De Benedetti L, Varesco L, Pellegata N S, Losi L, Gismondi V, Casarino L, Sciallero S, Bonelli L, Biticchi R, Bafico A
IST, National Cancer Institute, Genova, Italy.
Anticancer Res. 1993 May-Jun;13(3):667-70.
Twenty-four sporadic colorectal adenomas were analysed for the presence of allelic loss on the short arm of chromosome 17 as well as mutations in the K-ras and p53 genes. Chromosome 17p13 allelic loss was not present in 14 out of 14 informative cases. K-ras mutations were observed in 15 out of 24 cases. A p53 gene mutation (GGC-->GAC at codon 245) was detected in two biopsies taken at a four year interval from a recurrent rectal villous adenoma. Both biopsies also contained the same K-ras gene mutation (GGT-->GTT at codon 12). The data from the recurrent rectal adenoma provide in vivo evidence that K-ras and p53 heterozygous mutations confer a proliferative advantage but together are not sufficient for malignant transformation.
对24个散发性结肠直肠腺瘤进行分析，以检测17号染色体短臂上等位基因缺失情况以及K-ras和p53基因的突变。在14例信息充分的病例中，有14例不存在17号染色体p13等位基因缺失。24例中有15例观察到K-ras突变。在一例复发性直肠绒毛状腺瘤间隔四年采集的两份活检样本中检测到p53基因突变（密码子245处GGC→GAC）。两份活检样本还含有相同的K-ras基因突变（密码子12处GGT→GTT）。复发性直肠腺瘤的数据提供了体内证据，表明K-ras和p53杂合突变赋予增殖优势，但两者共同作用不足以导致恶性转化。
