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The etiology of prostate cancer (PCa) remains uncertain, and the role of diet is unclear. We aimed to evaluate the role of diet, through dietary patterns, on PCa, considering tumor aggressiveness and extension. The CAPLIFE study is a population-based case-control study including a total of 428 incident PCa cases and 393 controls aged 40-80 years. Dietary information was collected through a validated food frequency questionnaire. Three dietary patterns were identified through principal component analysis: "Mediterranean," "Western," and "Unhealthy," which were categorized into tertiles according to the control group cutoff points. Tumor aggressiveness and extension was determined. Logistic regression models were used to assess the association between dietary patterns and PCa. High adherence to an unhealthy dietary pattern was associated with higher odds of PCa, OR T3vsT1 = 1.52 (95% CI 1.02-2.27), especially for cases with ISUP 1-2 and localized PCa tumors. This association was not observed with a Western or Mediterranean pattern. In conclusion, adherence to an unhealthy diet appears to be associated with higher odds of PCa, especially for cases with ISUP 1-2 and localized PCa tumors.

In the past decade, evidence has accumulated about socio-economic inequalities in very diverse lung cancer outcomes. To better understand the global effects of socio-economic factors in lung cancer, we conducted an overview of systematic reviews. Four databases were searched for systematic reviews reporting on the relationship between measures of socio-economic status (SES) (individual or area-based) and diverse lung cancer outcomes, including epidemiological indicators and diagnosis- and treatment-related variables. AMSTAR-2 was used to assess the quality of the selected systematic reviews. Eight systematic reviews based on 220 original studies and 8 different indicators were identified. Compared to people with a high SES, people with a lower SES appear to be more likely to develop and die from lung cancer. People with lower SES also have lower cancer survival, most likely due to the lower likelihood of receiving both traditional and next-generation treatments, higher rates of comorbidities, and the higher likelihood of being admitted as emergency. People with a lower SES are generally not diagnosed at later stages, but this may change after broader implementation of lung cancer screening, as early evidence suggests that there may be socio-economic inequalities in its use.

This systematic review discusses long-term NSW and female BC risk, with special attention to differences between pre- and postmenopausal BC, to test the association with recent NSW. The review follows PRISMA guidelines (Prospero registry: CRD42018102515). We searched PubMed, Embase, and WOS for case-control, nested case-control, and cohort studies addressing long-term NSW (≥15 years) as risk exposure and female BC as outcome until 31 December 2020. Risk of bias was evaluated with the Newcastle-Ottawa scale. Eighteen studies were finally included (eight cohorts; five nested case-control; five case-control). We performed meta-analyses on long-term NSW and BC risk; overall and by menopausal status; a subanalysis on recent long-term NSW, based on studies involving predominantly women below retirement age; and a dose-response meta-analysis on NSW duration. The pooled estimate for long-term NSW and BC was 1.13 (95%CI = 1.01-1.27; 18 studies, I 2 = 56.8%, p = 0.002). BC risk increased 4.7% per 10 years of NSW (95%CI = 0.94-1.09; 16 studies, I 2 = 33.4%, p = 0.008). The pooled estimate for premenopausal BC was 1.27 (95%CI = 0.96-1.68; six studies, I 2 = 32.0%, p = 0.196) and for postmenopausal BC 1.05 (95%CI = 0.90-1.24,I 2 = 52.4%; seven studies, p = 0.050). For recent long-term exposure, the pooled estimate was 1.23 (95%CI = 1.06-1.42; 15 studies; I 2 = 48.4%, p = 0.018). Our results indicate that long-term NSW increases the risk for BC and that menopausal status and time since exposure might be relevant.

The aim of this study was to systematically review all evidence evaluating obesity as a prognostic factor for PC mortality. Cohort and case-control studies reporting mortality among PC patients stratified by body mass index (BMI) were included. The risk of mortality among obese patients (BMI ≥ 30) was compared with the risk for normal weight (BMI < 25) patients, pooling individual hazard ratios (HR) in random-effects meta-analyses. Reasons for heterogeneity were assessed in subgroup analyses. Dose-response associations for BMI per 5 kg/m 2 change were assessed. Among 7278 citations, 59 studies (280,199 patients) met inclusion criteria. Obesity was associated with increased PC-specific mortality (HR: 1.19, 95% CI: 1.10-1.28, I 2 : 44.4%) and all-cause mortality (HR: 1.09, 95% CI: 1.00-1.18, I 2 : 43.9%). There was a 9% increase (95% CI: 5-12%, I 2 : 39.4%) in PC-specific mortality and 3% increase (95% CI: 1-5%, I 2 : 24.3%) in all-cause mortality per 5 kg/m 2 increase in BMI. In analyses restricted to the higher quality subgroup (NOS ≥ 8), obesity was associated with increased PC-specific mortality (HR: 1.24, 95% CI: 1.14-1.35, I 2 : 0.0%) and maintained the dose-response relationship (HR: 1.11 per 5 kg/m 2 increase in BMI, 95% CI: 1.07-1.15, I 2 : 26.6%). Obesity had a moderate, consistent, temporal, and dose-response association with PC mortality. Weight control programs may have a role in improving PC survival.

Many adult cancer patients present one or more physical comorbidities. Besides interfering with treatment and prognosis, physical comorbidities could also increase the already heightened psychological risk of cancer patients. To test this possibility, we investigated the relationship between physical comorbidities with depression symptoms in a sample of 2073 adult cancer survivors drawn from the nationally representative National Health and Nutrition Examination Survey (NHANES) (2007-2018) in the U.S. Based on information regarding 16 chronic conditions, the number of comorbidities diagnosed before and after the cancer diagnosis was calculated. The number of comorbidities present at the moment of cancer diagnosis was significantly related to depression risk in recent but not in long-term survivors. Recent survivors who suffered multimorbidity had 3.48 (95% CI 1.26-9.55) times the odds of reporting significant depressive symptoms up to 5 years after the cancer diagnosis. The effect of comorbidities was strongest among survivors of breast cancer. The comorbidities with strongest influence on depression risk were stroke, kidney disease, hypertension, obesity, asthma, and arthritis. Information about comorbidities is usually readily available and could be useful in streamlining depression screening or targeting prevention efforts in cancer patients and survivors. A multidimensional model of the interaction between cancer and other physical comorbidities on mental health is proposed.