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PubMed2000

Association of vitamin D receptor gene polymorphism with prostate cancer and benign prostatic hyperplasia in a Japanese population.

Recent studies have suggested that vitamin D is an important determinant of prostate cancer risk and inherited polymorphisms in the 3'-untranslated region (3'UTR) of the vitamin D receptor (VDR) gene are associated with the risk and progression of prostate cancer. This study was conducted to explore the association of VDR gene polymorphisms with prostate cancer risk in Japanese men who are considered to be much less influenced by environmental risk factors for prostate cancer. We studied 222 prostate cancer patients, 209 benign prostatic hyperplasia (BPH) patients, 128 male controls who were over 60 years old and without any evidence of prostate cancer or BPH, and 198 female controls. A PCR-RFLP method was used to determine three VDR gene polymorphisms in the 3'UTR characterized by restriction enzymes BsmI, ApaI and TaqI. In the BsmI polymorphism, heterozygosity or homozygosity for the absence of the BsmI restriction site was associated with one-third the risk of prostate cancer (P < 0.0001; odds ratio, 3.31; 95% confidence interval, 2.05-5.32) and with one-half the risk of BPH (P < 0.005; odds ratio, 2.07; 95% confidence interval, 1.33-3.22) compared with the male controls. The TaqI and ApaI polymorphisms did not show any significant association with either prostate cancer or BPH. The results indicate that the BsmI polymorphism in the VDR gene plays a significant role in protection against prostate cancer and BPH. Because of the racial difference in the strength of the linkage disequilibrium between the three polymorphisms, additional studies are required to apply the present results to other racial-ethnic groups.

3' Untranslated Regions↗

PubMed2006

Detection of life-threatening prostate cancer with prostate-specific antigen velocity during a window of curability.

BACKGROUND: Prostate-specific antigen (PSA) level is typically used as a dichotomous test for prostate cancer, resulting in overdiagnosis for a substantial number of men. The rate at which serum PSA levels change (PSA velocity) may be an important indicator of the presence of life-threatening disease. METHODS: PSA velocity was determined in 980 men (856 without prostate cancer, 104 with prostate cancer who were alive or died of another cause, and 20 who died of prostate cancer) who were participants in the Baltimore Longitudinal Study of Aging for up to 39 years. The relative risks (RRs) of prostate cancer death and prostate cancer-specific survival stratified by PSA velocity were evaluated in the three groups of men by Cox regression and Kaplan-Meier analyses. Statistical tests were two-sided. RESULTS: PSA velocity measured 10-15 years before diagnosis (when most men had PSA levels below 4.0 ng/mL) was associated with cancer-specific survival 25 years later; survival was 92% (95% confidence interval [CI] = 84% to 96%) among men with PSA velocity of 0.35 ng/mL per year or less and 54% (95% CI = 15% to 82%) among men with PSA velocity above 0.35 ng/mL per year (P<.001). Furthermore, men with PSA velocity above 0.35 ng/mL per year had a higher relative risk of prostate cancer death than men with PSA velocity of 0.35 ng/mL per year or less (RR = 4.7, 95% CI = 1.3 to 16.5; P = .02); the rates per 100,000 person-years were 1240 for men with a PSA velocity above 0.35 ng/mL per year and 140 for men with a PSA velocity of 0.35 ng/mL per year or less. CONCLUSIONS: PSA velocity may help identify men with life-threatening prostate cancer during a period when their PSA levels are associated with the presence of curable disease.

Adult↗

PubMed2006

[Influence of androgen deprivation therapy on prostate volume in patients with prostate cancer undergoing prostate brachytherapy with permanent seed implantation].

OBJECTIVE: Enlarged prostate often causes pubic arch interference during needle insertion on transperineal interstitial permanent prostate brachytherapy. Pre-treatment hormonal therapy is necessary for downsizing the prostate gland in such cases. The degree of prostate downsizing with anti-androgen treatment before iodine 125 permanent seed implant brachytherapy and its relation to clinical as well as pathological parameters were assessed. METHODS: From September 2003 to March 2005, 110 patients underwent permanent seed implantation and 86 patients of all received antiandrogen depriviation prior to the treatment at our institute. Prostate volume was measured using transrectal ultrasound at the time of cancer diagnosis and before the seed implant. Correlations between prostate downsizing and clinical as well as pathological parameters were evaluated. RESULTS: Mean percent volume of the prostate after the size reduction with average of 6.0 months antiandrogen monotherapy, 7.7 months LHRH agoniost and 8.2 months maximum androgen blockage (MAB) was 83%, 63%, and 60%, respectively. Mann-Whitney U test revealed that the degree of prostate downsizing is significantly correlated with the prostate volume in patients with prostate cancer utilizing LHRH agonists. CONCLUSIONS: Antiandrogen monotherapy can be an alternative for prostate downsizing before interstitial brachytherapy. Utilizing LHRH agonists or MAB is recommended for cases with larger gland volume.

