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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.

Obesity is associated with negative prostate cancer outcomes (e.g., specific mortality, all-cause mortality, biochemical recurrence, etc.), according to the current scientific literature. Nevertheless, recommendations on weight loss and healthy lifestyles are poorly covered by clinicians. We aimed at identifying these recommendations from clinical practice guidelines (CPGs) for prostate cancer. We systematically searched MEDLINE, EMBASE, Web of Science, Scopus, guideline databases and online sources for CPGs updated from January 2015 to August 2021. The searches were independently conducted by two researchers, without language restrictions. A total of 97 prostate cancer guidelines, including 84 (86.6%) CPGs and 13 (13.4%) consensus statements, were included. Recommendations on reaching and maintaining a healthy weight or healthy lifestyles were provided by 7 (7.2%) and 13 (13.4%) documents, respectively. No differences regarding recommendations were found by type of document, year of publication or country. Our results suggest that professional societies and governments should update prostate cancer guidelines to include these recommendations for improving prostate cancer prognosis.

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 European Code against Cancer recommends not to smoke, to avoid alcohol consumption, to eat a healthy diet, and maintain a healthy weight to prevent cancer. To what extent is the public aware of the influence of these lifestyle factors on cancer development? The goal of the current study was to describe the perceived influence of four lifestyle factors (tobacco, alcohol, diet, and weight) on cancer development in the general population and identify factors related to low perceptions of influence. We analyzed data from the 2020 Onco-barometer (n = 4769), a representative population-based survey conducted in Spain. With the exception of smoking, lifestyle factors were among those with the least perceived influence, more so among the demographic groups at higher risk from cancer including men and older individuals (65+ years). Individuals from lower socio-economic groups were more likely to report not knowing what influence lifestyle factors have on cancer. Lower perceived influence was also consistently related to perceiving very low risk from cancer. Overall, although there is variation in perceptions regarding the different lifestyle factors, low perceived influence clusters among those at higher risk for cancer. These results signal the need for public health campaigns and messages informing the public about the preventive potential of lifestyle factors beyond avoiding tobacco consumption.

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.

To analyze the association between prostate cancer (PCa) risk and night shift work, chronotype, and sleep duration in the context of a population-based case-control study of incident prostate cancer in Spain, a total of 465 PCa cases and 410 controls were analyzed. Selection criteria were: (i) age 40-80 years, and (ii) residence in the coverage area of the reference hospitals for ≥6 months before recruitment. Exposure variables were: (i) night shift work (permanent or rotating); (ii) chronotype: morning, neither, or evening (Munich ChronoType Questionnaire) and (iii) sleep duration according to the recommendations of the American National Sleep Foundation. PCa aggressiveness was determined according to the International Society of Urology Pathology classification. Adjusted odds ratios (aOR) and 95% confidence intervals (95% CI) were estimated using logistic regression models. Night shift work was associated with PCa, aOR = 1.47 (95% CI 1.02-2.11), especially for rotating night shifts, aOR = 1.73 (95% CI 1.09-2.75). The magnitude of the association between ever night work and PCa was higher in evening subjects with aOR = 3.14 (95% CI 0.91-10.76) than in morning chronotypes with an aOR = 1.25 (95% CI 0.78-2.00). Working night shifts, especially rotating night shifts, could increase PCa risk. This risk may be higher in people with an evening chronotype., Competing Interests: The authors declare no conflict of interest.

We aimed to study the association between occupational exposure to pesticides and chronic lymphocytic leukemia (CLL) in Spain. Occupational exposure to pesticides (four insecticides, four herbicides and two fungicides) was evaluated using a job-exposure matrix for the Spanish population (MatEmESp) among 302 CLL cases and 1567 population controls in five regions of Spain, 2010-2013. Cumulative exposure scores (CES) were obtained by summing across the exposed jobs the product of prevalence, intensity and duration of exposure to each active substance. Principal components analysis (PCA) and logistic regression models adjusted for age, sex, region, education and occupational exposure to solvents were used. Around 20% of controls and 29% of cases were exposed to one or more pesticides. Compared to non-exposed, subjects in the highest tertile (3rd tertile) of CES of insecticides, herbicides, fungicides were more likely to have CLL [OR (95% CI), P-trend; 2.10 (1.38; 3.19), 0.002; 1.77 (1.12; 2.80), 0.12; and 1.67 (1.06; 2.64), 0.10, respectively). Following PCA, the first component (PC1, explaining 70% of the variation) equally led by seven active substances (the insecticide pyrethrin, all herbicides, all fungicides) was associated with a 26% higher odds of having CLL for 1-standard deviation increase in PC1 (95% CI: 1.14 to 1.40). These results confirm previous associations between CLL and exposure to pesticides and provide additional evidence by application groups and active substance. However, more research is needed to disentangle independent effects of individual active substances.

The International Agency of Research in Cancer (IARC) has recently confirmed shift work as a type 2A carcinogen. The results presented in published epidemiological studies regarding prostate cancer are inconsistent and the association remains controversial. The aims of this study were: (a) to investigate the possible association between shift work and prostate cancer incidence, identifying possible sources of heterogeneity; and (b) to analyze the potential effect of publication bias. A search for cohort and case-control studies published from January 1980 to November 2019 was conducted. The quality of the articles was assessed using the Newcastle-Ottawa Scale. Pooled OR were calculated using random-effects models. Heterogeneity was evaluated using Cochran's Q test and data were stratified by potential sources of heterogeneity. Publication bias was analyzed. Eighteen studies were included. No association was found between rotating/night-shift work and prostate cancer, pooled OR 1.07 (95%CI 0.99 to 1.15), I 2 = 45.7%, p = 0.016. Heterogeneity was eliminated when only cohort studies (pooled OR 1.03; 95%CI 0.96 to 1.10; I 2 = 18.9%, p = 0.264) or high-quality studies (pooled OR 0.99; 95%CI 0.89 to 1.08; I 2 = 0.0%, p = 0.571) were considered. A publication bias was detected. An association between shift work and prostate cancer cannot be confirmed with the available current data. Future analytical studies assessing more objective homogeneous exposure variables still seem necessary.