Primary Appointment

Dual/Joint/Adjunct Appointment

Lei Li, Ph.D. is a Professor in the Department of Experimental Radiation Oncology with a dual appointment as Professor in the Department of Genetics. He received his BS degree in Biology from Peking University and Ph.D degree from Chinese academy of Science, Institute of Biochemistry in Shanghai. Dr. Li came to the US for postdoctoral training and started his independent research in 1998. The main interest of his laboratory is molecular mechanisms of genomic instability and DNA repair. Work from his group is well-recognized in the field. His collaborators include Stephen Elledge (Harvard Medical School), Weidong Wang (National Institute of Health), Sandy Chang (Yale University), and Junjie Chen (MDACC).

We are interested in molecular mechanisms of DNA damage repair and cell cycle checkpoint mechanisms, properly dubbed "care takers" and "gate keepers" for the maintenance of genome integrity. Defects in these mechanisms cause genomic instability - a hallmark of cancer. Defective DNA repair or cell cycle checkpoint pathways allow DNA lesions to be converted to hereditary mutations during each round of cell division and allow these mutations to accumulate in proliferating cells. Ultimately, some cells, possessing effectual combinations of mutations, acquire tumorigenic competence and exhibit temporal-spatial disregulation of cell growth characteristic of cancer cells.We focus on how DNA damage is sensed and transduced into checkpoint signals. We are investigating a number of genes that are critical in the generation of checkpoint signal and maintenance of genomic stability. By constructing genetic models both in animals and in somatic cells, we are able to elucidate their mechanism of function and their impact in tumorigenesis with particular interests in how checkpoint signals can be originated from DNA lesions and disrupted replication process. A second area of our work is to explore how chromatin remodeling mechanisms interact with DNA repair and damage checkpoint pathways, since the highly compacted chromatin structure needs to be reconfigured to allowed access to DNA lesions. A third area of research deals with the repair of DNA interstrand cross-links, as many chemotherapy reagents are bifunctional DNA cross-linkers that covalently join the two strands of the double helix. We have identified a recombination-independent and error-prone pathway for the repair of DNA interstrand cross-links. Related to DNA interstrand crosslink processing, we are also investigating molecular mechanisms of Fanconi anemia, whose patient manifestations seem to reflect a deficiency in crosslink repair.

Academic Appointments

Last updated: 3/27/2013