Okamoto M, Ohtsu H, Miyaki M, Yonekawa H
Department of Laboratory Animal Science, Tokyo Metropolitan Institute of Medical Science, Japan.
Carcinogenesis. 1993 Jul;14(7):1483-6. doi: 10.1093/carcin/14.7.1483.
We examined allelic loss in colon tumors induced by 1,2-dimethylhydrazine (DMH) in F1 hybrid mice, using sequence-tagged microsatellite site (STMS) primers derived from the chromosomal region closely linked to the p53 locus. Polymerase chain reaction--single-strand conformation polymorphism (PCR-SSCP) analysis of 155 colonic tumors with two STMS markers revealed that no genetic alterations had occurred in these tumors, except for one case where one of the markers detected an increase of one CA repeat unit in one allele. No allelic loss at the loci closely linked to the p53 locus strongly suggests that allelic loss at the p53 locus is not involved in DMH-induced colon carcinogenesis in mice.
我们使用源自与p53基因座紧密连锁的染色体区域的序列标签微卫星位点（STMS）引物，检测了1,2 - 二甲基肼（DMH）诱导的F1杂交小鼠结肠肿瘤中的等位基因缺失情况。用两个STMS标记对155个结肠肿瘤进行聚合酶链反应 - 单链构象多态性（PCR - SSCP）分析，结果显示除1例肿瘤外，其余肿瘤均未发生基因改变，在该例中，其中一个标记检测到一个等位基因中的一个CA重复单元增加。与p53基因座紧密连锁的位点未发生等位基因缺失，这强烈表明p53基因座的等位基因缺失不参与小鼠DMH诱导的结肠癌发生过程。
