Abstract
Introduction: Several epidemiological studies have investigated whether reproductive and hormonal factors are associated with the risk of renal cell cancer (RCC) in women. Although the associations of most factors with RCC risk are inconsistent, most studies have observed a positive association between parity and RCC risk. We therefore examined the association of parity and other reproductive and hormonal factors with RCC risk in the Netherlands Cohort Study on Diet and Cancer (NLCS).
Methods: The NLCS was initiated in 1986. A self-administered questionnaire on diet and other risk factors for cancer was completed by 62,573 women, aged 55-69 at baseline. Data were processed and analyzed using the case-cohort approach; cases were enumerated for the entire cohort, and person years at risk were estimated using a subcohort. This subcohort was randomly sampled from the entire cohort immediately after the baseline measurement and has been being followed up for vital status. Cohort members who reported cancer at baseline were excluded from analysis. Follow-up for cancer was established by annual record linkages with the Netherlands Cancer Registry and the nationwide pathology registry. After 17.3 years of follow-up, data from 178 RCC cases and from 2,341 subcohort members were available for analysis. Rate ratios (RRs) and 95% Confidence Intervals (95% CI) were estimated using the Cox proportional hazards model, with multivariate adjustment for confounders.
Results: Age at menarche was not associated with RCC risk. Multivariate RRs for age at menopause, adjusted for age at baseline, history of hypertension and BMI, were 1.42 (95% CI: 0.90-2.25) for women with age at menopause 25-44 years, 1.60 (95% CI: 1.10-2.32) for women with age at menopause 45-49 years and 0.83 (95% CI: 0.38-1.78) for women with age at menopause 55 years and older, compared to the reference group (women with age at menopause 50-54 years). P-value for trend was 0.02.
Use of oral contraceptives and hormone replacement therapy were not associated with RCC risk.
With respect to parity, no association was found. Multivariate RR was 1.09 (95% CI: 0.71-1.67) for parous women compared to nulliparous women. Increasing number of childbirths was also not associated with RCC risk. Because BMI and hypertension could be intermediate factors in the relationship between parity and RCC risk, we also inspected models without adjustment for hypertension and BMI. Univariate RRs of the association between parity and RCC risk were not increased.
Despite the observed lack of association between parity and RCC risk, there were indications of effect-modification by BMI on the association between parity and RCC risk (p-value for interaction, 0.02). Normal weight women (BMI<25 kg/m2) with three or more children had a RR of 1.64 (95% CI: 1.03-2.64) compared to normal weight women with zero to two children.
Conclusion: We did not confirm the association between parity and RCC risk. With the exception of age at menopause, other reproductive and hormonal factors were not associated with RCC risk either.
Citation Information: Cancer Prev Res 2010;3(12 Suppl):B97.
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