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Prostate Cancer Risk (prostate + cancer_risk)
Selected AbstractsEmerging Evidence on the Role of Soy in Reducing Prostate Cancer RiskNUTRITION REVIEWS, Issue 4 2003Mark J. Messina PhD Soyfoods are a unique dietary source of isoflavones, which have both hormonal and non-hormonal effects relevant to prostate cancer prevention. In vitro, the main soybean isoflavone, genistein, inhibits prostate cancer cell growth; in animals, most but not all studies show isoflavone-rich soy protein and isolated isoflavones inhibit prostate tumor development. Currently, although only limited epidemiologic data indicate soy intake reduces prostate cancer risk, results from a pilot intervention trial suggest isoflavones may be beneficial to prostate cancer patients. For several reasons, men concerned about their prostate health may consider incorporating soy into their diet. [source] Association of prostate cancer with rapid N -acetyltransferase 1 (NAT1*10) in combination with slow N -acetyltransferase 2 acetylator genotypes in a pilot case-control studyENVIRONMENTAL AND MOLECULAR MUTAGENESIS, Issue 3 2002David W. Hein Abstract N -acetyltransferase-1 (NAT1) and N -acetyltransferase-2 (NAT2) are important in the metabolism of aromatic and heterocyclic amine carcinogens that induce prostate tumors in the rat. We investigated the association of genetic polymorphisms in NAT1 and NAT2, alone and in combination, with human prostate cancer. Incident prostate cancer cases and controls in a hospital-based case-control study were frequency-matched for age, race, and referral pattern. The frequency of slow acetylator NAT1 genotypes (NAT1*14, *15, *17) was 5.8% in controls but absent in cases. In contrast, in comparison with all other NAT1 genotypes the putative rapid acetylator NAT1 genotype (NAT1*10) was significantly higher in prostate cancer cases than controls (OR, 2.17; 95% CI, 1.08,4.33; P = 0.03). Combinations of NAT1*10 with NAT2 slow acetylator genotypes (OR, 5.08; 95% CI, 1.56,16.5; P = 0.008) or with NAT2 very slow (homozygous NAT2*5) acetylator genotypes (OR, 7.50; 95% CI, 1.55,15.4; P = 0.016) further increased prostate cancer risk. The results of this small pilot study suggest increased susceptibility to prostate cancer for subjects with combinations of NAT1*10 and slow (particularly very slow) NAT2 acetylator genotypes. This finding should be investigated further in larger cohorts and in other ethnic populations. Environ. Mol. Mutagen. 40:161,167, 2002. © 2002 Wiley-Liss, Inc. [source] Randomised clinical trial of isoflavones in reducing prostate cancer riskFOCUS ON ALTERNATIVE AND COMPLEMENTARY THERAPIES AN EVIDENCE-BASED APPROACH, Issue 4 2003NB Kumar [source] Prostate cancer and PSA among statin users in the Finnish prostate cancer screening trialINTERNATIONAL JOURNAL OF CANCER, Issue 7 2010Teemu J. Murtola Abstract Decreased risk of advanced prostate cancer has been reported among men using statins. However, the evidence on overall prostate cancer risk is conflicting. We compared the relative risk between current users and non-users of statins or other cholesterol-lowering medications in a population undergoing systematical prostate cancer screening. The study cohort comprised of 23,320 men participating in the screening arm of the Finnish prostate cancer screening trial during 1996,2004. Information on medication use was obtained from a comprehensive national prescription database. Cox proportional hazards regression was used to calculate multivariable adjusted hazard ratios (HRs) for prostate cancer. Serum prostate-specific antigen (PSA) level was compared between current users and non-users of cholesterol-lowering drugs. Compared with medication non-users, the overall prostate cancer incidence was decreased among statin users [HR 0.75, 95% confidence interval (CI) 0.63,0.89]. The inverse association was dose-dependent with cumulative amount of statin use, and strongest for low-grade and early stage tumors. The incidence was nonsignificantly lower also among users of other types of cholesterol-lowering drugs (HR 0.62, 95% CI 0.28,1.38), but without dose-dependence. Age-adjusted median serum PSA tended to be lower among users of cholesterol-lowering drugs, but the relative risk decrease among statin users was not related to decreased PSA. Overall incidence of prostate cancer was lowered among statin users when bias due to differential PSA testing between medication users and non-users was eliminated by systematical prostate cancer screening. Cholesterol-lowering with statins seems beneficial for prostate cancer prevention. [source] Physical activity and risk of prostate cancer in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohortINTERNATIONAL JOURNAL OF CANCER, Issue 4 2009Nina Føns Johnsen Abstract The evidence concerning the possible association between physical activity and the risk of prostate cancer is inconsistent and additional data are needed. We examined the association between risk of prostate cancer and physical activity at work and in leisure time in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. In our study, including 127,923 men aged 20,97 years from 8 European countries, 2,458 cases of prostate cancer were identified during 8.5 years of followup. Using the Cox proportional hazards model, we investigated the associations between prostate cancer incidence rate and occupational activity and leisure time activity in terms of participation in sports, cycling, walking and gardening; a metabolic equivalent (MET) score based on weekly time spent on the 4 activities; and a physical activity index. MET hours per week of leisure time activity, higher score in the physical activity index, participation in any of the 4 leisure time activities, and the number of leisure time activities in which the participants were active were not associated with prostate cancer incidence. However, higher level of occupational physical activity was associated with lower risk of advanced stage prostate cancer (ptrend = 0.024). In conclusion, our data support the hypothesis of an inverse association between advanced prostate cancer risk and occupational physical activity, but we found no support for an association between prostate cancer risk and leisure time physical activity. © 2009 UICC [source] Adipokine genes and prostate cancer