Apr;175(4):1199-200 [16515959.001]

(PMID = 16515983.001).

[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] 0 / Biomarkers, Tumor; 0 / Prostatic Secretory Proteins; 0 / beta-microseminoprotein; 9002-68-0 / Follicle Stimulating Hormone

   

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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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[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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[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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[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

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(PMID = 18674807.001).

[ISSN] 1527-9995

[Journal-full-title] Urology

[ISO-abbreviation] Urology

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

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

   

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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

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(PMID = 17176864.001).

[ISSN] 0018-1994

[Journal-full-title] Hinyokika kiyo. Acta urologica Japonica

[ISO-abbreviation] Hinyokika Kiyo

[Language] jpn

[Publication-type] English Abstract; Journal Article

[Publication-country] Japan

   

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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

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(PMID = 20664922.001).

[ISSN] 1791-2423

[Journal-full-title] International journal of oncology

[ISO-abbreviation] Int. J. Oncol.

[Language] eng

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

[Publication-country] Greece

[Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Isothiocyanates; 6U7TFK75KV / phenethyl isothiocyanate

   

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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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[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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[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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[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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[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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[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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[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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[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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[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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[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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[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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[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

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(PMID = 18472065.001).

[ISSN] 1166-7087

[Journal-full-title] Progrès en urologie : journal de l'Association française d'urologie et de la Société française d'urologie

[ISO-abbreviation] Prog. Urol.

[Language] fre

[Publication-type] English Abstract; Journal Article; Review

[Publication-country] France

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

[Number-of-references] 68

   

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[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

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[CommentIn] Eur Urol. 2009 Jun;55(6):1331-2 [19286304.001]

[CommentIn] Eur Urol. 2009 Jun;55(6):1331 [19286303.001]

(PMID = 19286302.001).

[ISSN] 1873-7560

[Journal-full-title] European urology

[ISO-abbreviation] Eur. Urol.

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] Switzerland

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

[Number-of-references] 75

   

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[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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Tumor suppressor genes retinoic acid receptor beta (RARbeta) and PDLIM4 are hypermethylated and silenced in prostate cancer (PCa) tissues and PCa cell lines compared to normal prostate cells.

METHODS: In this study, a benign prostate epithelial cell line RWPE1 was used as a model to study the epigenetic regulation of Myc on the RARbeta and PDLIM4 promoters.

[MeSH-major] DNA-Binding Proteins / genetics. Genes, myc. Prostate / physiology. Receptors, Retinoic Acid / genetics

[MeSH-minor] Blotting, Western. Cell Growth Processes / genetics. Cell Line. DNA / genetics. DNA (Cytosine-5-)-Methyltransferase / metabolism. DNA Methylation. Epigenesis, Genetic. Gene Expression Profiling. Humans. LIM Domain Proteins. Male. Polymerase Chain Reaction. Prostatic Neoplasms / genetics. Prostatic Neoplasms / pathology. Sequence Analysis, DNA. Transfection

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(PMID = 19623543.001).

[ISSN] 1097-0045

[Journal-full-title] The Prostate

[ISO-abbreviation] Prostate

[Language] eng

[Grant] United States / NCI NIH HHS / CA / CA 91956

[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 / DNA-Binding Proteins; 0 / LIM Domain Proteins; 0 / PDLIM4 protein, human; 0 / Receptors, Retinoic Acid; 0 / retinoic acid receptor beta; 9007-49-2 / DNA; EC 2.1.1.37 / DNA (Cytosine-5-)-Methyltransferase; EC 2.1.1.37 / DNA methyltransferase 3A; EC 2.1.1.37 / DNA methyltransferase 3B

   

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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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[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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[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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[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