Title of his talk: Systems biology approach to the discovery and implementation of targeted therapeutics.
Their research program aims to identify the mechanisms by which normal cells (lymphocytes) and tumor cells (ovarian and breast cancer) perceive and respond to their environment. In particular, they are investigating the signaling mechanisms utilized by the T-cell receptor CD28 and interleukin-2 receptor (IL-2R) in lymphocytes. During this process, they have cloned a number of different tyrosine kinases and are utilizing molecular mutagenesis and biochemical techniques to determine their mechanism of action. One of these unique kinases (EMT/ITK) is a major signaling molecule in T-cell activation; the other (TTK) plays a role in cell-cycle progression, particularly during the G2/M transition. They demonstrated that mice that lack the SHP-1 tyrosine phosphatase have a greatly elevated propensity to develop leukemias, lymphomas, and breast cancer. Further, the recently identified phosphatase tumor suppressor gene MMAC1 is deleted or mutated in a number of leukemias and T-cell lines. Strikingly, EMT, SHP-1, and MMAC1 all regulate signaling through a PI-3K pathway. The mission of the laboratory is to understand the mechanisms by which signal transduction is linked to proliferation, invasion, and programmed cell death in T lymphocytes and in breast and ovarian cancer.
Host: Anne-Lise Børresen-Dale, Department of Genetics, IFK, Montebello
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