riskINTERNATIONAL JOURNAL OF CANCER, Issue 4 2009Steven C. Moore Abstract Adiposity and adipocyte-derived cytokines have been implicated in prostate carcinogenesis. However, the relationship of adipokine gene variants with prostate cancer risk has not been thoroughly investigated. We therefore examined common variants of the IL6, LEP, LEPR, TNF and ADIPOQ genes in relation to prostate cancer in a case-control study nested within a large cohort of Finnish men. The study sample consisted of 1,053 cases of prostate cancer, diagnosed over an average 11 years of follow up, and 1,053 controls matched to the cases on age, intervention group and date of baseline blood draw. Logistic regression was used to model the relative odds of prostate cancer. We also examined genotypes in relation to serum insulin, IGF-1 and IGF-1:IGFBP-3 among 196 controls. Variant alleles at three loci (,14858A>G, ,13973A>C, ,13736C>A) in a potential regulatory region of the LEP gene conferred a statistically significant 20% reduced risk of prostate cancer. For example, at the ,14858A>G locus, heterozygotes and homozygotes for the A allele had an odds ratio (OR) of prostate cancer of 0.76 [95% confidence interval (CI) 0.62, 0.93] and 0.79 (95% CI 0.60, 1.04), respectively. At 13288G>A, relative to the GG genotype, the AA genotype was associated with a suggestive increased risk of prostate cancer (OR = 1.29; 95% CI 0.99,1.67; ptrend = 0.05). Polymorphisms in the IL6, LEPR, TNF and ADIPOQ genes were not associated with prostate cancer. Allelic variants in the LEP gene are related to prostate cancer risk, supporting a role for leptin in prostate carcinogenesis. © 2008 Wiley-Liss, Inc. [source] Genetic variation in the toll-like receptor gene cluster (TLR10-TLR1-TLR6) and prostate cancer riskINTERNATIONAL JOURNAL OF CANCER, Issue 11 2008Victoria L. Stevens Abstract Toll-like receptors (TLRs) are key players in the innate immune system and initiate the inflammatory response to foreign pathogens such as bacteria, fungi and viruses. The proposed role of chronic inflammation in prostate carcinogenesis has prompted investigation into the association of common genetic variation in TLRs with the risk of this cancer. We investigated the role of common SNPs in a gene cluster encoding the TLR10, TLR6 and TLR1 proteins in prostate cancer etiology among 1,414 cancer cases and 1,414 matched controls from the Cancer Prevention Study II Nutrition Cohort. Twenty-eight SNPs, which included the majority of the common nonsynonymous SNPs in the 54-kb gene region and haplotype-tagging SNPs that defined 5 specific haplotype blocks, were genotyped and their association with prostate cancer risk determined. Two SNPs in TLR10 [I369L (rs11096955) and N241H (rs11096957)] and 4 SNPs in TLR1 [N248S (rs4833095), S26L (rs5743596), rs5743595 and rs5743551] were associated with a statistically significant reduced risk of prostate cancer of 29,38% (for the homozygous variant genotype). The association of these SNPs was similar when the analysis was limited to cases with advanced prostate cancer. Haplotype analysis and linkage disequilibrium findings revealed that the 6 associated SNPs were not independent and represent a single association with reduced prostate cancer risk (OR = 0.55, 95% CI: 0.33, 0.90). Our study suggest that a common haplotype in the TLR10-TLR1-TLR6 gene cluster influences prostate cancer risk and clearly supports the need for further investigation of TLR genes in other populations. © 2008 Wiley-Liss, Inc. [source] Carbaryl exposure and incident cancer in the Agricultural Health StudyINTERNATIONAL JOURNAL OF CANCER, Issue 8 2007Rajeev Mahajan Abstract Carbaryl is a carbamate insecticide with a broad spectrum of uses in agricultural, commercial and household settings. It has previously been linked with non-Hodgkin lymphoma (NHL) but studies of cancer risk in humans are limited. We examined occupational carbaryl use and risk of all cancers in the Agricultural Health Study, a prospective study of a cohort of pesticide applicators in North Carolina and Iowa. This analysis included 21,416 subjects (1,291 cases) enrolled from 1993,1997 and followed for cancer incidence through 2003. Pesticide exposure and other data were collected using self-administered questionnaires. Poisson regression was used to calculate rate ratios (RRs) and 95% confidence intervals (CIs) while controlling for potential confounders. Carbaryl was not associated with cancer risk overall. Relative to subjects who never used carbaryl, melanoma risk was elevated with >175 lifetime exposure-days (RR = 4.11; 95%CI, 1.33,12.75; p -trend = 0.07), >10 years of use (RR = 3.19; 95%CI, 1.28,7.92; p -trend = 0.04), or ,10 days of use per year (RR = 5.50; 95%CI, 2.19,13.84; p -trend < 0.001). Risk remained after adjusting for sunlight exposure. Although not significant, there appeared to be a trend of decreasing prostate cancer risk with increasing level of exposure. A small increase in NHL risk was observed using some, but not all, exposure measures. No associations were observed with other examined cancer sites. Because the observed results were not hypothesized a priori and because of limited study of their biological plausibility, they should be interpreted with caution. © 2007 Wiley-Liss, Inc. [source] Risk factors for prostate cancer incidence and progression in the health professionals follow-up studyINTERNATIONAL JOURNAL OF CANCER, Issue 7 2007Edward Giovannucci Abstract Risk factors for prostate cancer could differ for various sub-groups, such as for "aggressive" and "non-aggressive" cancers or by grade or stage. Determinants of mortality could differ from those for incidence. Using data from the Health Professionals Follow-Up Study, we re-examined 10 factors (cigarette smoking history, physical activity, BMI, family history of prostate cancer, race, height, total energy consumption, and intakes of calcium, tomato sauce and ,-linolenic acid) using multivariable Cox regression in relation to multiple subcategories for prostate cancer risk. These were factors that we previously found to be predictors of prostate cancer incidence or advanced prostate cancer in this cohort, and that have some support in the literature. In this analysis, only 4 factors had a clear statistically significant association with overall incident prostate cancer: African,American race, positive family