Aged↗

PubMed1998

The precursor form of the human kallikrein 2, a kallikrein homologous to prostate-specific antigen, is present in human sera and is increased in prostate cancer and benign prostatic hyperplasia.

Prostate-specific antigen (PSA, hK3) is a diagnostic marker for prostatic cancer but lacks the specificity to sufficiently distinguish between prostatic cancer and benign prostatic hyperplasia (BPH). Human glandular kallikrein 2 (hK2) has been proposed as a potential diagnostic marker for prostate cancer that could complement the current PSA test. Recently we demonstrated that proPSA is present in prostate cancer sera. This study examines the expression of prohK2 in prostate cells and its presence in human sera. Western blot analysis was used to assess prohK2 expression in the human carcinoma cell line, LNCaP. A highly specific and sensitive dual monoclonal immunoassay for prohK2 was developed and used to assess the presence of prohK2 in human sera. prohK2 was detected in the spent media of LNCaP cells. Furthermore, prohK2 was present at immunodetectable concentrations in human sera, and its concentration was increased in prostatic cancer and BPH. These results indicate for the first time that prohK2 is secreted by human prostate cells and is a major component of uncomplexed (free) hK2 in human sera. In addition, prohK2 in human sera is associated with prostate disease and thus may be a useful marker for prostatic cancer and BPH.

Antibodies, Monoclonal↗

PubMed1999

Cancer surveillance series: interpreting trends in prostate cancer--part I: Evidence of the effects of screening in recent prostate cancer incidence, mortality, and survival rates.

BACKGROUND: The prostate-specific antigen test was approved by the U.S. Food and Drug Administration in 1986 to monitor the disease status in patients with prostate cancer and, in 1994, to aid in prostate cancer detection. However, after 1986, the test was performed on many men who had not been previously diagnosed with prostate cancer, apparently resulting in the diagnosis of a substantial number of early tumors. Our purpose is to provide insight into the effect of screening on prostate cancer rates. Detailed data are presented for whites because the size of the population allows for calculating statistically reliable rates; however, similar overall trends are seen for African-Americans and other races. METHODS: Prostate cancer incidence data from the National Cancer Institute's Surveillance, Epidemiology, and End Results Program and mortality data from the National Center for Health Statistics were analyzed. RESULTS/CONCLUSIONS: The following findings are consistent with a screening effect: 1) the recent decrease since 1991 in the incidence of distant stage disease, after not having been perturbed by screening; 2) the decline in the incidence of earlier stage disease beginning the following year (i.e., 1992); 3) the recent increases and decreases in prostate cancer incidence and mortality by age that appear to indicate a calendar period effect; and 4) trends in the incidence of distant stage disease by tumor grade and trends in the survival of patients with distant stage disease by calendar year that provide suggestive evidence of the tendency of screening to detect slower growing tumors. IMPLICATIONS: The decline in the incidence of distant stage disease holds the promise that testing for prostate-specific antigen may lead to a sustained decline in prostate cancer mortality. However, population data are complex, and it is difficult to confidently attribute relatively small changes in mortality to any one cause.

Black or African American↗

PubMed2001

Expression of adrenomedullin and peptide amidation activity in human prostate cancer and in human prostate cancer cell lines.

