Abstract Polymorphic variants in the PTEN (rs2735343), PI3K (rs2699887), AKT1 (rs2494750), AR (rs17302090), and AMACR (rs3195676) genes were evaluated as possible molecular markers of susceptibility, prognosis, and progression of prostate cancer (PCa), in a case-control study. Samples consisted of 277 patients with PCa and 277 controls from Londrina, PR, Brazil. SNPs were analyzed by real-time PCR. A family history of cancer, including PCa, as well as level of schooling were risk factors for PCa. The data were obtained via logistic regression, using odds ratios with a CI 95%. The genotypes of AKT1 and AKT1+AR demonstrated an association with protection for the disease. The combination of SNPs with the histopathological tumor data between allele variants of AMACR, AKT1+AR, and AKT1+AMACR indicated an association with protection against seminal vesicle invasion. The polymorphisms AKT1+AR and PI3K+AR were associated with protection against tumor bilaterality. The genotype combinations PTEN+AMACR and PTEN+AR were associated with the risk of extracapsular extension. Of the five genes studied, two were associated with protection for PCa, four were associated with protection for some prognostic variables, and only one was associated with risk. Thus, these SNPs are candidates for markers to discriminate men with better or worse prognosis for PCa.

PURPOSE: SUI (Stress Urinary Incontinence) results from sudden increases in intravesical peak pressures exceeding urethral resistance leading to involuntary urine loss. Obesity and smoking are well established reversible risk factors for SUI and may alter intravesical peak pressures. BMI, smoking status, and other clinical factors were studied to determine their relationship to CIPP (maximal Intravesical Peak Pressures generated by Cough) in SUI complaining women. MATERIALS AND METHODS: Three hundred nineteen women complaining of SUI were evaluated with medical history and urodynamics. Age, parity, comorbidities, previous surgery, BMI and history of smoking were obtained. The maximal intravesical peak pressures generated by cough (CIPP) and cough leak point pressure (CLPP) were acquired. Univariate and multivariate analysis were conducted. RESULTS: Current smokers and former smokers had similar CIPP (170cmH2O and 170cmH2O; p = 0.5, respectively); Those individuals who had never smoked had significantly lower CIPP (140cmH2O; p = 0.000 and p = 0.009 respectively). BMI was directly related to CIPP (r = 0.41; p = 0.000). Vaginal deliveries (r = -0.15, p = 0.08) and diabetes (r = 0.15, p = 0.016) were also directly related to CIPP on univariate analysis. Only smoking status (p = 0.000) and BMI (p = 0.000) were independently significantly related to CIPP on multivariate analysis. CONCLUSIONS: Obesity and smoking showed increased CIPP (maximal Intravesical Peak Pressures generated by Cough). While reduced BMI is related to lower CIPP, smoking cessation does not appear to diminish CIPP. These findings suggest that weight loss may reduce incontinence by CIPP modulation. However, the benefits of smoking cessation without additional lifestyle modification, may have no benefit to improve urinary incontinence.