history, higher tomato sauce intake (inversely) and ,-linolenic acid intake. In contrast, for fatal prostate cancer, recent smoking history, taller height, higher BMI, family history, and high intakes of total energy, calcium and ,-linolenic acid were associated with a statistically significant increased risk. Higher vigorous physical activity level was associated with lower risk. In relation to these risk factors, advanced stage at diagnosis was a good surrogate for fatal prostate cancer, but high-grade (Gleason , 7 or Gleason , 8) was not. Only for high calcium intake was there a close correspondence for associations among high-grade cancer, advanced and fatal prostate cancer. Tomato sauce (inversely) and ,-linolenic acid (positively) intakes were strong predictors of advanced cancer among those with low-grade cancers at diagnosis. Although the proportion of advanced stage cancers was much lower after PSA screening began, risk factors for advanced stage prostate cancers were similar in the pre-PSA and PSA era. The complexity of the clinical and pathologic manifestations of prostate cancer must be considered in the design and interpretation of studies. © 2007 Wiley-Liss, Inc. [source] 5,-Reductase type 2 gene variant associations with prostate cancer risk, circulating hormone levels and androgenetic alopeciaINTERNATIONAL JOURNAL OF CANCER, Issue 4 2007Vanessa M. Hayes Abstract Controversy exists over the significance of associations between the SRD5A2 (5,-reductase type 2) polymorphisms, A49T and V89L, and risk of prostate cancer. These potentially functional polymorphisms may alter life-long exposure to androgens with subsequent effects on male health and aging. The aim of this study was to examine the association of these variants with prostate cancer risk, plasma hormone levels and androgenetic alopecia. Subjects include 827 cases and 736 controls from an Australian population-based case,control study of prostate cancer. Information on prostate cancer risk factors and patterns of balding were collected. Plasma levels of testosterone, 3,-diol glucuronide (3,-diolG), dehydroepiandrosterone sulfate, androstenedione, sex hormone-binding globulin and estradiol were measured for controls. No associations with the V89L polymorphism were found. Carriers of the rarer A49T A allele were at a 60% higher risk of prostate cancer (OR = 1.60; 95% CI 1.09,2.36; p = 0.02) and 50% lower risk of vertex and frontal balding (p = 0.03) compared with men homozygous for the more common G allele. Although we found little evidence of association between this variant and plasma levels of 5 measured androgens, circulating 3,-diolG levels were 34% lower in A49T A allele carriers (p < 0.0001). Our study provides evidence that the SRD5A2 A49T A variant is associated with an increased risk of prostate cancer, lower levels of circulating 3,-diolG and decreased risk of baldness. These findings raise important questions with respect to previous assumptions concerning hormonal influences on prostate cancer risk in ageing males. © 2006 Wiley-Liss, Inc. [source] Alcohol consumption and risk of prostate cancer in middle-aged menINTERNATIONAL JOURNAL OF CANCER, Issue 1 2005W. Marieke Schoonen Abstract Alcohol consumption is a modifiable lifestyle factor that may affect prostate cancer risk. Alcohol alters the hormonal milieu and contains chemical substances such as flavonoids (red wine), which may alter tumor cell growth. Data from a population-based case-control study in King County, WA, were utilized to evaluate the association of alcohol consumption with prostate cancer in middle-aged men. A total of 753 newly diagnosed prostate cancer cases, 40,64 years of age, participated in the study. Seven hundred three control subjects, frequency matched to cases by age, were selected through random digit dialing. All participants completed an in-person interview on lifetime alcohol consumption and other risk factors for prostate cancer. Logistic regression models were used to estimate odds ratios (OR) and assess significance (95% confidence intervals [CI]). All tests of statistical significance were two-sided. No clear association with prostate cancer risk was seen for overall alcohol consumption. Each additional glass of red wine consumed per week showed a statistically significant 6% decrease in relative risk (OR = 0.94; 95% CI = 0.90,0.98), and there was evidence for a decline in risk estimates across increasing categories of red wine intake (trend p = 0.02). No clear associations were seen for consumption of beer or liquor. Our present study suggests that consumption of beer or liquor is not associated with prostate cancer. There may be, however, a reduced relative risk associated with increasing level of red wine consumption. Further research is needed to evaluate the potential negative association between red wine intake and prostate cancer risk. [source] Circulating enterolactone and prostate cancer risk: A Nordic nested case-control studyINTERNATIONAL JOURNAL OF CANCER, Issue 1 2002Pär Stattin Abstract Enterolactone, a phytoestrogen belonging to the class of lignans, is produced by the intestinal microflora from precursors in plant foods and has been implicated in protection against cancer. We study the effect of enterolactone on the risk of a subsequent diagnosis of prostate cancer. We conducted a longitudinal, nested case-control study by linkage of 3 biobanks to the cancer registries in Finland, Norway and Sweden, respectively. Enterolactone concentrations were measured by time-resolved fluoroimmunoassay in serum from 794 men who had a diagnosis of prostate cancer at a mean follow-up time of 14.2 years after blood collection and among 2,550 control men matched within each cohort for age (±2 years), date of blood collection (±2 months) and county. The median enterolactone concentrations did not differ between case and control subjects in the full study group (8.4 nmol/L [25th,75th percentile = 4.5,15.0] vs. 8.5 nmol/L [25th,75th percentile = 4.3,15.9]), nor in the national groups. Odds ratios of prostate cancer risk estimated by conditional logistic regression for increasing concentrations of enterolactone in quartiles in the full study group were 1.00 (referent), 1.21 (95% confidence interval [CI] = 0.96,1.52), 1.16 (95% CI = 0.91,1.47) and 1.08 (95% CI = 0.83,1.39). The OR estimate for the highest vs. the lowest