After therapeutic hormone deprivation, prostate cancer (CaP) cells often develop androgen-independent growth through not-well-defined mechanisms. The presence of neuroendocrine (NE) cells is often greater in prostate carcinoma than in normal prostate, and the frequency of NE cells correlates with tumor malignancy, loss of androgen sensitivity, increase of autocrine-paracrine activity, and poor prognosis. In some CaPs, neuropeptides have been previously implicated as growth factors. Peptidylglycine alpha-amidating monooxygenase (PAM) is the enzyme producing alpha-amidated bioactive peptides from their inactive glycine-extended precursors. In the present work, we demonstrate that androgen-independent PC-3 and DU145 cell lines, derived from human CaP, express PAM in vitro and in xenografts implanted in athymic nude mice, indicating that they are able to produce alpha-amidated peptides. Contrarily, barely detectable levels of PAM were found in the androgen-sensitive LNCaP cell line. We also show that whereas PC-3 and DU145 cells produce and secrete adrenomedullin (AM), a multifunctional amidated peptide, no expression was found in LNCaP cells. We further demonstrate that AM acts as a growth factor for DU145 cells, which suggests the existence of an autocrine loop mechanism that could potentially drive neoplastic growth. PAM mRNA levels were found to be 3-fold higher in prostate adenocarcinomas compared with that of human benign prostate hyperplasia (BPH) as demonstrated by real-time quantitative reverse transcription-PCR. The analysis of AM message expression in BPH and CaP (Gleason's score, 6-9) shows a clear distinction between benign and CaP. The expression was detected only in adenocarcinomas tissues with a marked increase in samples with a high Gleason's score. Immunocytochemically, AM was localized in the carcinomatous epithelial compartment. NE phenotype, assessed after the immunocytochemical localization of neuron-specific enolase (NSE), was found in both the epithelial and the stromal compartments of cancers; in BPH, only some spare basal cells were NSE-labeled. Cancer progression could be accelerated by peptides secreted by a population of cells capable of inducing androgen-independent tumoral growth via autocrine-paracrine mechanisms.

Adenocarcinoma↗

PubMed2007

Variation in the definition of biochemical recurrence in patients treated for localized prostate cancer: the American Urological Association Prostate Guidelines for Localized Prostate Cancer Update Panel report and recommendations for a standard in the reporting of surgical outcomes.

PURPOSE: The American Urological Association Prostate Guideline Update Panel was charged with updating the Guidelines for Clinically Localized Prostate Cancer. In assessing outcomes with treatment, it became apparent that a highly variable number of definitions exist with respect to biochemical recurrence. Herein, we review the variability in published definitions of biochemical recurrence and make recommendations directed toward improving this terminology by recommending a standard definition in patients treated with radical prostatectomy. MATERIALS AND METHODS: Four PubMed literature searches were performed between May 2001 and April, 2004 and covered articles published from 1991 through early 2004. The search terms included the MeSH major headings of prostate cancer and prostatic neoplasm. All potentially relevant articles were retrieved and a more detailed screen for relevance was performed. An article was considered relevant if it reported treatment outcomes of patients with clinical T1 or T2N0M0 prostate cancer. Data extractors recorded the definition of biochemical recurrence and definitions were then collapsed into categories representing the same criteria. The results of biochemical failure were subcategorized by initial treatment. RESULTS: Of 13,800 citations, a total of 436 articles were selected. Among these, a total of 145 articles contained 53 different definitions of biochemical recurrence for those treated with radical prostatectomy. Of these, the most common definition (35) was a prostate specific antigen of >0.2 ng/mL or a slight variation thereof. In addition, a total of 208 articles reported 99 different definitions of biochemical failure among those treated with radiation therapy. Of these, the American Society for Therapeutic Radiology and Oncology definition (70) and/or a variation thereof was the most commonly reported. In total, 166 different definitions of biochemical failure were identified. Following radical prostatectomy, the Panel recommends defining biochemical recurrence as an initial serum prostate specific antigen of > or =0.2 ng/mL, with a second confirmatory level of prostate specific antigen of >0.2 ng/mL. The Panel recommends the use of the American Society for Therapeutic Radiology and Oncology criteria for patients treated with radiation therapy and acknowledges that these criteria will soon be updated although not yet published. CONCLUSIONS: A high degree of variability in the definition of biochemical recurrence exists following treatment for localized prostate cancer. Strict definitions for biochemical recurrence are necessary to identify men at risk for disease progression and to allow meaningful comparisons among patients treated similarly. The Panel acknowledges the American Society for Therapeutic Radiology and Oncology criteria and future modifications thereof for those receiving radiation therapy and recommends the newly developed American Urological Association criteria for those treated with radical prostatectomy. The purpose for the establishment of this standard is for data reporting purposes and for comparison of similarly treated patients. It is not intended to represent a threshold value for which to initiate treatment. The Panel acknowledges that the clinical decision to initiate treatment will be dependent on multiple factors including patient and physician interaction rather than a specific prostate specific antigen threshold value.

