A prospective study of coffee and tea consumption and the risk of glioma in the UK Biobank.

BACKGROUND: Coffee and tea have been hypothesised to reduce the risk of some cancers; however, their impact on glioma is less well studied. METHODS: We examined associations between self-reported intake of tea and coffee in relation to glioma risk in the UK Biobank. We identified 487 incident glioma cases among 379,259 participants. Hazard ratios (HR) and 95% confidence intervals (CI) for glioma according to caffeinated beverage consumption were calculated using Cox proportional hazards regression with adjustment for age, gender, race and education; daily cups of tea or coffee were included in models considering the other beverage. RESULTS: Consuming 4 or more cups of tea was associated with reduced risk of glioma when compared to no tea consumption (HR = 0.69; 95% CI, 0.51-0.94). A significant inverse association was observed for glioblastoma (HR = 0.93 per 1 cup/d increment; 95% CI, 0.89-0.98) and among males for all gliomas combined (HR = 0.95 per 1 cup/d increment; 95% CI, 0.90-1.00). A suggestive inverse association was also observed with greater consumption of coffee (HR = 0.71; 95% CI, 0.49-1.05 for >4 versus 0 cups/d). Results were not materially changed with further adjustment for smoking, alcohol and body mass index. Associations were similar in 2-year and 3-year lagged analyses. CONCLUSIONS: In this prospective study, we found a significant inverse association between tea consumption and the risk of developing glioma, and a suggestive inverse association for the consumption of coffee. Further investigation on the possible preventive role of caffeine in glioma is warranted.

Commercial Gene Expression Tests for Prostate Cancer Prognosis Provide Paradoxical Estimates of Race-Specific Risk.

BACKGROUND: Commercial gene expression signatures of prostate cancer prognosis were developed and validated in cohorts of predominantly European American men (EAM). Limited research exists on the value of such signatures in African American men (AAM), who have poor prostate cancer outcomes. We explored differences in gene expression between EAM and AAM for three commercially available panels recommended by the National Comprehensive Cancer Network for prostate cancer prognosis. METHODS: A total of 232 EAM and 95 AAM patients provided radical prostatectomy specimens. Gene expression was quantified using NanoString for 60 genes spanning the Oncotype DX Prostate, Prolaris, and Decipher panels. A continuous expression-based risk score was approximated for each. Differential expression, intrapanel coexpression, and risk by race were assessed. RESULTS: Clinical and pathologic features were similar between AAM and EAM. Differential expression by race was observed for 48% of genes measured, although the magnitudes of expression differences were small. Coexpression patterns were more strongly preserved by race group for Oncotype DX and Decipher than Prolaris. Poorer prognosis was estimated in EAM versus AAM for Oncotype DX (P < 0.001), whereas negligible prognostic differences were predicted between AAM and EAM using Prolaris or Decipher (P > 0.05). CONCLUSIONS: Because of observed racial differences across three commercial gene expression panels for prostate cancer prognosis, caution is warranted when applying these panels in clinical decision-making in AAM. IMPACT: Differences in gene expression by race for three commercial panels for prostate cancer prognosis indicate that further study of their effectiveness in AAM with long-term follow-up is warranted.

Toenail selenium, genetic variation in selenoenzymes and risk and outcome in glioma.

BACKGROUND: Selenium is an essential trace element obtained through diet that plays a critical role in DNA synthesis and protection from oxidative damage. Selenium intake and polymorphisms in selenoproteins have been linked to the risk of certain cancers though data for glioma are sparse. METHODS: In a case-control study of glioma, we examined the associations of selenium in toenails and genetic variants in the selenoenzyme pathway with the risk of glioma and patient survival. A total of 423 genetic variants in 29 candidate genes in the selenoenzyme pathway were studied in 1547 glioma cases and 1014 healthy controls. Genetic associations were also examined in the UK Biobank cohort comprised of 313,868 persons with 322 incident glioma cases. Toenail selenium was measured in a subcohort of 300 glioma cases and 300 age-matched controls from the case-control study. RESULTS: None of the 423 variants studied were consistently associated with glioma risk in the case-control and cohort studies. Moreover, toenail selenium in the case-control study had no significant association with glioma risk (p trend = 0.70) or patient survival among 254 patients with high grade tumors (p trend = 0.70). CONCLUSION: The present study offers no support for the hypothesis that selenium plays a role in the onset of glioma or patient outcome.