Genetic mapping and physical cloning of UVB susceptibility region in mice

One of the most important goals of cancer research is to identify environme ntal and host factors that contribute to the malignant state. Human skin ca ncers are among the few tumor types for which the predominant environmental carcinogen is known. Ultraviolet light, a component of sunlight, is an imp ortant cause of skin cancer in humans. In humans and mice, ultraviolet B ra diation induces systematic and local immunosuppression. A consequence of th at is inappropriate immune surveillance of somatic tissues for evidence of malignantly transformed cells. The impairment of contact hypersensitivity, as it develops early and correlates well with tumor frequency in various mo use strains, has been used for over 15 y as a model of immunologic events o ccurring in photocarcinogenesis. In mice, as well as in humans, ultraviolet B radiation induced impairment of contact hypersensitivity is not uniform in all individuals; some individuals are susceptible to the deleterious eff ects of ultraviolet B, whereas others are resistant to ultraviolet B. We ha ve defined the genetic locus responsible for ultraviolet B susceptibility a nd resistance in mice within the Bat5 and H-2D segment of the mouse chromos ome 17.