Cold Spring Harbor Laboratory, USA
Posters & Accepted Abstracts: J Mol Genet Med
During the past decade, study of the rare inherited chromosome instability disorder, Fanconi Anemia (FA), has uncovered a novel DNA damage response pathway. Studies into the molecular basis of this disease have unmasked a network of DNA repair mechanisms that contributes to safeguarding the stability of the genome. To date, 19 genes have been identified that encode FA complementation group proteins, many of those have been linked to breast and ovarian cancer, acute myeloid leukemia, solid tumors and skin cancer. Previous studies from our group and others have identified a critical role of FANCM in repairing DNA interstrand crosslinks (ICLs) caused due to cisplatin, a chemotherapy drug used to treat different types of cancer. ICLs are among the most deleterious DNA lesions, since the covalent linkage formed between the Watson and Crick strands prevent DNA unwinding, posing formidable blocks to vital cellular processes such as genome duplication, cell cycle regulation, growth and division. In the presentation, I will summarize the recent progress in understanding the molecular pathogenesis of FA and discuss roles of FANCM as a breast cancer susceptibility gene.
Molecular and Genetic Medicine received 3571 citations as per Google Scholar report