van Wezel T, Ruivenkamp C A, Stassen A P, Moen C J, Demant P
Division of Molecular Genetics, The Netherlands Cancer Institute, Amsterdam.
Cancer Res. 1999 Sep 1;59(17):4216-8.
Germ-line mutations in APC and mismatch repair genes explain only a small percentage of all colorectal cancer cases. We have used the recombinant congenic strain mouse model to find new loci that are involved in the control of susceptibility to colon cancer. Five different colon cancer susceptibility genes, Scc1-Scc5, have been described previously using the recombinant congenic strains. Two of these loci, Scc4 and Scc5, show a reciprocal, genetic interaction. Here we report the mapping of four new colon tumor susceptibility genes: (a) Scc6 on chromosome 11; (b) Scc7 on chromosome 3; (c) Scc8 on chromosome 8; and (d) Scc9 on chromosome 10. Scc7 and Scc8 show a genetic interaction; Scc7 is only detected by virtue of its interaction with Scc8.
APC基因和错配修复基因中的种系突变仅占所有结直肠癌病例的一小部分。我们使用重组近交系小鼠模型来寻找参与控制结肠癌易感性的新基因座。先前已使用重组近交系描述了五个不同的结肠癌易感基因,即Scc1-Scc5。其中两个基因座,Scc4和Scc5,表现出相互的遗传相互作用。在此,我们报告了四个新的结肠肿瘤易感基因的定位:(a) 位于11号染色体上的Scc6;(b) 位于3号染色体上的Scc7;(c) 位于8号染色体上的Scc8;以及(d) 位于10号染色体上的Scc9。Scc7和Scc8表现出遗传相互作用;Scc7仅通过其与Scc8的相互作用才能被检测到。