Humans↗

PubMed2001

Human prostate cancer and benign prostatic hyperplasia: molecular dissection by gene expression profiling.

Critical aspects of the biology and molecular basis for prostate malignancy remain poorly understood. To reveal fundamental differences between benign and malignant growth of prostate cells, we performed gene expression profiling of primary human prostate cancer and benign prostatic hyperplasia (BPH) using cDNA microarrays consisting of 6500 human genes. Frozen prostate specimens were processed to facilitate extraction of RNA from regions of tissue enriched in either benign or malignant epithelial cell growth within a given specimen. Gene expression in each of the 16 prostate cancer and nine BPH specimens was compared with a common reference to generate normalized measures for each gene across all of the samples. Using an analysis of complete pairwise comparisons of expression profiles among all of the samples, we observed clearly discernable patterns of overall gene expression that differentiated prostate cancer from BPH. Further analysis of the data identified 210 genes with statistically significant differences in expression between prostate cancer and BPH. These genes include many not recognized previously as differentially expressed in prostate cancer and BPH, including hepsin, which codes for a transmembrane serine protease. This study reveals for the first time that significant and widespread differences in gene expression patterns exist between benign and malignant growth of the prostate gland. Gene expression analysis of prostate tissues should help to disclose the molecular mechanisms underlying prostate malignant growth and identify molecular markers for diagnostic, prognostic, and therapeutic use.

Gene Expression Profiling↗

PubMed1997

Serum-to-urinary prostate specific antigen ratio: its impact in distinguishing prostate cancer when serum prostate specific antigen level is 4 to 10 ng./ml.

PURPOSE: Benign prostatic hyperplasia (BPH) was shown to be associated with high concentrations of urinary prostate specific antigen (PSA). We investigated the serum-to-urinary PSA ratio in patients undergoing prostate biopsy to assess its efficacy in enhancing serum PSA specificity in the detection of prostate carcinoma. MATERIALS AND METHODS: From November 1995 through January 1996 consecutive patients undergoing prostate biopsy were prospectively included in the study. Serum and urine PSA levels were measured at our laboratory with the Tandem-R assay. Samples were drawn 24 hours before prostate biopsy and at a distance from prostatic manipulation or ejaculation. RESULTS: We studied 73 patients with BPH and 57 with prostate cancer. Differences between BPH and prostate cancer were statistically significant considering serum PSA or serum-to-urinary PSA ratios. In the 50 patients with a serum PSA of 4.0 to 10.0 ng./ml. (35 with BPH and 15 with prostate cancer) the differences between prostate cancer and BPH were still significant only when considering serum-to-urinary PSA ratio. Receiver operating characteristic curves showed that serum-to-urinary PSA ratio was a better predictor of prostate cancer than serum PSA. CONCLUSIONS: Our results suggest that the serum-to-urinary PSA ratio may be useful in distinguishing BPH from prostate cancer, particularly in the diagnostic gray zone of serum PSA between 4.0 and 10.0 ng./ml.

Aged↗

PubMed2001

Human prostate cancer cells lack feedback regulation of low-density lipoprotein receptor and its regulator, SREBP2.

The low-density lipoprotein receptor (LDLR) pathway provides cells with essential fatty acids for prostaglandin E2 (PGE2) synthesis. Regulation of LDLR expression by LDL was compared between the human normal and cancer prostate cells using semi-quantitative RT-PCR and LDL uptake assays. LDLR mRNA expression and LDL uptake by LDLR were down-regulated in the presence of exogenous LDL or whole serum in the normal prostate cells, but not in the prostate cancer cells. Addition of exogenous cholesterol down-regulated both LDLR and a potent regulator of the ldlr promoter, sterol regulatory element binding protein 2 (SREBP2), in normal cells but not in cancer cells. PGE2 synthesis in prostate cancer cells was significantly increased in response to LDL. Our study suggests that over-production of LDLR is an important mechanism in cancer cells for obtaining more essential fatty acids through LDLR endocytosis, allowing increased synthesis of prostaglandins, which subsequently stimulate cell growth. The data also suggest that the sterol regulatory element and SREBP2 play a role in the loss of sterol feedback regulation in cancer cells.

