Response

Extract

Oktay et al. raise two issues related to our recent study on risks of colorectal and other cancers after endometrial cancer for women with Lynch syndrome (1). Oktay et al. suggest that obesity and/or diet might have independently contributed to the increased risk of colorectal cancer we observed, given they are risk factors for endometrial and colorectal cancer for women in the general population (ie, they are potential confounders). We argue that these lifestyle factors are unlikely to have an impact on our estimation of cancer risks. First, one of our measures of association was a comparison between incidences of cancers after endometrial cancer for women with Lynch syndrome and incidences of cancers after endometrial cancer for women from the general population [see Table 3; SIR₂ for colorectal cancer = 36.3, 95% confidence interval = 25.8 to 49.6 (1)]. For this comparison, the only difference between the two groups of women was whether the women carried a germline mutation in a mismatch repair gene, which is not associated with body mass index or diet, and therefore this measure of association cannot be due to confounding with obesity or diet. Second, in contrast with women from the general population, we have reported in a previous study that obesity is not associated with an increased risk of endometrial cancer for women with Lynch syndrome (2). Third, in our study of women with Lynch syndrome and history of endometrial cancer, there was no difference in body mass index at age 20 years between those who did and did not develop colorectal cancer (mean = 22, standard deviation [SD] = 3.7 vs mean = 22, SD = 4.0kg/m²; P = .61). Similarly there was no difference in recent body mass index (within 2 years before interview) between those who did and did not develop colorectal cancer (mean = 27, SD = 6.0 vs mean = 27, SD = 5.9kg/m²; P = .51). There was also no evidence of difference in intakes of fruit, vegetables, and red meat between those with and without colorectal cancer (data not shown).