International Mammalian Genome Society

17th International Mouse Genome Conference

9-12 November 2003, Braunschweig, Germany


POSTER 158 - GENETICS OF SKIN TUMOR PROMOTION SUSCEPTIBILITY

Angel J M
The University of Texas MD Anderson Cancer Center, Science Park-Research Division

Co-Authors: Riggs P K, Caballero M, DiGiovanni J
Institutions: The University of Texas MD Anderson Cancer Center, Science Park-Research Division

Cancer susceptibility in the general population is a function of multiple, poorly penetrant modifier genes each of which contributes to, but is not solely responsible for predisposition to developing a particular type of cancer after exposure to certain environmental carcinogenic agents. Genetic differences in susceptibility to two-stage skin carcinogenesis have been known for many years and the major contribution to susceptibility appears to be at the level of tumor promotion. Studies suggest that susceptibility to 12-O-tetradecanoylphorbol-13-acetate (TPA) skin tumor promotion is a multigenic trait. Loci that modify the susceptibility to TPA skin tumor promotion have been mapped to chromosomes 1, 2, 9, and 19 in genetic crosses of sensitive DBA/2 with relatively resistant C57BL/6 mice. One promotion susceptibility locus, Psl1, was mapped to an ~40 cM region of distal chromosome 9. Results from tumor studies using interval specific congenic mouse strains suggest that at least two genes that modify the response to TPA skin tumor promotion map within this 40 cM region of distal chromosome 9. A large number of genes mapping to this region have been associated with skin phenotypes or cancer development. Furthermore, cDNA microarray analysis identified several genes mapping to this region that are differentially expressed in the epidermis of sensitive and resistant mice treated with TPA. Supported by NIEHS grant ES08355, NIEHS Center grant ES07784, and M.D. Anderson Cancer Center Core grant CA16672.


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