Colombatti A, Collavo D, Biasi G, Chieco-Bianchi L
Int J Cancer. 1975 Sep 15;16(3):435-41. doi: 10.1002/ijc.2910160310.
We have shown in the preceding paper that AKR mice are highly resistant to M-MSV tumor development, and that resistance is transmitted as a dominant character. In the present studies the tumor-response pattern of F1 hybrids between resistant AKR and susceptible strains (C57Bl/6, BALB/c and B10BR) following injection with Moloney mouse sarcoma virus (M-MSV) resembles that of the non-AKR parent. Segregation is observed in first backcross (Bc1) and F2 mice, and the segregation ratios up to Bc3 mice fit a one-gene model. The data of triple cross hybrids suggests that this dominant susceptibility gene inhibits the phenotypic expression of M-MSV tumor resistance in some susceptible Fv1bb strains as well as in their hybrids with AKR. Neither Fv-1 nor H-2 exerts any significant influence on this complex system.
我们在前一篇论文中表明，AKR小鼠对M-MSV肿瘤的发生具有高度抗性，且这种抗性作为显性性状遗传。在本研究中，抗性AKR与易感品系（C57Bl/6、BALB/c和B10BR）之间的F1杂种在注射莫洛尼氏小鼠肉瘤病毒（M-MSV）后的肿瘤反应模式类似于非AKR亲本。在第一代回交（Bc1）和F2小鼠中观察到分离现象，并且直到Bc3小鼠的分离比例符合单基因模型。三杂交杂种的数据表明，这个显性易感基因在一些易感Fv1bb品系及其与AKR的杂种中抑制了M-MSV肿瘤抗性的表型表达。Fv-1和H-2对这个复杂系统均未产生任何显著影响。