quartile of enterolactone in separate analyses of the Norwegian, Finnish and Swedish cohort was 1.21 (95% CI = 0.91,1.60), 1.02 (95% CI = 0.59,1.76) and 0.87 (95% CI = 0.45,1.67), respectively. No support for the hypothesis that high circulating enterolactone is protective against prostate cancer was found. © 2002 Wiley-Liss, Inc. [source] The association between leukocyte telomere length and cigarette smoking, dietary and physical variables, and risk of prostate cancerAGING CELL, Issue 4 2009Lisa Mirabello Summary Telomeres consist of nucleotide repeats and a protein complex at chromosome ends that are essential to maintaining chromosomal integrity. Several studies have suggested that subjects with shorter telomeres are at increased risk of bladder and lung cancer. In comparison to normal tissues, telomeres are shorter in high-grade intraepithelial neoplasia and prostate cancer. We examined prostate cancer risk associated with relative telomere length as determined by quantitative PCR on prediagnostic buffy coat DNA isolated from 612 advanced prostate cancer cases and 1049 age-matched, cancer-free controls from the PLCO Cancer Screening Trial. Telomere length was analyzed as both a continuous and a categorical variable with adjustment for potential confounders. Statistically significant inverse correlations between telomere length, age and smoking status were observed in cases and controls. Telomere length was not associated with prostate cancer risk (at the median, OR = 0.85, 95% CI: 0.67, 1.08); associations were similar when telomere length was evaluated as a continuous variable or by quartiles. The relationships between telomere length and inflammation-related factors, diet, exercise, body mass index, and other lifestyle variables were explored since many of these have previously been associated with shorter telomeres. Healthy lifestyle factors (i.e., lower BMI, more exercise, tobacco abstinence, diets high in fruit and vegetables) tended to be associated with greater telomere length. This study found no statistically significant association between leukocyte telomere length and advanced prostate cancer risk. However, correlations of telomere length with healthy lifestyles were noted, suggesting the role of these factors in telomere biology maintenance and potentially impacting overall health status. [source] Can the Mediterranean diet prevent prostate cancer?MOLECULAR NUTRITION & FOOD RESEARCH (FORMERLY NAHRUNG/FOOD), Issue 2 2009Catherine Itsiopoulos Abstract Prostate cancer is the second most common cancer in men worldwide. Despite the global importance of this cancer, until recently little was known about risk factors apart from the well-established factors: age, family history and country of birth. The large worldwide variation in prostate cancer risk and increased risk in migrants moving from low to high risk countries provides strong support for modifiable environmental factors. We have based our review on the findings of a systematic review undertaken by an expert panel on behalf of the World Cancer Research Fund and the American Institute for Cancer Research, and new data since then, linking identified foods and nutrients with prostate cancer. Evidence indicates that foods containing lycopene, as well as selenium and foods containing it, probably protect against prostate cancer, and excess consumption of foods or supplements containing calcium are a probable cause of this cancer. The expert panel also concluded that it is unlikely that ,-carotene (whether from foods or supplements) has a substantial effect on the risk of this cancer. A recent review on environmental factors in human prostate cancer also found that there were protective effects of vitamin E, pulses, soy foods and high plasma 1,25-dihydroxyvitamin D levels. The Mediterranean diet is abundant in foods that may protect against prostate cancer and is associated with longevity and reduced cardiovascular and cancer mortality. Compared with many Western countries Greece has lower prostate cancer mortality and Greek migrant men in Australia have retained their low risk for prostate cancer. Consumption of a traditional Mediterranean diet, rich in bioactive nutrients, may confer protection to Greek migrant men, and this dietary pattern offers a palatable alternative for prevention of this disease. [source] Correlations of dietary patterns with prostate healthMOLECULAR NUTRITION & FOOD RESEARCH (FORMERLY NAHRUNG/FOOD), Issue 1 2008Maria Stacewicz-Sapuntzakis Abstract Both genetic and environmental influences may be involved in etiology of prostate health and prostate cancer. These include ethnic origin, family history, smoking, and diet. Adiposity and excess energy intake are potentially distinct risk factors and positive associations with prostate cancer risk for both were observed among case-control and cohort studies. Some epidemiological studies support an association between dietary fat, particularly saturated or animal fats, and prostate cancer risk. Of these, several suggest reduced risk with low-fat diets high in n-3 fatty acids and increased risk with high-fat diets rich in n-6 fatty acids. Others suggested association with higher meat intake, possibly due to heterocyclic amines and polycyclic aromatic hydrocarbons, produced during grilling or frying. Positive association of prostate cancer risk with dairy intake could involve ,-methylacyl-CoA racemase activity (required for ,-oxidation of phytanic acid present in dairy products and red meat) or the suppression of vitamin D activity by calcium. Inverse associations were observed with dietary intake of plant foods. These include cereals, soy products, and fruit and vegetable sources of carotenoids. Numerous plant constituents may act synergistically in the prevention and inhibition of prostate disorders. These diet-risk associations may lead to future individualized diet recommendations based upon genetic polymorphisms. [source] Emerging Evidence on the Role of Soy in Reducing Prostate Cancer RiskNUTRITION REVIEWS, Issue 4 2003Mark J. Messina PhD Soyfoods are a unique dietary source of isoflavones, which have both hormonal and non-hormonal effects relevant to prostate cancer prevention. In vitro, the main soybean isoflavone, genistein, inhibits prostate cancer cell growth; in animals, most but not all studies show isoflavone-rich soy protein and isolated