Estrogen Receptor Alterations in Benign Breast Lesions and the Risk of Subsequent Breast Cancer
Abstract
Enhanced estrogen responsiveness of the breast, which may contribute to breast cancer development, could result from changes in estrogen receptor ER-alpha or ER-beta expression, or mutation of ER which may lead to receptor hypersensitivity, e.g., the ER-alpha A908G mutation. We are investigating whether ER markers may serve independently or jointly with histopathology to improve predictive capability for breast cancer. The present study is based on a cohort of 6800 women biopsied for benign breast disease at the Mayo Clinic between 1967 and 1981, and were followed until 1987 for breast cancer. During this time period, 226 cases of breast cancer were identified, and age/race-matched women who did not develop cancer were selected as controls. We have measured expression of ER-a by immunohistochemistry in benign breast lesions and surrounding normal breast epithelium of postmenopausal cases and controls, and have been screening benign and malignant breast tissues for the ER-a A908G mutation. Thus far, we have identified the A908G mutation in benign breast biopsies exhibiting hyperplasia and/or apocrine metaplasia, and in malignant breast tumors, including lobular tumors. Immunohistochemical expression of ER-beta has not been successful, therefore, we propose to genotype CYP19/aromatase for the C/T variant in exon 10 in cases and controls.
Document Details
- Document Type
- Technical Report
- Publication Date
- May 01, 2004
- Accession Number
- ADA426789
Entities
People
- Kathleen Conway-dorsey
Organizations
- University of North Carolina at Chapel Hill