Molecular Markers for Breast Cancer Susceptibility.
Abstract
This proposal is based upon the hypothesis that the protective effects of an early pregnancy and lactation on the incidence of breast cancer result from estrogen (E) and progesterone (P)-induced differentiation and the resultant loss of cells susceptible to carcinogenesis. These effects of E and P are mediated by the induction of specific "local mediators", i.e., growth factors that act via autocrine and paracrine mechanisms to influence terminal duct (TD) and end bud growth (TEB) and differentiation. These rapidly proliferating cells are the most susceptible to neoplastic transformation. No molecular markers are available to identify and follow the fate of these susceptible cells, yet this information is required to develop effective diagnostic tools and preventive therapies for breast cancer. Thus, the initial objective of this grant is to identify molecular markers for TEB and TD cells in order to follow their fate during mammary development and carcinogenesis. During the first year of this proposal we have validated the feasibility of manually dissecting end bud, mid-gland and stromal subfractions from the mammary glands of 45-50 day old Wistar Furth rats, and the isolation of intact RNA and nuclear matrix proteins from these fractions. We have performed confocal microscopic and differential display PCR and 2D-PAGE analyses and identified differences in gene expression in these fractions. DNA sequencing of unique DD-PCR products has identified a novel member of the rho-GAP family designated p190-B that may be selectively expressed in TEBs.
Document Details
- Document Type
- Technical Report
- Publication Date
- Sep 01, 1995
- Accession Number
- ADA302265
Entities
People
- Jeffrey M. Rosen
Organizations
- Baylor College of Medicine