|Office:||University of Massachusetts Medical School
364 Plantatio Street, LRB-415
Worcester, MA 01605
My laboratory focuses on understanding how tumor suppressor proteins function to maintain genomic integrity and suppress cancer. In particular, we focus on the hereditary breast and ovarian cancer genes, BRCA1, BRCA2 and the BRCA1-associated helicase, FANCJ (BACH1/ BRIP1). Bi-allelic loss of these genes also causes Fanconi anemia (FA), a rare chromosomal instability and cancer syndrome. Our work on FANCJ revealed that DNA repair defects underlie both hereditary breast cancer and FA. Currently, we are employing biochemical and whole-genome screening technologies, to uncover mechanisms regulating DNA repair choice and how cancer cells evade toxic chemotherapies.
The laboratory is interested in a range of DNA repair-related topics including (i) the role of FANCJ in DNA repair, DNA damage tolerance, and checkpoint signaling and how these functions contribute to tumor suppression (ii) how FANCJ function is regulated by direct interactions with BRCA1 and MLH1, a mismatch repair protein, (iii) the relationship between FANCJ, BRCA1, and MLH1 in DNA crosslink repair, (iv) identifying novel FANCJ protein modifications or interacting partners that contribute to the function of FANCJ in the DNA damage response (v) understanding the underlying defects associated with loss of function of proteins in the BRCA-FA pathway and whether these defects can be suppressed and (vi) performing functional genomic screens to uncover mechanisms regulating DNA damage repair pathways and how DNA repair defective cancer cells develop resistance to therapy.
A post-doctoral position and graduate laboratory rotation are available.