| First Author | Handel-Fernandez ME | Year | 1999 |
| Journal | J Invest Dermatol | Volume | 113 |
| Issue | 2 | Pages | 224-9 |
| PubMed ID | 10469308 | Mgi Jnum | J:56747 |
| Mgi Id | MGI:1342377 | Doi | 10.1046/j.1523-1747.1999.00683.x |
| Citation | Handel-Fernandez ME, et al. (1999) Genetic mapping and physical cloning of UVB susceptibility region in mice. J Invest Dermatol 113(2):224-9 |
| abstractText | One of the most important goals of cancer research is to identify environmental and host factors that contribute to the malignant state. Human skin cancers are among the few tumor types for which the predominant environmental carcinogen is known. Ultraviolet light, a component of sunlight, is an important cause of skin cancer in humans. In humans and mice, ultraviolet B radiation induces systematic and local immunosuppression. A consequence of that 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 mouse strains, has been used for over 15 y as a model of immunologic events occurring 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 effects of ultraviolet B, whereas others are resistant to ultraviolet B. We have defined the genetic locus responsible for ultraviolet B susceptibility and resistance in mice within the Bat5 and H-2D segment of the mouse chromosome 17. |