CCAAT-Enhancer-Binding Proteins↗

PubMed1996

The CaPSURE database: a methodology for clinical practice and research in prostate cancer. CaPSURE Research Panel. Cancer of the Prostate Strategic Urologic Research Endeavor.

OBJECTIVES: Implicit in the modern concept of patient outcome assessment is a shift from primary reliance on clinical indicators to a broader definition that includes physical, psychological, and social well-being. This is especially true of prostate cancer, where treatment can profoundly alter patient well-being. We have initiated a longitudinal observational database, CaPSURE (Cancer of the Prostate Strategic Urologic Research Endeavor) to document the impact of prostate cancer on resource utilization, clinical outcomes, health-related quality of life and survival in typical practice settings. METHODS: Observational databases have been used in the treatment of other conditions. We have incorporated many well-tested elements in our study. Data are collected from two sources: the physician and the patient. The urologist enrolls eligible patients into the study, completes a medical history, and records current status, treatment, and laboratory results at each office visit. Patients complete quarterly questionnaires on health-related quality of life, resource utilization, work loss, and satisfaction with care. RESULTS: Currently 21 sites participate in CaPSURE with 1419 patients enrolled by April 1996. Twenty percent of patients are newly diagnosed with prostate cancer. Time since diagnosis averages 3.0 years (SD = 3.1); mean age at diagnosis is 68.9 years (SD = 7.9, range = 39.6 to 90.7). The majority of patients (72%) are diagnosed with Stage B cancer. Patients receive a variety of treatments including surgery, irradiation, hormonal therapy, and watchful waiting. CONCLUSIONS: Information available from CaPSURE will assist practicing urologists who must make clinical decisions on the basis of data such as the results of treatment in typical care settings, the effect of prostate cancer and its treatment methods on patient quality of life, and the effect on health care costs of the early detection of prostate cancer.

Adult↗

PubMed1999

Prostate specific antigen density for discriminating prostate cancer from benign prostatic hyperplasia in the gray zone of prostate-specific antigen.

Serum prostate specific antigen (PSA) is currently the best blood marker for prostate cancer. However, low specificity for detection of prostate cancer, especially in the gray zone of PSA, is a problem. We evaluated the clinical significance of PSA density (PSAD) in gray zone PSA cases with conversion of serum PSA to a Stanford reference value. In a series of histologically confirmed 63 benign prostatic hyperplasia (BPH) patients and 234 prostate cancer patients, 36 BPH patients and 25 prostate cancer patients had gray zone PSA levels. Serum PSA was measured with the Markit-F or Markit-M PA assay. All data were converted to Stanford reference values. We used transabdominal ultrasound to determine prostate volume. PSAD was determined as the serum PSA/prostate volume ratio. The mean PSA values for BPH and prostate cancer were 6.42 +/- 1.80 and 7.80 +/- 2.15 ng/ml (p = 0.0116), respectively, and prostate volume was 33.4 +/- 14.1 ml and 17.1 +/- 8.2 ml, respectively (p < 0.0001). The mean PSAD for prostate cancer was 0.572 +/- 0.363 while that for BPH was 0.218 +/- 0.085 (p = 0.0001). Cut-off values with sensitivity > 90% were 0.218 for PSAD and 30 ml for prostate volume. At these cut-off values, specificity reached 56% for each marker. In discriminating prostate cancer from BPH in the gray zone of PSA, PSAD demonstrated better performance than PSA.

Aged↗

PubMed2006

Occupational risk factors for prostate cancer and benign prostatic hyperplasia: a case-control study in Western Australia.

OBJECTIVE: To assess the association of selected occupational exposures with risk of prostate cancer and with risk of benign prostatic hyperplasia (BPH). METHODS: This population-based case-control study recruited 606 men with a diagnosis of confirmed prostate cancer, 400 men who had undergone their first prostatectomy for BPH and 471 male controls randomly selected from the electoral roll between 1 August 2001 and 1 October 2002 in Western Australia. chi(2) tests and logistic regressions were used for univariate and multivariate analyses to investigate the association of the two outcomes with occupational exposure to pesticides, fertilisers, metals, wood dust, oils, diesel exhaust and polyaromatic hydrocarbons (PAHs). RESULTS: Exposure to toxic metals at a non-substantial level increased the risk of BPH (odds ratio (OR) 1.39, 95% confidence interval (CI) 1.1 to 1.84) and led to a non-significant excess risk of prostate cancer (OR 1.25, 95% CI 0.96 to 1.61). Non-significant excess risks were observed for prostate cancer after exposure to oils other than mineral oil (OR 1.54, 95% CI 0.95 to 2.51) and for BPH after exposure to PAHs (OR 1.20, 95% CI 0.91 to 1.58). A non-statistically significant protective effect for prostate cancer was seen after exposure to organophosphate pesticides (OR 0. 69, 95% CI 0.43 to 1.12). No other associations were found for either prostate cancer or BPH and no dose-response relationships were seen for the exposures investigated. CONCLUSIONS: These results do not provide evidence that any of the occupational factors examined are risk factors for either prostate cancer or BPH.

