Christine Canman

Christine Canman, Ph.D.

Associate Professor of Pharmacology


Dr. Canman received her B.S. degree in Microbiology from the University of Illinois in 1987 and Ph.D. degree in Pharmacology in 1992 from the University of Michigan. She then trained under the mentorship of Dr. Michael B. Kastan as a postdoctoral fellow at Johns Hopkins University from 1993 - 1998. There she investigated signaling pathways induced by ionizing radiation and mediated by the Ataxia Telangiectasia Mutated protein kinase. Dr. Canman then joined the faculty at St. Jude Children’s Research Hospital as an Assistant Member and continued her research in understanding signaling pathways related to the maintenance of genome stability and responses to ionizing radiation. From 2002-2004, Dr. Canman participated in Oncology Drug Discovery at Pfizer in Ann Arbor. There, she worked the development of tyrosine kinase inhibitors for cancer treatment. In 2004, Dr. Canman became an Assistant Professor in the Department of Pharmacology at the University of Michigan where she continues to investigate cellular mechanisms that promote genome stability and resistance to standard chemotherapeutic agents. Dr. Canman is currently the Associate Director of the Doctoral Program in Cancer Biology and directs Cancer Biology 554.

Research Interests

Research in the Canman laboratory focuses on the mechanisms by which cells tolerate DNA damage and replication stress. The induction of DNA damage and replication stress are primary mechanisms by which many anticancer agents and ionizing radiation function therapeutically. In addition, replication of the genome can be hazardous, in that many secondary DNA structures may form that create replication fork blockade and pausing of DNA polymerases (e.g. G4 DNA quadruplexes). We study how specialized DNA polymerases, also known as translesion DNA synthesis (TLS) polymerases, play roles in facilitating tolerance to replication stress and DNA damage as well as promoting chemo and radioresistance of cancer cells. The broad implication of this research is that understanding the role TLS polymerases play in promoting survival and genome stability may lead to the identification of novel pathways that cancer cells specifically require for survival and proliferation.