Experimental ultraviolet radiation carcinogenesis: I. Relationship of the major histocompatibility complex to tumor latency and immunogenecity.
The induction of skin tumors by ultraviolet radiation (UV) was compared concurrently in 3 inbred mouse strains (BALB/c, C3H, and C57BL/10) and 7 related H-2 (major histocompatibility complex) congenic strains of mice. The latency period for UV-tumor induction was observed to be shorter in BALB/c mice compared with that in C3H and C57BL/10 animals. Similarly, tumor latency periods in the different H-2 congenic mouse strains tested were comparable to those of their related background strain. The proportion of squamous cell carcinomas to spindle cell fibrosarcomas, as well as the ratio of progressor and regressor tumors, as determined by their ability to grow when transplanted into normal syngenic mice, were comparable for those strains of mice that shared common genetic backgrounds. Interestingly, for all strains of mice analyzed UV-regressor and UV-progressor tumors were found to arise randomly throughout the latency period. These studies suggest that, at least for the three parameters tested, genes or gene products encoded within the major histocompatibility complex do not influence either latency period, histologic type or immunogenicity of UV-induced skin tumors.
D000818:Animals; D008285:Major Histocompatibility Complex; D051379:Mice; D008815:Mice, Inbred Strains; D009368:Neoplasm Transplantation; D009381:Neoplasms, Radiation-Induced / Q000235:genetics* / Q000276:immunology; D012878:Skin Neoplasms / Q000209:etiology / Q000235:genetics* / Q000276:immunology; D013045:Species Specificity; D013997:Time Factors; D014466:Ultraviolet Rays / Q000009:adverse effects*