isoflavones inhibit prostate tumor development. Currently, although only limited epidemiologic data indicate soy intake reduces prostate cancer risk, results from a pilot intervention trial suggest isoflavones may be beneficial to prostate cancer patients. For several reasons, men concerned about their prostate health may consider incorporating soy into their diet. [source] Population differences in the testosterone levels of young men are associated with prostate cancer disparities in older menAMERICAN JOURNAL OF HUMAN BIOLOGY, Issue 4 2010Louis Calistro Alvarado Although there is evidence that greater exposure to testosterone is associated with an increased risk of prostate cancer, a recent analysis of 18 prospective studies found no relationship between levels of endogenous sex hormones and prostate cancer development. However, the reviewed studies were subject to methodological constraints that would obscure any potential relationship between prostate cancer and androgenic hormones. If prostate cancer risk is mediated by lifetime exposure to testosterone, then case-control studies that concentrate on endogenous sex hormones near the ages that prostate cancer is diagnosed would provide limited information on cumulative testosterone exposure across the lifespan. Alternately, early adulthood has been suggested as the most salient period to evaluate the influence of steroid physiology on prostate carcinogenesis. As such, an exhaustive literature search was completed to obtain testosterone values reported for study samples of younger men, along with prostate cancer incidences for the larger populations from which the study populations were sampled. A novel analytical method was developed to standardize, organize, and examine 12 studies reporting testosterone levels for 28 population samples. Study populations were generally apportioned according to ethnicity and geographic residence: Americans of African, Asian, Caucasian, and Hispanic ancestry from several different regions within the United States as well as men from China, Germany, Japan, Kuwait, New Zealand, South Korea, and Sweden. Population differences in the testosterone levels of young men were significantly associated with population disparities in the prostate cancer incidence of older men (Spearman's rho = 0.634, p = 0.002). Am. J. Hum. Biol. 2010. © 2010 Wiley-Liss, Inc. [source] Diet and prostate cancer risk with specific focus on dairy products and dietary calcium: A case,control studyTHE PROSTATE, Issue 10 2010Sara Raimondi Abstract BACKGROUND Despite the prevalence of prostate cancer worldwide, only a few risk factors have been well-established. The role of diet, especially of dairy products, in the etiology of prostate cancer is still controversial. METHODS This study assessed the association of dietary components, particularly dairy products and dietary calcium, on prostate cancer risk in a case,control study of 197 cases and an equal number of individually matched controls recruited in Montreal, Canada. A semi-quantitative food frequency questionnaire was administered in which the usual consumption frequency and amounts consumed of more than 200 food items were recorded. RESULTS We found a twofold increased risk of prostate cancer associated with an increased intake of dairy products {Odds Ratio (OR),=,2.19; 95% Confidence Intervals (CI) 1.22,3.94}. A significant trend of decreasing prostate cancer risk with higher intake was found for legumes, nuts, finfish/shellfish and for ,-tocopherol after adjustment for calcium intake. Milk was the only dairy product significantly associated with prostate cancer risk, with OR,=,2.27; 95% CI (1.25,4.09) for the highest versus lowest quartiles of consumption. Calcium, the main micronutrient contained in dairy products, showed only a borderline association with prostate cancer risk (P,=,0.09), with slightly higher risk for higher calcium intake. In conclusion, this study supports the hypothesis that dairy products, especially milk, are involved in the etiology of prostate cancer. However, the mechanisms by which the various nutrients in dairy products and total diet may interact to influence this risk remain unknown. Prostate 70: 1054,1065, 2010. © 2010 Wiley-Liss, Inc. [source] HNF1B and JAZF1 genes, diabetes, and prostate cancer risk,THE PROSTATE, Issue 6 2010Victoria L. Stevens Abstract BACKGROUND Epidemiologic studies have shown that men with type II diabetes have a lower risk of prostate cancer than non-diabetic men. Recently, common variants in two genes, HNF1B and JAZF1, were found to be associated with both of these diseases. METHODS We examined whether the relationship between HNF1B and JAZF1 variants and decreased prostate cancer risk may potentially be mediated through diabetes in two large prospective studies, the Cancer Prevention Study II Nutrition Cohort and the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial. RESULTS Three HNF1B SNPS, rs11649743, rs4430796, and rs7501939, were associated with decreased risk of prostate cancer and were also associated, with marginal statistical significance, with increased risk of diabetes. The JAZF1 SNPs rs6968704 and rs10486567 were associated with decreased risk of prostate cancer but were not associated with diabetes. All five SNP,prostate cancer relationships did not substantially differ when the analyses were stratified by diabetic status or when diabetic status was controlled for in the model. Furthermore, the association of diabetes with prostate cancer was not altered when the SNPs were included in the logistic model. CONCLUSIONS These findings indicate that the HNF1B variants are directly associated with both diabetes and prostate cancer, that diabetes does not mediate these gene variant,prostate cancer relationships, and the relationship between these diseases is not mediated through these gene variants. Prostate 70: 601,607, 2010. © 2009 Wiley-Liss, Inc. [source] A functional polymorphism in Pre-miR-146a gene is associated with prostate cancer risk and mature miR-146a expression in vivo,THE PROSTATE, Issue 5 2010Bin Xu Abstract BACKGROUND A G,>,C polymorphism (rs2910164) which is located in the sequence of miR-146a precursor, results in a change from a G:U pair to a C:U mismatch in its stem region. To explore whether rs2910164 plays any role in prostate cancer (CaP), we analyzed the association between