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.

Prostate cancer is the second most common neoplasia amongst men worldwide. Hereditary susceptibility and ancestral heritage are well-established risk factors that explain the disparity trends across different ethnicities, populations, and regions even within the same country. The Y-chromosome has been considered a prototype biomarker for male health. African, European, Middle Eastern, and Hispanic ancestries exhibit the highest incidences of such neoplasia; Asians have the lowest rates. Nonetheless, the contribution of ancestry patterns has been scarcely explored among Latino males. The Mexican population has an extremely diverse genetic architecture where all the aforementioned ancestral backgrounds converge. Trans-ethnic research could illuminate the aetiology of prostate cancer, involving the migratory patterns, founder effects, and the ethnic contributions to its disparate incidence rates. The contribution of the ancestral heritage to prostate cancer risk were explored through a case-control study (152 cases and 372 controls) study in Mexican Mestizo males. Seventeen microsatellites were used to trace back the ancestral heritage using two Bayesian predictor methods. The lineage R1a seems to contribute to prostate cancer (OR_adjusted:8.04, _95%CI:1.41–45.80) development, whereas E1b1a/E1b1b and GHIJ contributed to well-differentiated (Gleason ≤ 7), and late-onset prostate cancer. Meta-analyses reinforced our findings. The mentioned lineages exhibited a connection with the Middle Eastern and North African populations that enriched the patrilineal diversity to the southeast region of the Iberian Peninsula. This ancestral legacy arrived at the New World with the Spanish and Sephardim migrations. Our findings reinforced the contribution of family history and ethnic background to prostate cancer risk, although should be confirmed using a large sample size. Nonetheless, given its complex aetiology, in addition to the genetic component, the lifestyle and xenobiotic exposition could also influence the obtained results.

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 semi-quantitative FFQ with a frame reference of 3 years 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 (FDIP) were determined through principal component analysis, and their association with PC was estimated using logistic regression models. Three FDIP were identified: gallate pattern (GP) characterised by (–)-epicatechin-3-O-gallate, (–)-epigallocatechin-3-O-gallate and (+)-gallocatechin; luteolin pattern (LP) characterised by luteolin and (–)-epigallocatechin-3-O-gallate; and a mixed pattern (MP) that included (+)-catechin, (–)-epicatechin and quercetin. A higher GP (OR_{T3 v.T1} = 0·47; 95 % CI 0·33, 0·66) and LP intake (OR_{T3 v. T1} = 0·39; 95 % CI 0·27, 0·59) were associated with a decreased PC likelihood. In contrast, a higher MP intake (OR_{T3 v. 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.

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.