Risk Of Incident Prostate Cancer Research Articles

Long-Term Prediction of Prostate Cancer Up to 25 Years Before Diagnosis of Prostate Cancer Using Prostate Kallikreins Measured at Age 44 to 50 Years

We examined whether prostate-specific antigen (PSA) forms and human kallikrein 2 (hK2) measured at age 44 to 50 years predict long-term risk of incident prostate cancer. From 1974 to 1986, 21,277 men age 50 years in Malmö, Sweden, enrolled onto a cardiovascular study (74% participation). The rate of PSA screening in this population is low. According to the Swedish Cancer Registry, 498 were later diagnosed with prostate cancer. We measured hK2, free PSA, and total PSA (tPSA) in archived blood plasma from 462 participants later diagnosed with prostate cancer and from 1,222 matched controls. Conditional logistic regression was used to test for association of prostate cancer with hK2 and PSA forms measured at baseline. Median delay between venipuncture and prostate cancer diagnosis was 18 years. hK2 and all PSA forms were strongly associated with prostate cancer (all P < .0005). None of the 90 anthropometric, lifestyle, biochemical, and medical history variables measured at baseline was importantly predictive. A tPSA increase of 1 ng/mL was associated with an increase in odds of cancer of 3.69 (95% CI, 2.99 to 4.56); addition of other PSA forms or hK2 did not add to the predictive value of tPSA. tPSA remained predictive for men diagnosed > or = 20 years after venipuncture, and the predictive value remained unchanged in an analysis restricted to palpable disease. A single PSA test at age 44 to 50 years predicts subsequent clinically diagnosed prostate cancer. This raises the possibility of risk stratification for prostate cancer screening programs.

The UGT2B17 gene deletion polymorphism and risk of prostate cancer : A case–control study in Caucasians

Background: UDP-glucuronosyltransferase (UGT) 2B17 is a phase II metabolizing enzyme that mediates the glucuronidation of C 19 steroids. A deletion polymorphism in the UGT2B17 gene is associated with a substantial reduction in glucuronidation activity in vitro. Methods: We examined the association between the UGT2B17 deletion polymorphism and the risk of incident prostate cancer in a population-based study from central Arkansas that included 411 Caucasian cases and 397 Caucasian controls. We developed a novel high-throughput procedure that uses real-time PCR and allelic discrimination for genotyping analysis. Results: The prevalence of the UGT2B17 deletion [(0/0)] was 12% in the controls, which was consistent with previous population estimates and with Hardy Weinberg equilibrium. There was no association between the UGT2B17 deletion polymorphism and prostate cancer risk in unconditional logistic regression analysis. Compared to the wild-type group (+/+), the adjusted odds ratio (OR) was 0.89 (95% CI = 0.55–1.45) for the homozygous deletion (0/0), and the OR was 0.99 (95% CI = 0.73–1.35) for the heterozygote group (+/0). Conclusion: These findings show that the UGT2B17 deletion polymorphism is not associated with prostate cancer risk in Caucasians.

History of Diabetes, Clinical Features of Prostate Cancer, and Prostate Cancer Recurrence-Data from CaPSURETM (United States)

There is a growing epidemiologic literature suggesting an inverse association between history of diabetes and risk of incident prostate cancer. To our knowledge, the relationship between diabetes and tumor features and risk of recurrence among men with prostate cancer has not been examined previously. We hypothesized that men with diabetes would present with more favorable prostate cancer and experience lower risk of recurrence. We identified 691 men with diabetes at the time of prostate cancer diagnosis, among 6722 men diagnosed with prostate cancer in 1989 to 2002 within CaPSURE(TM), a community-based prostate cancer registry study. We compared clinical and socio-demographic variables by diabetes status, using chi2 tests, t-tests, and multinomial logistic regression. We examined recurrence rates for prostate cancer among patients with and without diabetes using Kaplan-Meier log-rank tests and Cox proportional hazard models. In multivariate analyses, history of diabetes was not associated with any diagnostic clinical parameter, and treatment-specific recurrence rates for prostate cancer generally did not differ by diabetes history. Among men with low-prognostic risk or who were younger at prostate cancer diagnosis, being diabetic (versus not) was associated with an elevated risk of recurrence after radiation therapy, in multivariate analyses. Contrary to data suggesting that diabetes may be modestly protective against risk of incident prostate cancer, we did not observe any evidence of an inverse association between history of diabetes and aggressiveness at diagnosis or risk of recurrence, in this population of men with prostate cancer.