miR-146a polymorphism and risk of CaP and the expression of miR-146a with different genotypes in CaP tissues in southern Chinese Han population. MATERIALS AND METHODS Two hundred fifty-one CaP and 280 control subjects were included in the cancer association study, and 15 CaP tissue samples were used to test the expression of the miRNA precursors by real-time quantitative reverse transcription PCR. RESULTS We found that subjects carrying CC homozygotes had a 0.65-fold reduced risk (95% CI,=,0.43,0.99) than those carrying GG/GC genotypes (P,=,0.03), and the C allele displayed a lower prevalence of CaP compared with the G allele (OR,=,0.73, 95% CI,=,0.57,0.94, P,=,0.01). Moreover, hsa-miR-146a quantification showed that homozygous carriers of the C-variant had significantly decreased miRNA levels compared to the carriers of the GG/GC genotype. CONCLUSIONS The natural genetic variation in pre-miR-146a affects the amount of mature miR-146a, contributes to the genetic predisposition to CaP. Prostate 70: 467,472, 2010. © 2009 Wiley-Liss, Inc. [source] Chromosome 8q24 risk variants in hereditary and non-hereditary prostate cancer patients,THE PROSTATE, Issue 5 2008Jielin Sun Abstract Background Multiple variants in three regions at 8q24 are consistently found to be associated with prostate cancer (PCa) risk in population-based association studies. The role that these variants may play in familial prostate cancer risk has not been extensively investigated. Methods We evaluated 12 SNPs at three 8q24 regions using population-based association and family-based linkage and association methods in hereditary PCa (HPC) probands and their families, non-HPC patients, and unaffected screened controls, all recruited at Johns Hopkins Hospital. Results For multiple variants in Region 1 (e.g., rs1447295) and Region 2 (e.g., rs16901979), we found statistically significantly higher frequencies of previously identified risk alleles and genotypes in HPC probands than in unaffected controls. Furthermore, in Region 2 the risk alleles were statistically significantly more frequent in HPC probands than in non-HPC patients. Family-based transmission tests found risk alleles of SNPs in Region 2, but not in Regions 1 and 3, were significantly over-transmitted to affected men in these families. We found little evidence supporting PCa linkage at 8q24 in 168 HPC families, in part explained by the observation of multiple, different risk allele-containing haplotypes segregating in the vast majority of these families. Conclusions Our study further supports the presence of PCa susceptibility loci at 8q24, particular at Region 2, and also provides evidence that these SNPs play an important role in familial prostate cancer. Large family-based studies are needed to confirm our novel findings. Prostate 68: 489,497, 2008. © 2008 Wiley-Liss, Inc. [source] Vitamin D receptor (VDR) gene polymorphisms and haplotypes, interactions with plasma 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D, and prostate cancer riskTHE PROSTATE, Issue 9 2007Bahar Mikhak Abstract BACKGROUND The vitamin D receptor (VDR) is required for actions of vitamin D. The binding of 1,25-dihydroxyvitamin D to the VDR on prostatic epithelial cells prompts the regulation of cancer-related genes. METHODS We conducted a nested case-control study in the Health Professionals Follow-up Study to investigate the role of the VDR Cdx2, Fok1, and Bsm1 gene polymorphisms and associated haplotypes and their interaction with plasma vitamin D metabolites in relation to prostate cancer (PC) risk. RESULTS No association was found between these SNPs or their associated haplotypes and all PC subtypes except that haplotype 2 (A-f-b) with Cdx2 A, Fok1 f, and Bsm1 b alleles and haplotype 3 (A-F-B) with Cdx2 A, Fok1 F and Bsm1 B alleles compared to the most common haplotype (A-F-b), were associated with reduced risk of aggressive PC (high stage or Gleason sum ,7; P,=,0.02), both with two alleles suspected of being low risk. Carriers of the variant Cdx2 A allele who were deficient in plasma 25-hydroxyvitamin D (,15 ng/ml) compared to non-carriers with normal 25-hydroxyvitamin D, had a lower risk of total and poorly differentiated PCs (Gleason sum ,7) (P for interaction,=,0.02 and 0.04, respectively). Plasma 1,25-dihydroxyvitamin D deficiency (,26 pg/ml) was associated with a threefold risk of poorly differentiated PC (P for interaction,=,0.01) when comparing carriers of the Cdx2 A allele to non-carriers with normal 1,25-dihydroxyvitamin D. CONCLUSION In this population of men, none of the VDR polymorphisms studied was associated with susceptibility to PC. Prostate 67: 911,923, 2007. © 2007 Wiley-Liss, Inc. [source] Glutathione S-transferase M1, T1, and P1 polymorphisms and prostate cancer risk in middle-aged menTHE PROSTATE, Issue 2 2006Ilir Agalliu Abstract BACKGROUND The glutathione S-transferase (GST) enzymes detoxify several carcinogens. Genetic polymorphisms in GSTM1, T1, and P1 (Ile105Val) have been associated with prostate cancer, however, results have been inconsistent across studies. METHODS Data from a population-based case-control study in King County, Washington, were used to further evaluate the relationships between these GST polymorphisms and prostate cancer. Incident cases (n,=,590) were 40,64 years old, diagnosed from 1993 through 1996, and identified via the SEER cancer registry. Controls (n,=,538) were identified via random digit dialing, and frequency age-matched to cases. Logistic regression was used to estimate odds ratios (OR) and 95% confidence intervals (CI). RESULTS Risk of prostate cancer was moderately increased among Caucasians with the GSTM1 -null genotype (OR,=,1.54; 95% CI 1.19,2.01). There were no associations for either GSTT1 or P1(Ile105Val). The association between the GSTM1 -null genotype and prostate cancer was not different according to cancer aggressiveness defined by stage at diagnosis and Gleason score. Among GSTM1 -null Caucasians, the relative risk of prostate cancer increased linearly with increasing pack-years of smoking (P -value for trend,=,0.007), with the highest ORs observed for smokers of >30 pack-years. CONCLUSIONS Findings suggest that the GSTM1 -null genotype defines a subgroup of men at higher risk of prostate cancer, particularly if they are heavy smokers. © 2005 Wiley-Liss, inc. [source] Longitudinal PSA changes in men with