E. Boulton et al., Susceptibility to radiation-induced leukaemia/lymphoma is genetically separable from sensitivity to radiation-induced genomic instability, INT J RAD B, 77(1), 2001, pp. 21-29
Purpose : To determine whether there is a relationship between the genetics
underlying the susceptibility to radiation-induced leukaemia in CBA/H (acu
te myeloid leukaemia, AML) and C57BL/6 (thymic lymphoma, TL) mice, and the
genetics underlying the sensitivity of CBA/H (sensitive) and C57BL/6 (resis
tant) mice to radiation-induced chromosomal instability.
Materials and methods: CBA/H, (CBA/H x C57BL/6) F-1, F-1 x CBA/H, F-1 x C57
BL/6 and F-1 x F-1 mice were exposed to a single acute dose of 3.0 Gy X-ray
s. AML and TL were diagnosed over the subsequent 30 months.
Results: There was no statistically significant difference in the incidence
of AML in F-1, F-1 x F-1, F-1 x CBA/H and F-1 x C57BL/6 mice, which was si
milar to 50% that in CBA/H mice. AML susceptibility is therefore a dominant
polygenic trait, and both susceptibility and resistance (variable penetran
ce) CBA/H and C57BL/6 loci are involved. The incidence of TL in the F-1 and
F-1 x CBA/H mice was negligible, indicating that TL susceptibility is a re
cessive trait. As the TL incidence in the F-1 x C57BL/6 mice was about half
that in C57BL/6 mice, one recessive locus is probably involved.
Conclusions : AML susceptibility in CBA/H mice is a dominant trait in contr
ast to the recessive inheritance of CBA/H sensitivity to radiation-induced
chromosomal instability. TL-susceptibility in C57BL/6 is a recessive trait
in contrast to the dominant inheritance of C57BL/6 resistance to radiation-
induced chromosomal instability.