Obesity and the risk of prostate cancer (United States)

The role of obesity in prostate cancer etiology remains controversial. A recent report suggested that obese men younger than age 60 may have a lower risk of developing prostate cancer than men the same age who are not obese. The current study used a nested, matched case-control study design and data collected in the General Practice Research Database between January 1991 and December 2001 to assess the association between body mass index (BMI) and the risk of incident prostate cancer. Seven hundred and thirty cases of prostate cancer with adequate information on BMI were identified and matched to 2740 controls on age, sex, general practice, and index date. Obese men (BMI > or = 30.0 kilograms [kg]/square of height in meters [m(2)]) were at lower risk of developing prostate cancer (AOR=0.78, 95% CI: 0.56, 1.09) compared to normal weight men (BMI=23.0-24.9 kg/m(2)), and the data best fit an inverse quadratic model for the relation between BMI and the risk of prostate cancer. This study provides modest support for a protective association between obesity and the risk of incident prostate cancer.

Alcohol intake, drinking patterns, and risk of prostate cancer in a large prospective cohort study.

Alcohol drinking has been extensively studied in relation to prostate cancer, yet findings on the direction of the association are equivocal. Previous studies have not examined drinking patterns. Thus, the authors prospectively evaluated the associations between these factors and risk of incident prostate cancer (n = 2,479) in a cohort study of 47,843 US men (1986-1998). The men completed a questionnaire at baseline that included information on consumption of specific types of alcohol and frequency of use. The authors estimated hazard ratios using Cox proportional hazards regression for average alcohol intake and number of days per week on which alcohol was consumed stratified by average weekly intake (<105 g/week vs. > or = 105 g/week). Compared with nondrinking, the hazard ratio for consumption increased slightly from an average of 5.0-14.9 g/day (hazard ratio (HR) = 1.05, 95% confidence interval (CI): 0.94, 1.18) to 30.0-49.9 g/day (HR = 1.13, 95% CI: 0.96, 1.33), but it was not increased at > or = 50 g/day (HR = 1.00, 95% CI: 0.77, 1.31) after adjustment for recent smoking and other factors. Compared with abstainers, risk was greatest among men who consumed an average of > or = 105 g/week but who drank on only 1-2 days per week (HR = 1.64, 95% CI: 1.13, 2.38). These results suggest that moderate or greater alcohol consumption is not a strong contributor to prostate cancer risk, except possibly in men who consume large amounts infrequently.

Hypertension, Heart Rate, Use of Antihypertensives, and Incident Prostate Cancer

PURPOSE: Recent studies have reported conflicting results on a possible relationship between hypertension, heart rate, and prostate cancer. A model has been developed suggesting that high blood pressure and high heart rate may both be markers for increased central sympathetic nervous activity, which may result in androgen-mediated stimulation of prostate cancer growth. METHODS: In this study we examined the associations between hypertension, heart rate, use of antihypertensive medications, and incident prostate cancer in a cohort of 2442 men. Data from the Cardiovascular Health Study (CHS), an NHLBI-sponsored observational study of adults age 65 or older in four U.S. communities, were analyzed using Cox proportional hazards regression. Seated systolic and diastolic blood pressures were measured using a standardized protocol at the initial clinical examination and annually at follow-up visits. Medications data were transcribed by trained interviewers from prescription medication containers brought into the clinic by participants. RESULTS: A total of 209 cases of incident prostate cancer were identified from either an ICD-9 code of 185 in hospital medical records (n = 130) or by self-report from annual surveillance interviews (n = 79). An average of 5.6 years of follow-up was available for analyses. No associations between blood pressure measures at entry into the study and prostate cancer were found, although these results may have been affected by subsequent treatment of hypertension. An association between resting heart rate (HR) equal to or greater than 80 beats per minute and incident prostate cancer was found compared to men with a rate of less than 60 beats per minute (HR: 1.6, 95% confidence interval [CI]: 1.03–2.5). An inverse association was found between risk of incident prostate cancer and use of any antihypertensive medication (HR: 0.7, 95% CI: 0.5–0.9). A test of heterogeneity found no difference between use of the specific classes of antihypertensive medication and the association with prostate cancer risk. CONCLUSIONS: These data tend to support the hypothesized causal pathway between vascular disease markers and prostate cancer.