The Cantor lab performs mechanistic studies to uncover how the hereditary breast cancer genes protect the genome and suppress cancer. Through biochemical protein purification strategies and genome-wide RNA interference (RNAi) screens, the lab seeks to identify novel genes and pathways that function with the hereditary breast cancer genes in DNA repair and tumors suppression. Importantly, these approaches have provided insight towards the regulation of DNA repair pathways, how this regulation is altered in cancer, and how cancer cells evade therapies.
- Cantor, SB, Bell, D, Ganesan, S, Kass, E, Drapkin, R, Grossman, S, Wahrer, D, Sgroi, D, Lane, W, Haber, D, Livingston, D. BACH1, a novel helicase–like protein, interacts directly with BRCA1 and contributes to its DNA repair function. Cell. 2001; 105:149.
- Litman, R, Peng, M, Jin, Z, Zhang, F, Zhang, J, Powell, S, Andreassen, PR, Cantor, SB. BACH1 is critical for homologous recombination and appears to be the Fanconi anemia gene product FANCJ. Cancer Cell. 2005; 8:255–265.
- Min Peng, Jenny Xie, Anna Ucher, Janet Stavnezer & Cantor SB, Crosstalk between BRCA-Fanconi anemia and mismatch repair pathways prevents MSH2-dependent aberrant DNA damage responses. EMBO J. 2014 June 25: 10.15252/embj.201387530.
- Guillemette S, Serra R, Peng M, Hayes JA, Konstantinopoulos PA, Green MR, and. Cantor SB, Resistance to therapy in BRCA2 mutant cells due to loss of the nucleosome-remodeling factor CHD4, Genes and Development, 2015 Mar 1;29(5):489-94.