Luongo C, Moser A R, Gledhill S, Dove W F
McArdle Laboratory for Cancer Research, University of Wisconsin Medical School, Madison 53706.
Cancer Res. 1994 Nov 15;54(22):5947-52.
Allelic loss at the Apc locus in spontaneously occurring intestinal adenomas from mice heterozygous for the ApcMin nonsense mutation was analyzed using a site-specific quantitative polymerase chain reaction assay. All 97 of the intestinal adenomas analyzed showed extensive loss of the wild-type Apc (Apc+) allele. Quantitative polymerase chain reaction analysis of loci linked to Apc indicated loss of the chromosome carrying Apc+. Only one copy of the homologue carrying ApcMin remained in the intestinal adenomas. Possible reasons for the difference in the mechanism of Apc+ loss between human and Min mouse intestinal adenomas are discussed.
使用位点特异性定量聚合酶链反应分析方法,对携带ApcMin无义突变的杂合子小鼠自发产生的肠道腺瘤中Apc基因座的等位基因缺失情况进行了分析。所分析的97个肠道腺瘤均显示野生型Apc(Apc+)等位基因广泛缺失。对与Apc连锁的基因座进行定量聚合酶链反应分析表明,携带Apc+的染色体发生了缺失。在肠道腺瘤中仅保留了携带ApcMin的同源染色体的一个拷贝。文中讨论了人类和Min小鼠肠道腺瘤中Apc+缺失机制存在差异的可能原因。