Annual Meeting

November 13-16, 2012
Hilton San Francisco Financial District, San Francisco, CA

sponsored by
AVON Foundation
Speaker Abstracts

Early Life Factors and Reproductive Timing: Evidence on Menarche and Menopause.

Mary Beth Terry, PhD, Columbia University

Accumulating evidence from both human population and animal studies supports a role for the prenatal and early life environment in influencing breast cancer risk. Timing of menarche and menopause are also important predictors of breast cancer risk. Prenatal and early life factors that have been associated with breast cancer risk have not always been associated with age at menarche and intermediate markers of breast cancer risk like breast density in the same way. Even less is known about how these same early life factors are related to timing of menopause. As reproductive timing influences breast cancer risk, we examined whether prenatal exposures such as exposure to maternal smoking and early life growth were associated with markers of reproductive timing and breast cancer risk as measured by mammographic density. Specifically, we followed women who were born between 1959 and 1967 and whose mothers participated in either the Collaborative Perinatal Project (Boston and Providence sites) or the Childhood Health and Development Study in California (n=1,134, age range at interview from 39 to 49 years at interview). Cigarette smoking was reported by mothers at the time of their pregnancy; 40% of mothers smoked while pregnant. Other pregnancy exposures including maternal weight gain and pregnancy conditions were collected prospectively; birth and infant childhood growth measures were collected until age 5 years of age. In this presentation, selected exposures will be compared and contrasted across measures of age at menarche, menopausal transition, and mammographic density. For example, within this population, rapid growth during infancy was associated with earlier age at menarche, later age at menopause, but lower overall mammographic density. Implications of these opposing effects will be discussed within the context of interpreting the effect of early life exposures on overall breast cancer risk across the lifecourse.

Supported by NIH R01CA104842 and DOD 170210357

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