Lack of EGFR gene mutations in exons 19 and 21 in esophageal (Barrett's) adenocarcinomas
Lack of EGFR gene mutations in exons 19 and 21 in esophageal (Barrett's) adenocarcinomas
复制标题
DOI：
10.1111/j.1442-2050.2007.00630.x
复制
发表时间：
2007-01-01
影响因子：
2.6
通讯作者：
Sarbia, M.
中科院分区：
文献类型：
--
作者：
Puehringer-Oppermann, F. A.;Stein, H. J.;Sarbia, M.
表皮生长因子受体在几种肿瘤中过度表达，是酪氨酸激酶抑制剂吉非替尼的靶点。该受体在食管腺癌中也有过度表达。在非小细胞肺癌中，位于激活环中的表皮生长因子受体酪氨酸激酶和富含甘氨酸的P环中的特定体细胞突变导致对吉非替尼的敏感性增强。用变性高压液相色谱技术分析了105例食管腺癌组织中表皮生长因子受体酪氨酸激酶基因的第19和21外显子。我们发现在密码子754中腺嘌呤到鸟嘌呤外显子19只有一个沉默突变，导致K替换为K，其余的样本为野生型。总而言之，在食道腺癌(Barrett‘s)中，与非小细胞肺癌患者对吉非替尼的敏感性相关的EGFR酪氨酸激酶域的突变并不存在。
Epidermal growth factor receptor is over-expressed in several tumors and is the target for the tyrosine kinase inhibitor gefitinib. This receptor is also over-expressed in esophageal adenocarcinomas. In non-small cell lung cancer, specific somatic mutations residing in the epidermal growth factor receptor tyrosine kinase in the activation loop and the glycine-rich P-loop, are responsible for an enhanced sensitivity toward gefitinib. We analyzed exons 19 and 21 coding for the receptor tyrosine kinase of the epidermal growth factor gene in 105 samples of esophageal (Barrett's) adenocarcinoma by denaturing high-pressure liquid chromatography. We found only one silent mutation in exon 19 of adenine to guanine in codon 754 leading to a substitution of K to K, the rest of the sample being wild-type genotype. In conclusion, mutations within the tyrosine kinase domain of EGFR associated with sensitivity of non-small cell lung cancer patients to gefitinib are not present in esophageal (Barrett's) adenocarcinoma.