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BRCA1 and/or BRCA2 (BRCA1/2) mutations induce alterations in DNA repair pathways, thereby forcing cells to use more error-prone repair pathways such as nonhomologous end-joining and/or single-strand annealing rather than recombination between homologous DNA sequences ( 1 ) . In conjunction with these recognized effects on DNA integrity, Friedenson notes that the point estimates of the odds ratios (ORs) for BRCA1/2 carriers from our case–control study of colorectal cancer were slightly higher for those younger than 65 years than for those 65 years old or older and suggests that colorectal cancer within BRCA1/2 mutation carriers might progress more rapidly. Although this is a reasonable theoretical possibility, we would like to highlight that the statistical evidence Friedenson cites from our study in support of this argument is weak ( 2 ) . We did not observe a statistically significantly increased risk of colorectal cancer among either younger or older subjects who carry BRCA1/2 mutations (for those <65 years old, OR = 3.14, 95% confidence interval [CI] = 0.64 to 15.43; for those ≥65 years old, OR = 0.96, 95% CI = 0.48 to 1.91), and the interaction term testing the hypothesis that these results differed from one another was not statistically significant ( P = .22) ( 2 ) .

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