Gleeson C M, Sloan J M, McGuigan J A, Ritchie A J, Russell S E
Department of Medical Genetics, Queen's University of Belfast, Belfast City Hospital, Northern Ireland.
Cancer Res. 1995 Aug 1;55(15):3406-11.
This study examined the association between 17p allelic loss and p53 gene mutation in a series of 16 esophageal adenocarcinomas arising on a background of Barrett's esophagus. Two highly polymorphic dinucleotide repeat polymorphisms mapping to 17p13 were analyzed to assess the frequency of 17p allelic loss in these tumors. Mutations in the p53 gene were detected by direct DNA sequencing. Ninety-four % (15 of 16) of samples were informative at one or both polymorphic loci. Allelic loss at one or both loci was detected in 80% (12 of 15) of samples. Mutations were detected in 69% (11 of 16) esophageal adenocarcinomas, and there was a close association between 17p allelic loss and p53 gene mutation (P = 0.00879; Fisher's Exact Test). The tumors that were analyzed demonstrated a specific p53 mutation spectrum, with G:C to A:T base transitions at CpG dinucleotides accounting for 80% (8 of 10) of single-base substitutions. In three cases, the same p53 mutation was detected in both high-grade dysplasia and adjacent tumor. These results indicate that p53 gene alterations contribute to the development of esophageal adenocarcinoma and precede the development of invasive carcinoma in patients with Barrett's esophagus.
本研究检测了16例起源于巴雷特食管的食管腺癌中17p等位基因缺失与p53基因突变之间的关联。分析了两个定位于17p13的高度多态性二核苷酸重复多态性,以评估这些肿瘤中17p等位基因缺失的频率。通过直接DNA测序检测p53基因的突变。94%(16例中的15例)样本在一个或两个多态性位点具有信息性。在80%(15例中的12例)样本中检测到一个或两个位点的等位基因缺失。在69%(16例中的11例)食管腺癌中检测到突变,并且17p等位基因缺失与p53基因突变之间存在密切关联(P = 0.00879;Fisher精确检验)。所分析的肿瘤表现出特定的p53突变谱,CpG二核苷酸处的G:C到A:T碱基转换占单碱基替换的80%(10例中的8例)。在3例病例中,在高级别异型增生和相邻肿瘤中均检测到相同的p53突变。这些结果表明,p53基因改变促成了食管腺癌的发生,并在巴雷特食管患者浸润性癌发生之前出现。