and without prostate cancer: Assessment of prostate cancer riskTHE PROSTATE, Issue 3 2005Andreas P. Berger Abstract BACKGROUND To determine longitudinal PSA changes over a period of 10 years in patients with and without prostate cancer. METHODS Serial PSA measurements performed over 10 years were evaluated in 353 men who eventually developed prostate cancer and in 2.462 participants of a screening program without prostatic malignancy. RESULTS In men with cancer, mean tPSA increased from 2.28 ng/ml at 10 years before diagnosis to 6.37 ng/ml at the time of postive biopsy (PSA velocity: 0.409 ng/ml/year). PSA velocity was significantly associated with Gleason scores and pathologic stage. In the benign group (n,=,2.462), mean tPSA increased from 1.18 to 1.49 ng/ml over a period of 10 years (PSA velocity of 0.03 ng/ml/year). Of the subjects with tPSA levels of 2 ng/ml or less, 2 years prior to cancer diagnosis, 11.4% had tPSA values of more than 4 ng/ml at the time of biopsy. Of the 972 men with tPSA below 1 ng/ml 2 years before the most recent measurement was obtained, 966 (99.4%) had no evidence of prostate cancer 2 years later, while six were found to have malignancies (0.6%). CONCLUSIONS Longitudinal PSA changes in men with and without prostate cancer are significantly different. Annual testing may not be required in men with baseline tPSA levels of 1 ng/ml or below, whereas in patients with levels higher than 1 ng/ml, it seems to be indicated because of the significant percentage of men presenting with tPSA levels of more than 4 ng/ml two years later. © 2005 Wiley-Liss, Inc. [source] Evaluation of the Prostate Cancer Prevention Trial Risk calculator in a high-risk screening populationBJU INTERNATIONAL, Issue 3 2010David J. Kaplan Study Type , Diagnostic (exploratory cohort) Level of Evidence 2b OBJECTIVE To evaluate the Prostate Cancer Prevention Trial (PCPT) risk calculator in a screening cohort of young, racially diverse, high-risk men with a low baseline prostate-specific antigen (PSA) level and enrolled in the Prostate Cancer Risk Assessment Program (PRAP). The PCPT calculator provides an assessment of prostate cancer risk based on age, PSA level, race, previous biopsy, and family history. PATIENTS AND METHODS Eligibility for PRAP includes men aged 35,69 years who are African-American, have a family history of prostate cancer, or have a known BRCA1/2 mutation. PCPT risk scores were determined for PRAP participants, and were compared to observed prostate cancer rates. RESULTS In all, 624 participants were evaluated, including 382 (61.2%) African-American men and 242 (38.7%) men with a family history of prostate cancer; the median (range) age was 49.0 (34.0,69.0) years and the median PSA level 0.9 (0.1,27.2) ng/mL. The PCPT risk score correlated with prostate cancer diagnosis, as the median baseline risk score in patients diagnosed with prostate cancer was 31.3%, vs 14.2% in patients not diagnosed with prostate cancer (P < 0.001). The PCPT calculator similarly stratified the risk of diagnosis of Gleason score ,7 disease, as the median risk score was 36.2% in patients diagnosed with Gleason ,7 prostate cancer vs 15.2% in all other participants (P < 0.001). CONCLUSION The PCPT risk calculator score was found to stratify prostate cancer risk in a cohort of young, primarily African-American men with a low baseline PSA level. These results support further evaluation of this predictive tool for assessing the risk of prostate cancer in high-risk men. [source] 16 Kallikrein 15 (KLK15) in prostate cancer: in silico analysis and single nucleotide polymorphism verificationBJU INTERNATIONAL, Issue 2006M.A. KEDDA Introduction:, Prostate cancer is the most common cancer in Caucasian men and there is strong evidence that kallikreins are part of an enzymatic cascade pathway activated in this disease. Altered KLK15 expression has been associated with cancer progression and grade and we postulate that single nucleotide polymorphisms (SNPs) in the KLK15 gene, will alter gene expression and will be associated with prostate cancer susceptibility and prognosis. Materials and Methods:, We have used in silico prediction of function of wildtype and variant promoter sequences through assessment of hormone receptor elements and transcription factor binding sites; as well as prediction of likely splice variants through genomic, splicing and EST databases and web sites, and multiple sequence alignment packages. We have also used PCR and sequence analysis to further characterise the promoter region of the gene. Results:,In silico analysis of the KLK15 gene has identified the following: two putative promoter regions, two putative androgen response elements (AREs) and four putative estrogen response elements (EREs); two clusters of cis elements; and 109 SNPs. Forty-seven SNPs alter transcription factor sites (22 gain sites), 20 gain/increase probability of an ERE and three alter nuclear hormone receptor binding sites. Three new EST clones have been identified by analysis of gene expression in CGAP databases and suggest a new KLK15 splice variant, with a different start site. Conclusion:, We have identified a number of new SNPs in the KLK15 gene, which may be functionally important and, in collaboration with the Queensland Cancer Fund (ProsCan Study), we will further investigate the association of these SNPs with prostate cancer risk and prognosis. [source] Diet, anthropometric measures and prostate cancer risk: a review of prospective cohort and intervention studiesBJU INTERNATIONAL, Issue 8 2004P.C. Dagnelie ABSTRACT We reviewed 37 prospective cohort and four intervention studies on potential dietary risk factors for prostate cancer, published between 1966 and September 2003. Some studies were limited by small size, crude measurement of dietary exposure and limited control for confounders. Intervention and prospective cohort studies support a protective role against prostate cancer for selenium, and possibly for vitamin E, pulses and tomatoes/lycopene. Overall consumption of meat, eggs, vegetables, fruit, coffee, tea, carotenoids and vitamins A, C and D was not consistently related to prostate cancer risk. Intervention studies also indicate that supplementation with ,-carotene does not lower prostate cancer risk, except possibly in men with low ,-carotene status at baseline. For specific types of meat, alcoholic