Nagata Y, Abe M, Motoshima K, Nakayama E, Shiku H
Department of Oncology, Nagasaki University School of Medicine.
Jpn J Cancer Res. 1990 Feb;81(2):135-40. doi: 10.1111/j.1349-7006.1990.tb02539.x.
Point mutations at codons 12 and 13 of c-Ki-ras gene were analyzed in human pancreatic cancer. DNAs obtained from sample tissues were amplified by means of polymerase chain reaction and were analyzed by dot blot hybridization assays with oligonucleotide probes appropriate for detecting mutations at these codons. Out of 38 evaluated cases, point mutations at codon 12 were found in 35 cases; these mutations resulted in changes of the coded amino acid to aspartic acid in 24 cases, to valine in 9 cases, to arginine in 2 cases and to cysteine in one case. In one case, a glycine-to-aspartic acid mutation was found at codon 13. In two cases, two distinct mutations were simultaneously present. The frequency pattern of mutations at codon 12 was somewhat different from those given in two previous reports on the similar analysis of pancreatic cancers in European countries. This may indicate the presence of possible genetic or non-genetic factors in determining preferential mutational patterns at these particular codons.
在人类胰腺癌中分析了c-Ki-ras基因第12和13密码子的点突变。从样本组织中获取的DNA通过聚合酶链反应进行扩增,并用适合检测这些密码子突变的寡核苷酸探针通过斑点印迹杂交分析进行分析。在38例评估病例中,35例在第12密码子处发现点突变;这些突变导致编码氨基酸在24例中变为天冬氨酸,9例中变为缬氨酸,2例中变为精氨酸,1例中变为半胱氨酸。在1例中,第13密码子处发现甘氨酸到天冬氨酸的突变。在2例中,同时存在两种不同的突变。第12密码子的突变频率模式与之前两篇关于欧洲国家胰腺癌类似分析的报告中给出的模式略有不同。这可能表明在决定这些特定密码子的优先突变模式时存在可能的遗传或非遗传因素。