Latency, Histology, and Antigenicity of Tumors Induced by Ultraviolet Light in Three Inbred Mouse Strains1

duced a systemic change in the animals that interfered with tumor rejection (12). The fact that these tumors were so highly antigenic suggested that host defense mechanisms may be of critical importance in the development of these skin cancers (4). There is a good possibility that our findings in the murine system on tumor antigenicity and the systemic immunological effects of UV treatment (4) will be applicable to UV-induced skin cancers in humans. Although there are several fundamental differences between UV carcinogene sis in humans and rodents, particularly with regard to the histological types of tumors (3), the mechanism of transfor mation and the immunological parameters are likely to be universal. Several studies present similar reports of the association between UV radiation and the immune system in rodents and humans. Nathanson et a!. (15) and Koranda et a!. (9) reported that treatment of mice with immunosup pressive agents accelerated the development and increased the incidence of UV-induced skin tumors. Their experimen tal studies corroborate the clinical observation that renal transplant patients who receive chronic immunosuppres sive therapy seem to develop a high frequency of UV-associ ated skin cancers (13, 14, 20). In addition, studies with guinea pigs showed that UV treatment suppressed the elici tation of a contact hypersensitivity response to 2,4-dini trochlorobenzene at the site of irradiation (6). Similarly, the cutaneous delayed hypersensitivity reaction to streptoki nase-streptodornase was suppressed in a human subject afterUV irradiation (7). This study is the 1st step in an investigation of the influ ence of genetic background on the susceptibility of mice to uV carcinogenesis. Becausethereis reasonto believethat immunolgical factors can contribute to tumor induction, it was desirable to test the generality of the earlier observa tions in C3Hf mice (10, 12) by examining the antigenicity of tumors from other strains. In these experiments the tumor incidence, the site and rate of tumor development, and the histological types of tumors were compared in 3 inbred strains of mice with different coat colors [BALB/cAnN (here after referred to as BALB/c) albino; C3H/HeN mammary tumor virus negative (hereafter referred to as C3H1 agouti; and C57BL/6N (hereafter referred to as C57BL/6) blackj. In addition, the relative antigenicity of primary tumors induced in each strain was assessed by comparing tumor growth in normal and immunosuppressed syngeneic recipients.