To study the mechanisms of carcinogen-induced genetic recombination, we use human cells engineered to contain two defective copies of a selectable gene, stably integrated into a chromosome. Only cells that successfully combine the first part of one gene and the last part of the other gene can survive selection and form a colony. The system gives us a quantitative measure of the frequency of recombination induced by various carcinogens, and allows us to determine the nature of the recombination event. Integration of this recombination substrate into human cells that are deficient in various processes such as nucleotide excision repair, mismatch repair, p53, etc., or lack a particular DNA polymerase enables us to determine the role of these processes in recombination. They are assisted by research assistants and undergraduate students.
Funding comes mainly from federal grants for research.
Students interested in carcinogenesis and these related basic science areas are encouraged to discuss their interests with one of the directors and carry out a rotation in the laboratory to become acquainted with the research being conducted. Please, close the new window to come back to this page. Lack of correlation between degree of interference with transcription and rate of strand specific repair in the HPRT gene of diploid human fibroblasts. B.S. Tung, W.G. McGregor, Y.-C. Wang, V.M. Maher, and J.J. McCormick . Comparison of the rate of excision of major UV photoproducts in the strands of the human HPRT gene of normal and xeroderma pigmentosum variant cells.