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We are interested in the molecular basis of cell death and proliferation control during the genotoxic stress response. Our laboratory is primarily using two human tumor models: (i) Chronic lymphocytic leukemia (CLL) for leukemia, and (ii) prostate cancer, for epithelial tumors. For leukemia, we seek to understand therapeutic resistance and how the BCL-2 family and autophagy regulation contributes to it. Overcoming such resistance with rational, targeted approaches, is a desired outcome for translation of these findings into clinical setting. Specifically: 1) We study the role of BCL-xL and MCL-1 in resistance to and sensitization to BCL-2 homology domain 3 (BH3) mimetics, 2) We study autophagy as a mechanism of resistance, and 3) We seek to lay the foundations for optimizing the use of BCL-2 targeting agents by integrating gene expression data obtained from cell lines with that from patients treated in the clinic or ex vivo. Understanding the critical BCL-2 family protein associations according to differing cell sensitivities will allow development of molecular and pharmacologic approaches for their effective targeting. We recently identified a previously unexplored connection between autophagy and DNA damage response, via the deubiquitinase USP14. We are now extending the role of USP14 in DNA repair and immunity. By characterizing apoptotic and autophagy pathways in lymphoid malignancies, we seek to ultimately use them to predict response and thus personalize the selection of targeted therapeutic agents. For prostate, we are pursuing in addition to similar studies in autophagy also how it impact on repair of DNA damage, and ultimately to the outcome of radiotherapy. We seek to understand the DNA damage signals incurred by mammalian cells following ionizing radiation (IR). We are interested in IR-regulated genes, with a focus on those that have an important role in cell cycle checkpoints, cell proliferation, apoptosis (Bcl-2 family), and autophagy (ATG family, Beclin, mTOR). A third project focuses on a tumor-specific cell death ligand,Apo2L/TRAIL and its role in apoptosis, autophagy and potential for cancer therapy.
We are interested in the molecular basis of cell death and proliferation control during the genotoxic stress response. Our laboratory is primarily using two human tumor models: (i) Chronic lymphocytic leukemia (CLL) for leukemia, and (ii) prostate cancer, for epithelial tumors. For leukemia, we seek to understand therapeutic resistance and how the BCL-2 family and autophagy regulation contributes to it. Overcoming such resistance with rational, targeted approaches, is a desired outcome for translation of these findings into clinical setting. Specifically: 1) We study the role of BCL-xL and MCL-1 in resistance to and sensitization to BCL-2 homology domain 3 (BH3) mimetics, 2) We study autophagy as a mechanism of resistance, and 3) We seek to lay the foundations for optimizing the use of BCL-2 targeting agents by integrating gene expression data obtained from cell lines with that from patients treated in the clinic or ex vivo. Understanding the critical BCL-2 family protein associations according to differing cell sensitivities will allow development of molecular and pharmacologic approaches for their effective targeting. We recently identified a previously unexplored connection between autophagy and DNA damage response, via the deubiquitinase USP14. We are now extending the role of USP14 in DNA repair and immunity. By characterizing apoptotic and autophagy pathways in lymphoid malignancies, we seek to ultimately use them to predict response and thus personalize the selection of targeted therapeutic agents. For prostate, we are pursuing in addition to similar studies in autophagy also how it impact on repair of DNA damage, and ultimately to the outcome of radiotherapy. We seek to understand the DNA damage signals incurred by mammalian cells following ionizing radiation (IR). We are interested in IR-regulated genes, with a focus on those that have an important role in cell cycle checkpoints, cell proliferation, apoptosis (Bcl-2 family), and autophagy (ATG family, Beclin, mTOR). A third project focuses on a tumor-specific cell death ligand,Apo2L/TRAIL and its role in apoptosis, autophagy and potential for cancer therapy.
Research Interests
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