Overview Academic/Research Interest Areas

Etiology of DNA damage-induced chromosomal rearrangements common to leukemias, lymphomas, and soft-tissue sarcomas: The long-term objective of my research is to understand the mechanisms used by hematopoietic cells to repair of one type of DNA damage -- the double-strand break (DSB)-- and the initial molecular events that lead to genomic rearrangements such as translocations, which are a hallmark of leukemias, lymphomas, and soft-tissue sarcomas. Radiation and DNA damaging agents are common therapy in the treatment of human cancers. Exposure to these agents also leads to chromosomal DSBs that may be aberrantly repaired to produce rearrangements and oncogenic transformation and tumor formation. Recent data from my lab indicates that chromosomal rearrangements analogous to those observed in hematopoietic malignancies are readily formed during DSB repair in both human and mouse hematopoietic stem cell-enriched populations. However, the majority of these rearrangements are not sufficient for malignant progression. My lab uses multiple genetic approaches in cultured cell lines and genestically engineered mice to identify the initial events that promote the formation of DNA damage-induced chromosomal rearrangements, and the cooperative mutations or predisposing factors that can promote (or suppress) transformation of cells that acquire them. This research will provide an understanding of the earliest events in DNA repair and the development of certain tumors, particularly therapy-related and infant leukemia, and may lead to new approaches to therapy and prevention.

Recent Publications

Richardson, C., Moynahan, M., Jasin, M. Double-strand break repair by interchromosomal recombination: Suppression of chromosomal translocations. Genes & Dev. 12:3831-3842, 1998.

Richardson, C., and Jasin, M. Frequent chromosomal translocations induced by DNA double-strand breaks. Nature 405: 697-700, 2000.

Richardson, C., and Jasin, M. Coupled homologous and nonhomologous repair of a double-strand break preserves genomic integrity in mammalian cells. Mol. Cell. Biol. 20: 9068-9075, 2000.

Elliott, B., Richardson, C., Jasin, M. Chromosomal translocation mechanisms at intronic alu elements in mammalian cells. Mol. Cell 17: 885-894, 2005.

Richardson, C. , Stark, J., Ommundsen, M., Jasin, M. Over-expression of Rad51 promotes alternative DSB repair and genome instability. Oncogene 23: 546-553, 2004.

Richardson, C., Horikoshi, N., and Pandita, T. The DSB response network in meiosis. DNA Repair 3: 1149-1164, 2004.

Educational Background

A.B., Department of Molecular Biology, Princeton University, 1990

Ph.D., Department of Genetics & Development, Columbia University, 1995