Molecular Therapeutics



The Division of Molecular Therapeutics investigates the molecular and cellular determinants that lead to tumor formation and that dictate cellular responses to cytotoxic stresses. Emphasis is placed on translating information gained on the latter topic to the development of novel therapeutic approaches to cancer.

The Division of Molecular Therapeutics is a laboratory-based research group within the Department of Oncology. Basic science investigations focus on the molecular differences between normal cells and tumor cells and on the molecular mechanisms that determine cellular responses to DNA damage and other cytotoxic stresses. Current areas of interest include investigations of oncogenes and tumor suppressor genes in tumor development, such as telomerase, the retinoblastoma gene and protein, the p53 gene and protein, the ATM and ATR genes and proteins, and the Brca1 protein. There is also a particular focus on the molecular controls of cellular responses to ionizing irradiation, which has implications for both tumor formation and tumor responses to chemotherapy and radiation therapy. Identification of the steps involved in signaling pathways initiated by radiation and other cytotoxic stresses also provide new potential targets for the design of novel drugs that can be used to enhance the sensitivity of tumor cells to radiation or chemotherapy.

Complementary studies within the Division are directed toward modeling High-Risk pediatric leukemias with the aim of gaining insights into mechanisms of leukemogenesis. There is a particular interest in modeling BCR-ABL-dependent lymphoid leukemia with the use of genetic tools that target pathways known to be deregulated in this disease. These engineered model systems also facilitate the implementation of pre-clinical ‘therapeutic trials’ to understand the dynamics of drug responsiveness and interrogate mechanism of drug resistance in vivo.  Collaborative studies aim to develop and implement novel therapeutic strategies to overcome drug resistance in these models. 


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