Michael Haffner

About Michael Haffner

Genomic rearrangements that lead to the juxtaposition of two non-neighbor genes such as TMPRSS2 and ERG are some of the most common alterations in prostate cancer. The origin of these rearrangements remains unclear. There is growing evidence to suggest a new model for the generation of these genomic rearrangements that requires stimulation of normal prostate cells with androgens resulting in the formation of breaks in the DNA to recruitment of the DNA break-repair machinery to imperfect DNA repair that allows two un-related genes to fuse together and promote cancer progression. Dr. Haffner is evaluating the roles of TOP2B and the DNA damage/repair pathways in cancer progression which may result in a new strategy for therapeutically targeting advanced prostate cancer. In the second part of his research, he will exploit AR-signaling associated DNA breaks for therapeutic targeting in the setting of advanced prostate cancer.