drinks, dairy products, fat and anthropometric measures, most cohort studies suggest either an increased risk or no relation with prostate cancer. For calcium, two cohort studies suggest an increased risk at very high calcium intakes (>2000 mg/day). In conclusion, prospective studies are consistent with a protective role for selenium, and possibly vitamin E, pulses and tomatoes/lycopene, in the aetiology of prostate cancer. Studies are inconclusive on the role of meat, dairy products, fat, vegetables, fruits, alcohol and anthropometric measures, whereas a very high calcium intake appears to be positively associated with prostate cancer risk. [source] Association between leptin receptor gene polymorphisms and early-onset prostate cancerBJU INTERNATIONAL, Issue 1 2003Z. Kote-Jarai Significant tissue loss is a consistent feature of ureteric obstruction with, most studies showing increased programmed cell death or apoptosis of kidney epithelial cells. The study by Chuang et al. showed that there is also muscular damage during obstruction, specifically of the ureteric myocytes. More importantly they show for the first time that this induction of cell death is associated with the increased expression of cytochrome c and the caspases, key proteins that drive the induction of apoptosis. Admittedly they do not show whether cytochrome c is released from the mitochondria or that the caspases are truly activated, important events in the cell death pathway, but an increase in their expression does indicate their role in this process. Understanding the pathways leading to tissue loss during ureteric obstruction has important implications in the development of novel treatments for this condition. OBJECTIVE To report a case-control study examining the relationship between polymorphisms in the leptin receptor (OBR) gene and the development of young-onset prostate cancer, because epidemiological studies report that prostate cancer risk is associated with animal fat intake, and thus we investigated if this association occurs via this genetic mechanism. PATIENTS, SUBJECTS AND METHODS The Lys109Arg (OBR1) and Gln223Arg (OBR2) polymorphisms in the coding region of OBR were studied in blood DNA from 271 patients with prostate cancer aged < 56 years at diagnosis and 277 geographically matched control subjects. Cases were collected through the Cancer Research UK/British Prostate Group Familial Prostate Cancer Study. Blood DNA was genotyped using the polymerase chain reaction and a restriction enzyme digest. RESULTS There was no statistically significant association between the OBR genotype and prostate cancer risk; men homozygous for 109Arg genotype had a slightly increased risk for prostate cancer, with a relative risk (95% confidence interval) of 1.36 (0.65,2.85), and those homozygous for the 223Arg allele had some reduction in prostate cancer risk, at 0.82 (0.58,1.26), but neither was statistically significant. CONCLUSION This case-control study showed no significant association between leptin receptor gene polymorphisms and the risk of young-onset prostate cancer, suggesting that genetic variations in OBR are unlikely to have a major role in the development of early-onset prostate cancer in the UK. [source] Obesity in relation to prostate cancer risk: comparison with a population having benign prostatic hyperplasiaBJU INTERNATIONAL, Issue 6 2003J. Irani Objective To analyse the relationship between obesity and prostate cancer, when compared with men with benign prostatic hyperplasia (BPH). Patients and methods The records were reviewed of consecutive patients with histologically confirmed prostate cancer admitted for prostate surgery between January 1993 and February 1999. Controls were selected from patients who were hospitalized at the same time for the surgical treatment of BPH. One control was matched to each case by age. Obesity was defined as a body mass index (BMI) of> 29 kg/m2. Results The study included 194 cases and 194 controls; their median (range) age at operation was 69.5 (50,88) years in both groups, and the BMI 26.1 (16.6,38.1) kg/m2 in the cancer and 25.7 (15.1,36.8) kg/m2 in the BPH group. The difference between the groups was not significant (P = 0.06). Obesity was significantly associated with prostate cancer, with an odds ratio (95% confidence interval) of 2.47 (1.41,4.34). Cases with advanced disease had a higher BMI than those with localized disease, but when age was considered the difference was not significant. Conclusion In general the BMI was not significantly associated with prostate cancer when compared with men having BPH. However, obese men had 2.5 times the risk of having prostate cancer. [source] Serum phytoestrogens and prostate cancer risk in a nested case-control study among Japanese menCANCER SCIENCE, Issue 1 2004Kotaro Ozasa The purpose of this study was to examine whether a high serum concentration of phytoestrogens reduces the risk of prostate cancer in a case-control study nested in a community-based cohort in Japan (Japan Collaborative Cohort (JACC) Study). Information on lifestyles and sera of the subjects were collected in 1988,90, and they were followed up to 1999. Incident and dead cases of prostate cancer and controls were matched for study area and age. Phytoestrogens and sex hormones in sera stored at ,80°C were measured in 2002. Of 14,105 male subjects of the cohort who donated their sera, 52 cases and 151 controls were identified. Three datasets were analyzed; 1) all subjects, 2) 40 cases and 101 controls after excluding subjects with low testosterone levels who were suspected of having had medical intervention, and 3) 28 cases and 69 controls with prostate specific antigen level of ,10.0 ng/ml. The odds ratio (OR) for the highest level to the lowest was 0.38 (95% confidence interval (CI); 0.13, 1.13) for genistein, 0.41 (0.15, 1.11) for daidzein, and 0.34 (0.11, 1.10) for equol for the second dataset. Genistein and daidzein showed similar findings in the third one. Equol and equol/daidzein ratio showed consistent findings in all three datasets (OR=0.39, 95% CI; 0.13, 0.89, trend P=0.02 for the first dataset). Their effects seemed to be independent of serum sex hormones. In conclusion, serum genistein, daidzein, and equol seemed to dose-dependently reduce prostate cancer risk. (Cancer Sci 2004; 95: 65,71) [source] | ||||||||||||||||||||||||||||