Karin Scarpinato, Ph.D.
Mismatch repair (MMR) proteins play a dual role as tumor suppressors. Their repair function ensures genome stability, while their participation in a DNA damage response pathway initiates cell death of damaged cells after exposure to chemotherapeutic agents. Defects in MMR proteins result in increased genome instability and evasion of apoptosis, promoted carcinogenesis failure of chemotherapeutic treatment and secondary tumor growth with an often selective growth advantage of MMR-deficient cancer cells under treatment conditions. Research in the lab is focused on two main projects: (1) the mechanistic aspects of the DNA damage response pathway and its coordination with DNA repair, and (2) the contribution, detection and identification of MMR defects in non-HNPCC tumors.
