Background Patients with cancer may be at high risk of adverse outcomes from SARS-CoV-2 infection. We analyzed a cohort of patients with cancer and COVID-19 reported to the COVID-19 and Cancer Consortium (CCC19) to identify prognostic clinical factors, including laboratory measurements and anti-cancer therapies. Patients and Methods Patients with active or historical cancer and a laboratory-confirmed SARS-CoV-2 diagnosis recorded between March 17-November 18, 2020 were included. The primary outcome was COVID-19 severity measured on an ordinal scale (uncomplicated, hospitalized, admitted to intensive care unit, mechanically ventilated, died within 30 days). Multivariable regression models included demographics, cancer status, anti-cancer therapy and timing, COVID-19-directed therapies, and laboratory measurements (among hospitalized patients). Results 4,966 patients were included (median age 66 years, 51% female, 50% non-Hispanic white); 2,872 (58%) were hospitalized and 695 (14%) died; 61% had cancer that was present, diagnosed, or treated within the year prior to COVID-19 diagnosis. Older age, male sex, obesity, cardiovascular and pulmonary comorbidities, renal disease, diabetes mellitus, non-Hispanic Black race, Hispanic ethnicity, worse ECOG performance status, recent cytotoxic chemotherapy, and hematologic malignancy were associated with higher COVID-19 severity. Among hospitalized patients, low or high absolute lymphocyte count, high absolute neutrophil count, low platelet count, abnormal creatinine, troponin, LDH, and CRP were associated with higher COVID-19 severity. Patients diagnosed early in the COVID-19 pandemic (January-April 2020) had worse outcomes than those diagnosed later. Specific anti-cancer therapies (e.g. R-CHOP, platinum combined with etoposide, and DNA methyltransferase inhibitors) were associated with high 30-day all-cause mortality. Conclusions Clinical factors (e.g. older age, hematological malignancy, recent chemotherapy) and laboratory measurements were associated with poor outcomes among patients with cancer and COVID-19. Although further studies are needed, caution may be required in utilizing particular anti-cancer therapies.

2-Amino-1-methyl-6-phenylimidazo [4,5-b]pyridine (PhIP) is the major heterocyclic amine generated from cooking meats at high temperatures, and dietary exposures have been shown to induce prostate cancer in rats. PhIP derives its carcinogenic potential through the formation of PhIP-DNA adducts. The purpose of this study was to examine whether self-reported consumption and preparation doneness of grilled meats were associated with PhIP-DNA adduct levels in prostate epithelial cells. The study population consisted of 268 AfricanAmerican and Caucasian men who underwent radical prostatectomy for prostate cancer. PhIP-DNA adducts in tumor and adjacent nontumor cells were measured using immunohistochemical methods, and dietary meat intake information was based on food frequency questionnaires. Data were analyzed using multivariate linear regression models. After adjusting for age at prostatectomy and race, grilled meat consumption (P = 0.002) was significantly associated with higher adduct levels in tumor cells, but this association seemed to be primarily due to consumption of grilled red meats (P = 0.001) as opposed to grilled white meat consumption (P = 0.15). Among the specific food items, grilled hamburger consumption had the most significant association with adduct level in tumor cells (P = 0.002). Similar trends in positive associations with grilled meat consumption and adduct levels were observed in nontumor cells, but none of these associations reached statistical significance. Our results suggest that dietary interventions targeted at lower consumption of grilled red meats may reduce prostate cancer risk via the PhIP prostate carcinogenic pathway. (Cancer Epidemiol Biomarkers Prev 2007;16(4):803 -8)

Condensed Abstract-Men who carry the GSTP1 Val 105 variant who are exposed at high levels to occupational PAH are at increased risk for prostate cancer. This increased risk is more pronounced in men under age 60 or with a family history of prostate cancer.Background-Variation in the glutathione S-transferase (GSTP1) gene and occupational polycyclic aromatic hydrocarbons (PAH) exposure are putative prostate cancer risk factors. An Ile/ Val polymorphism in codon 105 of GSTP1 affects its enzymatic activity toward PAH detoxification, a possible mechanism in prostate carcinogenesis.

Objectives-Metabolic syndrome refers to cluster of conditions serving as risk factors for cardiovascular disease. Metabolic syndrome is prevalent in the United States and the spectrum of specific features has been shown to differ by race and ethnicity. A number of recent reports link metabolic syndrome to prostate cancer, however most studies do not have racially diverse populations to explore differences in risk.Methods-A case-control study was conducted to test the association between metabolic syndrome features and prostate cancer among 637 cases and 244 controls, with African Americans comprising 43% of the study population.Results-Metabolic syndrome, defined using a modified version of the ATP III criteria, was marginally associated with increased risk of prostate cancer in African Americans (OR=1.71; 95% CI=0.97, 3.01), but not Caucasians (OR=1.02; 95%CI=0.64, 1.62). After stratifying cases on stage at diagnosis, African American men with organ confined disease were more likely to have a history of metabolic syndrome compared to controls (OR=1.82; 95% CI=1.02, 3.23), but no association was observed among those with advanced stage disease (OR=0.93; 95%CI=0.31, 2.77). When evaluating specific features of metabolic syndrome, obesity was inversely related to prostate cancer among Caucasians (OR = 0.51, 95% CI=0.33, 0.80), but unrelated to risk among African Americans (OR=1.15; 95% CI=0.70, 1.89).Conclusions-In this investigation, metabolic syndrome was associated with prostate cancer risk in African American men, but not Caucasians. The prevalence of this syndrome, coupled with the racial disparity and prostate cancer incidence and outcomes after diagnosis warrant further investigation.