021.1 Hormone: Cell Interaction – Plasma Membrane Response to Extracellular Signal – Action of Prostaglandins and Catecholamines
Instructor: Dr. Peter Polgar
Location: BUSM, K212
Number of Students: One
Period to be Offered: Contact Dr. Polgar
Description of Elective:
The project would involve some aspect of the biochemistry of interaction of the prostaglandins and catecholamines with cells in culture. The hormone-cell relationship would be determined in terms of hormone binding to the cell surface, response of the cyclic AMP and GMP systems and the control of cell division in normal and transformed human fibroblasts.
024.16 Molecular and Cellular Changes in Breast Cancer
Instructor: Abdulmaged Traish, Ph.D.
Number of Students: 2 per semester
Period to be Offered: Fall and Spring semester
Description of Elective:
This elective will consist of discussions, readings and laboratory work on the receptor levels and other tumor markers in breast cancer and animal tissues. In many patients, breast cancer is a systemic disease at diagnosis, and may not be curable by local treatment alone. A number of therapeutic modalities are used in management of breast cancer patients including adjuvant chemotherapy, radiation therapy, endocrine therapy or a combination of such treatments. These treatments have been shown to prolong disease-free survival (DFS) and overall survival of breast cancer patients. There is a lack of definitive tumor markers which identify those patients in which cancer will likely recur without treatment . While pathological breast cancer staging (tumor size, nodal status, and presence and site of metastasis) remain among the most reliable methods of predicting disease outcome, knowledge of other tumor markers may provide additional prognostic information. There is a critical need for identification of specific tumor markers whose expression directly contributes to the malignant process. Identification of tumor markers may permit their use as targets for therapeutic strategies. We have isolated, partially characterized and cloned the cDNA for a 55 kDa nuclear protein from human breast tumor cells (henceforth referred to as nmt55). We have found that this protein is expressed in most ER+ tumors but not in ER- tumors. We postulate that loss of nmt55 expression is associated with molecular and cellular changes linked to cellular differentiation leading to loss of ER expression, development of hormone-independent tumor growth and metastases.