This lab investigates DNA damage response and repair network signaling in carcinogenesis, drug resistance and molecular cancer therapeutics. DNA damage response and repair signaling genes are tumor suppressors that constantly protect chromosomal DNA from environmental and metabolically generated genotoxins and from oncogenic replication stress. Mutations in these genes manifest into genome instability syndromes such as Fanconi anemia (FA) and Breast and Ovarian Cancer early onset (BRCA). In contrast, tumor cells also acquire resistance to chemo and radiation therapy by altered regulation of cell cycle checkpoints and DNA repair networks. These mechanisms and their regulation are highly complex, and often they are differentially regulated in tumor cells, particularly in the context of oncogenic or growth factor signals they adopt.
The basic science projects in this lab focus on the regulation of Fanconi anemia (FA) and Breast cancer (BRCA) mutated (FA-BRCA) tumor suppressor networks by post-translational modifications.
The translational research projects focus on identifying the role of tumor signaling (ex. Hedgehog, mTOR, oncogenic and metabolic stress, epigenetics and hypoxia) on cell cycle checkpoints and DNA repair networks in cancer cells and developing rationally designed therapeutic combinations to effectively kill tumor cells by chemo and radiation therapy.
Komaraiah Palle, Ph.D.
Assistant Professor of Oncologic Sciences
Abraham Mitchell Cancer Research Scholar
Kaushlendra Tripathi, Ph.D.
David W. Clark, Ph.D.
Chinnadurai Mani, Ph.D.
Ranganatha Somasagara, Ph.D.
Sebastian M. Spencer
Cellular and Biomolecular Imaging Facility
Mass Spectrometry and Proteomics Core Laboratory
NIH/NIGMS R01 R01 GM98956 (Palle)
Goal: To elucidate Rad18 mediated ubiquitin signaling mechanisms in regulation of DNA repair networks in response to replication stress and replication coupled DNA double strand breaks induced by chemotherapeutic agents such as Topo inhibitors and crosslinking agents.
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