Peter Demant

Biography

Peter Demant is a distinguished Member in the Department of Molecular and Cellular Biology at Roswell Park Cancer Institute. He received MD (Medicine) from Charles University Medical School, Prague, Czech Republic, 1963 and PhD (Genetics and Immunology) Institute of Experimental Biology and Genetics, Prague, Czech Republic, 1967. His research interest include: the study of the genes in host genome, which control the development of cancer. We aim to map and subsequently clone such genes, understand the way they interact with different molecular pathways during tumor development and progression, and determine what their relationship is to processes of regulation of cellular homeostasis at different developmental stages. The first evidence for the role of genetic factors in cancer has been obtained in familial cancer syndromes, which are caused by germ-line mutations in tumor suppressor or mismatch repair genes like APC, Rb, NF2, MSH2. However, these syndromes account for a small part of all cancers. The largest proportion of cancers is of non-familial, sporadic, type. Nevertheless, also in these apparently non-inherited cancers the host genetic factors play an important role (e.g., Lichtenstein et al., New Eng J Med 343:78, 2000). Moreover, especially in the breast cancer there is extended evidence that many, and probably most, cases of the apparently non-familial breast cancer appear in the genetically predisposed individuals (Peto and Mack, Nat Genet 26:411-414, 2000; Pharoah et al., Nat Genet 31:33-36, 2002). The largest part of this predisposition is caused by presently unknown genes. In contrast to the germ-line mutations of oncogenes or tumor suppressor and mismatch repair genes, the genes affecting development and progression of sporadic cancers are multiple and have smaller effects. Therefore, they are difficult to detect in classical family and population studies, and they have to be analyzed in experimental animals, which offer the advantage of defined genetic constitution, possibility of producing informative crosses, and standardized tumor-induction procedures (Demant, Nat Rev Genet 4:721-734, 2003). We used recombinant congenic strains of mice to map and identify lung and colon cancer susceptibility genes in mice and subsequently to search for their homologues in humans.

Research Interest

Cancer Susceptibility Genes in Mice and Their Human Homologues