胃癌及癌前病变中10q23.3杂合性缺失与肿瘤抑制基因PTEN突变
Loss of heterozygosity on 10q23.3 and mutation of tumor suppressor gene PTEN in gastric cancer and precancerous lesions.
作者信息
Li Yi-Ling, Tian Zhong, Wu Dong-Ying, Fu Bao-Yu, Xin Yan
机构信息
Department of Gastroenterology, First Hospital of China Medical University, Shenyang 110001, Liaoning Province, China.
出版信息
World J Gastroenterol. 2005 Jan 14;11(2):285-8. doi: 10.3748/wjg.v11.i2.285.
AIM
To investigate the loss of heterozygosity (LOH) and mutation of tumor suppressor gene PTEN in gastric cancer and precancerous lesions.
METHODS
Thirty cases of normal gastric mucosa, advanced and early stage gastric cancer, intestinal metaplasia, atrophic gastritis, and atypical hyperplasia were analyzed for PTEN LOH and mutations within the entire coding region of PTEN gene by PCR-SSCP denaturing PAGE gel electrophoresis, and PTEN mutation was detected by PCR-SSCP sequencing followed by silver staining.
RESULTS
LOH rate found in respectively atrophic gastritis was 10% (3/30), intestinal metaplasia 10% (3/30), atypical hyperplasia 13.3% (4/30), early stage gastric cancer 20% (6/30), and advanced stage gastric cancer 33.3% (9/30), None of the precancerous lesions and early stage gastric cancer showed PTEN mutations, but 10% (3/30) of the advanced stage gastric cancers, which were all positive for LOH, showed PTEN mutation.
CONCLUSION
LOH of PTEN gene appears in precancerous lesions, and PTEN mutations are restricted to advanced gastric cancer, LOH and mutation of PTEN gene are closely related to the infiltration and metastasis of gastric cancer.
目的
研究胃癌及癌前病变中杂合性缺失（LOH）及抑癌基因PTEN的突变情况。
方法
采用PCR-SSCP变性聚丙烯酰胺凝胶电泳分析30例正常胃黏膜、进展期和早期胃癌、肠化生、萎缩性胃炎及非典型增生中PTEN基因整个编码区内的LOH及突变情况，通过PCR-SSCP测序及银染检测PTEN突变。
结果
萎缩性胃炎、肠化生、非典型增生、早期胃癌及进展期胃癌的LOH发生率分别为10%（3/30）、10%（3/30）、13.3%（4/30）、20%（6/30）及33.3%（9/30）。癌前病变及早期胃癌均未发现PTEN突变，但进展期胃癌中有10%（3/30）出现PTEN突变，且均为LOH阳性。
结论
PTEN基因的LOH出现在癌前病变中，PTEN突变仅限于进展期胃癌，PTEN基因的LOH及突变与胃癌的浸润和转移密切相关。
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