Practice question

Bisphenol A acts as xenoestrogen binding estrogen receptors alpha and beta with ability to activate estrogene-responsive genes promoting mammary epithelial proliferation. Prenatal BPA exposure during mammary placode development causes epigenetic changes including demethylation of promoter regions, increased number of terminal end buds which remain highly sensitive to estrogen. Upon pubertal estrogen rise, these hyperresponsive buds undergo excessive ductal branching and hyperplasia predisposing to neoplastic transformation. Epidemiologic and animal data link early BPA exposure to increased breast cancer incidence later in life through endocrine imprinting mechanism promoting hormone-dependent mammary tumorigenesis in adults.