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Effect of parent genetic background on latency and antigenicity of UV‐induced tumors originating in F 1 hybrids
Author(s) -
Kitajima Toshiyuki,
Iwashiro Michihiro,
Kuribayashi Kagcmasa,
Imamura Sadao
Publication year - 1995
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/j.1600-0625.1995.tb00220.x
Subject(s) - antigenicity , hybrid , latency stage , ratón , biology , microbiology and biotechnology , ultraviolet radiation , cancer research , antigen , chemistry , immunology , medicine , botany , radiochemistry
Wide variations in susceptibility to skin tumor development by chronic ultraviolet light (UV) exposure and antigenicity of induced tumors which is estimated by tumor rejection in syngeneic recipients have been recognized among various murine strains. To examine the effect of parent genetic background on latency and antigenicity of UV‐induced tumors originating in F 1 hybrids, we induced skin tumors in three mouse strains: BALB/c, C57BL/6, (B6), and C3H/HeMs (C3H/He), and their F 1 , hybrids: (BALB/c×C3H/He)F 1 , (CC3F 1 ), (BALB/c×B6)F 1 , (CB6F 1 ) and (C3H/He×B6)F 1 , (C3B6F 1 ) by exposing mice to UV radiation (0.44 mW/ cm 2 for 1 h) three times a week, and analyzed whether the UV‐induccd tumors originating in F 1 hybrids possess the similar property in latency or antigenicity as seen in the UV‐induced tumors derived from the parent strains. The latency of tumor induction by chronic UV exposure in C3H/He, BALB/c and their F 1 , hybrid CC3F 1 , was relatively short whereas that of B6 was relatively long, and that of F 1 , hybrids with B6 (CB6F, and C3B6F 1 ) was intermediate. On the other hand, the low antigenicity as progressive growth behavior of UV‐induced tumors in syngeneic recipients was observed not only in tumors derived from C3H/He but also in those from F, hybrids with C3H/He (C3B6F 1 , and CC3F 1 ) whereas most tumors derived from B6, BALB/c and their F 1 hybrid CC3F 1 were highly antigenic as to be rejected in syngeneic recipients. These findings suggest that the parent genetic quality regulating the susceptibility to tumor induction by chronic UV exposure is co‐dominantly inherited into F 1 hybrids. On the other hand, that providing the progressive growth behavior of induced tumors appears to be a dominant effect.