Age Distribution↗

PubMed2002

Thrombospondin-1, vascular endothelial growth factor expression and their relationship with p53 status in prostate cancer and benign prostatic hyperplasia.

OBJECTIVE: To evaluate the expression of thrombospondin-1 (TSP-1, a potent inhibitor of angiogenesis) and vascular endothelial growth factor (VEGF, an important angiogenic factor in solid tumours) in prostate cancer, and their relationship with p53 status. PATIENTS AND METHODS: Using immunohistochemistry, the expression of VEGF, TSP-1 and p53 was assessed in 82 archival tissue specimens from 23 patients with benign prostatic hyperplasia (BPH), 22 with localized prostate cancer and 37 with metastatic prostate cancer. Seven of the last group had received androgen deprivation therapy. The relationship between the expression of VEGF, TSP-1 and p53 status was also evaluated with tumour grade and stage in patients with prostate cancer. RESULTS: The seven patients receiving hormonal treatment were excluded from the analysis because androgen deprivation significantly increased TSP-1 and decreased VEGF expression (both P < 0.01). Immunohistochemical analysis showed significantly higher VEGF and significantly lower TSP-1 expression (both P < 0.01) in prostate cancer than in BPH tissues. There was also significantly higher VEGF and significantly lower TSP-1 expression (both P < 0.05) in tissues from metastatic than localized prostate cancer. There was no significant correlation between VEGF or TSP-1 expression and Gleason score, but a significant inverse correlation between TSP-1 and VEGF expression. There was a significant association between VEGF expression and p53 status (P < 0.05), but TSP-1 expression was not associated with p53 status. CONCLUSIONS: Angiogenic factors, including VEGF and TSP-1, might be important in the development and progression of prostate cancer. These changes seem to be influenced by p53 status. Identifying the angiogenic factors involved in prostate cancer might lead to the development of diagnostic or therapeutic strategies based on anti-angiogenesis.

Adenocarcinoma↗

PubMed2003

CYP17 polymorphisms in relation to risks of prostate cancer and benign prostatic hyperplasia: a population-based study in China.

Because androgens likely play a key role in prostate growth and prostate cancer development, variants of genes involved in androgen biosynthesis may be related to prostate cancer risk. The enzyme P450c17alpha, encoded by the CYP17 gene, catalyzes the conversion of progesterone and pregnenolone into precursors of potent androgens. In the 5' promoter region of the CYP17 gene, a T (A1 allele) to C substitution (A2 allele) has been hypothesized to increase CYP17 gene expression, resulting in higher levels of androgens. To investigate a possible role of CYP17 in prostate diseases, we evaluated the risk of prostate cancer and benign prostatic hyperplasia (BPH) in relation to variation in CYP17 genotype in a population-based case-control study conducted in Shanghai, China. The study included 174 prostate cancer cases, 182 BPH cases and 274 population controls. We observed no statistically significant overall associations of CYP17 genotypes with prostate cancer risk, although associations of the A1/A1 (odds ratio (OR) =1.42, 95% confidence interval (CI) 0.83-2.48) and A1/A2 (OR 1.41, 95% CI 0.91-2.17) genotypes with prostate cancer were suggested. A similar association of the A1/A1 genotype with BPH was suggested. We found no associations of CYP17 genotypes with serum sex hormone levels or other biomarkers after correction for multiple comparisons. Large population-based studies are needed to clarify whether CYP17 plays a role in prostate cancer risk and whether genotype effects vary in different racial/ethnic and other subgroups.

Aged↗

PubMed2002

Significance of vitamin D receptor gene polymorphism for risk and disease severity of prostate cancer and benign prostatic hyperplasia in Japanese.

