Summary Background Aspirin is associated with decreased risk of colorectal cancer (CRC), potentially by modulating the gut microbiome. Aims To evaluate the effect of aspirin on the gut microbiome in a double‐blinded, randomised placebo‐controlled pilot trial. Methods Healthy volunteers aged 50‐75 received a standard dose of aspirin (325 mg, N = 30) or placebo (N = 20) once daily for 6 weeks and provided stool samples every 3 weeks for 12 weeks. Serial measurements of gut microbial community composition and bacterial abundance were derived from 16S rRNA sequences. Linear discriminant analysis of effect size (LEfSe) was tested for between‐arm differences in bacterial abundance. Mixed‐effect regression with binomial distribution estimated the effect of aspirin use on changes in the relative abundance of individual bacterial taxa via an interaction term (treatment × time). Results Over the study period, there were differences in microbial composition in the aspirin vs placebo arm. After treatment, four taxa were differentially abundant across arms: Prevotella, Veillonella, Clostridium XlVa and Clostridium XVIII clusters. Of pre‐specified bacteria associated with CRC (n = 8) or aspirin intake (n = 4) in published studies, interactions were significant for four taxa, suggesting relative increases in Akkermansia, Prevotella and Ruminococcaceae and relative decreases in Parabacteroides, Bacteroides and Dorea in the aspirin vs placebo arm. Conclusion Compared to placebo, aspirin intake influenced several microbial taxa (Ruminococcaceae, Clostridium XlVa, Parabacteroides and Dorea) in a direction consistent with a priori hypothesis based on their association with CRC. This suggests that aspirin may influence CRC development through an effect on the gut microbiome. The findings need replication in a larger trial.
Background Adherence to the World Cancer Research Fund (WCRF)/American Institute for Cancer Research (AICR) cancer prevention recommendations is associated with colorectal cancer (CRC) risk in whites, but only 1 previous study has reported on this link in African Americans. This study assessed the association between the 2018 WCRF/AICR guidelines and CRC incidence in African Americans (26.5%) and whites (73.5%) in the Atherosclerosis Risk in Communities prospective cohort (n = 13,822). Methods A total of 368 incident CRC cases (268 among whites and 100 among African Americans) were identified between the baseline (1987) and 2012. A baseline adherence score was created for 7 WCRF/AICR guidelines (each contributing 0, 0.5, or 1 point to the score, with higher scores corresponding to greater adherence). Adherence scores were also categorized as tertiles (0.0‐3.0, 3.5‐4.0, and 4.5‐7.0). Cox proportional hazards regression was used to calculate hazard ratios (HRs) and 95% confidence intervals (CIs) for the total cohort and with stratification by race. Results After adjustments for age, sex, race, center, smoking, education, intake of aspirin, calcium, total calories, diabetes status, and, in women, hormone replacement therapy, greater adherence was associated with decreased CRC risk. The HRs per 1‐unit increment in score were 0.88 (95% CI, 0.80‐0.97) for the whole cohort, 0.89 (95% CI, 0.73‐1.09) for African Americans, and 0.88 (95% CI, 0.77‐0.99) for whites. Similar associations between higher adherence scores and decreased cancer risk were observed for men and women and for colon cancer but not for rectal cancer. Conclusions Greater adherence to the cancer prevention recommendations appears to be associated with decreased CRC risk for both African Americans and whites.
Background: Laboratory and epidemiologic research suggests a protective role of magnesium in colorectal cancer development. We estimated the associations of serum and dietary magnesium with colorectal cancer incidence in the Atherosclerosis Risk in Communities (ARIC) study.
Background Pancreatic tumor cells may avoid immune surveillance by releasing the transmembrane major histocompatibility complex class I chain-related A (MICA) protein in soluble form (s-MICA). We hypothesized that the presence of the A5.1 polymorphism in the MICA gene, which encodes a truncated MICA protein, is associated with higher s-MICA levels and increased pancreatic cancer risk. Methods MICA alleles and s-MICA levels were measured in 121 pancreatic cancer cases and 419 controls. General linear regression with a log transformation assessed geometric means of s-MICA levels across MICA alleles. Unconditional logistic regression was used to calculate the odds ratio (OR) and 95% confidence intervals (CI) for pancreatic cancer associated with MICA alleles. Results After multivariate adjustment, participants with at least one copy of the A5.1 allele versus no A5.1 allele had 1.35 (95% CI: 1.05–1.74) times greater s-MICA levels (1.65 times higher for cases and 1.28, for controls) and increased risk of pancreatic cancer (OR = 1.91, 95% CI: 1.05–3.48). Conclusions Our study suggests higher risk of pancreatic cancer among those with the MICA A5.1 polymorphism, which may be explained by an increase in s-MICA secretion and impaired immune response. Impact These findings provide further evidence at the genetic and molecular level of the important role of MICA in pancreatic cancer development, and may have important implications with regards to pancreatic cancer screening.
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