Epidemiological studies related to androgens and prostate cancer have focused on serum determination of testosterone, androstenedione, and dehydroepiandrosterone, with inconsistent results. Herein, we hypothesized that differences in androgen biosynthetic and metabolic pathways, rather than differences in specific androgen concentrations, are associated with prostatic carcinogenesis. Therefore, spot urine samples from 111 incident prostate cancer cases with Gleason score at diagnosis and 227 healthy population controls, were analyzed. Urinary androgen concentrations (ng/mg creatinine) were determined by ultra-performance liquid chromatography-tandem mass spectrometry. Using a factor analysis, we identified three androgen urinary excretion patterns. In a subsample, we evaluated a modification effect of the androgen receptor CAG polymorphism. Pattern I, characterized by androstenedione and testosterone hydroxylated metabolites (11β-OHT; 2β-OHT; 15β-OHT; 2α-OHT; 6β-OHT), was associated with high prostate cancer odds among carriers of androgen receptor gene (CAG)>19 repeats (OR: 3.67 95% CI: 1.23-11.0; p for interaction=0.009). Conversely, higher testosterone excretion (pattern III), was marginally associated with lower (OR: 0.35 95% CI:0.12-1.00, p for trend=0.08) poorly differentiated prostate cancer (Gleason ≥8). No clear association was observed with pattern II (dehydroepiandrosterone; 16α and 16β-OHT). Our results were consistent with the previous evidence which suggests that the C11-oxy backdoor pathway is important for prostatic carcinogenesis. Androgen urine excretion analysis could be useful for prostate cancer diagnosis, treatment, and prognosis; however, further studies with a larger number of samples and the urinary determination of 11-ketoandrogens are necessary.
Flavonoids are a broad group of bioactive compounds with anticarcinogenic effects on the prostate that have been scarcely evaluated in Latin American populations. Our objective was to evaluate the association between dietary patterns of flavonoid intake and prostate cancer (PC) in a population-based case-control study carried out in Mexico City. Based on a semiquantitative food-frequency questionnaire with a frame reference of 3 y before diagnosis or interview, we used an updated database for estimating the daily intake (mg/d) of flavones, flavonols, and flavanols for 395 confirmed incident PC cases and 797 population controls matched by age (±5 years). Histological PC differentiation was evaluated using the Gleason score at diagnosis. Flavonoid dietary intake patterns (FDIPs) were determined through principal component analysis, and their association with PC was estimated using logistic regression models. Three FDIPs were identified: gallate pattern (GP) characterized by (-)-epicatechin-3-O-gallate, (-)-epigallocatechin-3-O-gallate and (+)-gallocatechin; luteolin pattern (LP) characterized by luteolin and (-)-epigallocatechin-3-O-gallate; and a mixed pattern (MP) that included (+)-catechin, (-) -epicatechin, and quercetin. A higher GP (OR T3 vs.T1=0.47; 95% CI 0.33-0.66) and LP intake (OR T3 vs. T1=0.39; 95% CI 0.27-0.59) were associated with a decreased PC likelihood. In contrast, a higher MP intake (OR T3 vs. T1=2.32; 95% CI 1.67-3.23) increased PC likelihood. The possible differential and synergistic anticarcinogenic role of flavonoid compounds in PC deserves further study.
BackgroundThe interplay between pubertal events patterns (PEP) and prostate cancer (PCa) remains poorly understood. Therefore, we investigated the association of PEP with the odds of PCa, and PCa histological differentiation in men residents of Mexico city.MethodsIn this case–control study, we analyzed the information of 371 incident prostate cancer cases and 775 controls matched on age (±5 years). High‐grade prostate cancer was classified with Gleason score at diagnosis as ≥8. With information related to beard growth, age at maximum height attainment, and acne severity, the k‐medoids algorithm was used to identify three mutually exclusive PEP (early, intermediate, and late). This association was evaluated using multivariable nonconditional logistic regression models.ResultsMen with late PEP, characterized by age at maximum height attainment at around 23 years and no history of acne, was inversely associated with incident (odds ratio [OR]: 0.27; 95% confidence interval [CI]: 0.15–0.48, p trend <0.01) and high‐grade prostate cancer (OR: 0.24; 95% CI: 0.09–0.59, p trend <0.01). Similar associations were observed even after adjusting by IGF‐1 (OR: 0.19; 95% CI: 0.06–0.58) and androgens excretion (OR: 0.21; 95% CI: 0.06–0.66). Only the association between the absence of acne and prostate cancer remained significant after adjustment by these biomarkers.ConclusionsThis study suggests that pubertal characteristics might be helpful in identifying risk groups, among which, secondary prevention strategies could be applied. Also, the results agree with previous work suggesting other potential biological mechanisms involved in the etiology of prostate cancer such as the infectious and inflammatory pathways.
Objective. To estimate prostate cancer (PC) survival in Mexico and explore survival disparities according to the marginalization level of residence place. Materials and methods. A nationwide administrative claims database (4 110 men) whose PC treatment was financed by Seguro Popular between 2012-2016, was cross-linked to the National Mortality Registry up to December 2019. Patients were classified according to their oncological risk at diagnosis and the marginalization level of the residence municipality. Cox proportional hazards regression was used to estimate multivariable survival functions. Results. Five-years PC survival (69%; 95%CI: 68,71%) ranged from 72% to 54% at very low and very high marginalization, respectively (p for trend<0.001). The lowest PC survival was observed in men with high-risk PC (47%; 95%CI: 33,66%) residents in very high marginalization municipalities. Conclusions. Overall, PC survival was lower than that reported in other Latin American countries. The distribution of oncologic risk and survival differences across marginalization levels suggests limited early detection and cancer health disparities.
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