OBJECTIVE: Recent studies have demonstrated an association between vitamin D receptor (VDR) genotype and prostate cancer. Currently, there is a scarcity of data regarding the association of VDR genotype with benign prostatic hyperplasia (BPH). The purpose of this study was to investigate the TaqI VDR polymorphism in Japanese prostate cancer patients, Japanese BPH patients and Japanese controls in order to determine if an association exists between VDR genotype and the risk of developing prostate cancer and BPH as well as disease severity. METHODS: 110 prostate cancer patients, 83 BPH patients and 90 male age-matched controls were genotyped for a previously described TaqI restriction fragment length polymorphism at codon 352 in exon 9 of the VDR gene. Products were digested into T allele or t allele according to the absence or presence of a TaqI restriction site with individuals being classified as TT, Tt or tt. RESULTS: The frequency of the genotype tt was higher in the control group (6.7%) compared to patients with prostate cancer (1.8%) and BPH (3.6%) but this was not statistically significant. However, the frequency of the genotype TT was significantly higher among prostate cancer patients with locally advanced or metastatic disease (T3/ T4/N1/M1) compared to controls (p = 0.001). In addition, the genotype TT was significantly higher among prostate cancer patients with a high Gleason grade of tumor (grade 5) compared to controls (p = 0.0001). In addition, the genotype TT was statistically higher in BPH patients with high prostate volume (volume >50 cm(3)) compared to controls (p = 0.001). CONCLUSION: These data demonstrate that VDR genotype plays an important role in determining the risk of more advanced and aggressive prostate cancer as well as prostatic enlargement in Japanese men.

Aged↗

PubMed1999

Cancer surveillance series: interpreting trends in prostate cancer--part II: Cause of death misclassification and the recent rise and fall in prostate cancer mortality.

BACKGROUND: The rise and fall of prostate cancer mortality correspond closely to the rise and fall of newly diagnosed cases. To understand this phenomenon, we explored the role that screening, treatment, iatrogenic (i.e., treatment-induced) deaths, and attribution bias (incorrect labeling of death from other causes as death from prostate cancer) have played in recent mortality trends. METHODS: Join point regression is utilized to assess the recent rise and fall in mortality and the relationship of total U.S. trends to those areas served by the National Cancer Institute's Surveillance, Epidemiology, and End Results (SEER) Cancer Registry Program. Incidence-based mortality (IBM) is estimated with the use of prostate cancer data from the SEER Program to partition (from overall prostate cancer mortality trends) the contribution of cases diagnosed since the widespread use of prostate-specific antigen (PSA) testing starting in 1987. IBM is also used to examine the contribution of stage at diagnosis to the recent prostate cancer mortality trends. RESULTS: IBM for cases diagnosed since 1987 rose above the pre-1987 secular (i.e., background) trend, peaked in the early 1990s, and almost returned to the secular trend by 1994. This rise and fall of IBM track with the pool of prevalent cases diagnosed within the prior 2 years. IBM for cases diagnosed with metastatic disease fell starting in 1991, while IBM for those diagnosed with localized/regional disease was relatively flat. CONCLUSIONS: The rise and fall in prostate cancer mortality observed since the introduction of PSA testing in the general population are consistent with a hypothesis that a fixed percent of the rising and falling pool of recently diagnosed patients who die of other causes may be mislabeled as dying of prostate cancer. The decline in IBM for distant stage disease and flat IBM trends for localized/regional disease provide some evidence of improved prognosis for screen-detected cases, although alternative interpretations are possible.

Age Distribution↗

PubMed2006

On the importance of being ethnic: coping with the threat of prostate cancer in relation to prostate cancer screening.

The relation between coping with a possible prostate cancer diagnosis and screening behavior was examined in men from seven precise ethnic groups. Five coping styles differed in their likelihood of use across ethnic groups and had somewhat different associations with frequency of prostate-specific antigen (PSA) testing. As expected, PSA test frequency differed among men from different ethnic groups and was differentially predicted by coping styles. Analyzing the results using typical groups of White, Black, and Hispanic, rather than precise ethnic groups, obscured these results. Researchers investigating psychological variables in preventive health behaviors must analyze diversity within the framework provided by ethnic specificity. Such an approach will guide the development and provision of interventions that are more sensitive to the characteristics of specific ethnic groups of at risk men.

Acculturation↗