Associate Professor of BiochemistryDirector, Molecular Cancer Therapeutics ProgramPhD, Molecular Neurobiology, 1998, The RoyalKarolinska for Medical Research, Stockholm, SwedenPostdoc, Cancer Biology, 1999-2002, Dana FarberCancer Institute, Boston, MA, Instructor 2002-06, Medicine, Harvard Medical School, Boston, MA,
Contact information2500 N. Jackson State St., G362Jackson, MS 39216Phone:(601) 815-6814E-mail: email@example.com
Recently, we discovered the novel oncogene, BRCA1-IRIS. Overexpression of BRCA1-IRIS in mammary or ovarian epithelial cells triggers aggressive traits, suggesting that BRCA1-IRIS is involved in the induction of metastasis in breast and ovarian cancer. The goal of our lab is to understand the cellular and molecular basis for BRCA1-IRIS' effects on mammary and ovarian epithelial cells, and to use this information to develop a BRCA1-IRIS-specific inhibitor for clinical use in preventing metastasis in cancer patients. We also rediscovered Geminin as an oncogene. Besides being an endogenous DNA-replication inhibitor, we found that Geminin is also involved in promoting cytokinesis and cell division when expressed at normal levels. In cancer cells, e.g. breast and ovarian cancer cells, Geminin overexpression causes cytokinesis to skip, resulting in tetraploid/aneuploid cells. Increasing amounts of evidence point to aneuploidy as a major cause of cancer metastasis. During the cell cycle, Geminin solubility oscillates, with soluble protein during S phase and insoluble protein in G2/M phase, in a phosphorylation -dependant manner. In G2/M, Geminin is bound to chromatin, centromeres and centrosomes and at the midbody during cytokinesis. When overexpressed, Geminin inhibits the function of several important mitotic-inducing proteins, such as Topoisomerase IIÎ± and Aurora B kinase, leading to cytokinesis-skipping and the formation of tetraploid/aneuploid cells, and most likely metastatic cells in vivo. Our broader goals are to map these interactions on a molecular level, and use this information to find drugs or drug regimes that can inhibit Geminin or any of its interacting partners in cancer cells. Again, the ultimate goal is to find a drug to prevent the metastatic effects of Geminin in a clinical setting, saving patient lives.
2500 North State Street
Jackson, MS 39216
General Information: 601-984-1000
Patient Appointments: 888-815-2005