Cell-Cell Adhesion and Breast Cancer
Final rept. 15 Dec 1994-14 Dec 1999
GEORGETOWN UNIV WASHINGTON DC
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Our original hypothesis was that breast tumor progression is more realistically modeled by a defect in cell-cell adhesion that results from an alteration in any one or more of the steps molecules required for E-cadherin function rather than loss of E-cadherin alone. This hypothesis has been borne out by our work over the past five years. In particular our discovery that increased expression of the mesenchymal cadherin 11 is associated with invasive breast cancer represents a paradigm shift in this area. We are now testing the effects of small molecule cadherin-11 disruptors. The past five years has also seen the expansion of the field to encompass the intracellular signaling and oncogenic activities of the cadherin-associated molecule beta-catenin. Our contributions in this area include the discovery of a key role for beta-catenin in the regulation of the cell cycle and contact inhibition. A recurring theme in the area of cancer treatment is the relationship between environmental influences such as diet and the molecular pathways that cause cancer. We have published several papers in this area and have demonstrated a direct relationship between the retinoid alpha receptor and beta-catenin itself. These results have major implications in the area of cancer prevention.
- Anatomy and Physiology
- Medicine and Medical Research