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《Chinese Journal of Cancer》 2001-06
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Studies on Inactivation of p16/CDKN2 Gene in Non-Small Cell Lung Cancer

AN Qian, DONG Xiang-yang, ZHANG Jian-jun, HUANG Jin-feng, LI Li, CHENG Shu-jun, GAO Yan-ning (Cancer Institute (Hospital), Peking Union Medical College/ Chinese Academy of Medical Sciences, Beijing 100021, P. R. China)  
Objective: This study was designed to investigate the mechanisms of the p16 inactivation in Chinese non-small cell lung cancer (NSCLC) patients and the role of the pl6 as a tumor suppressor gene (TSG) in the genesis of Chinese NSCLC. Method: The genetic and epigenetic alterations of pl6 gene were examined in 17 cases of primary lung cancers by using the methods of microsatellite analysis and methylation-specific PCR (MSP), and P16 protein expression was determined with immunohistochemical staining (IHC). ResultS: Among 13 informative cases, 9 (69. 2% ) had loss of heterozygosity (LOH) for D9S1748, the closest flanking marker to pl6 gene. Among 17 tumor samples, 12 (70. 6% ) displayed promoter methylation from MSP analysis. In total, 82. 4% (14/17 ) of the cases had one or two genetic/ epigenetic alterations of pl6 gene. The results from IHC indicated that 76. 5% (13/17) of these tumor samples had negative P16 protein expression. Among these pl6 protein negative cases, 92. 3% (12/ 13 ) carried at least one of these aberrations. The data showed a good correlation between the results of IHC and molecular analyses. Conclusion: This study suggests that the pl6 may play a critical role in the genesis of Chinese NSCLC, and loss of one allele in addition to promoter hypermethylation of another allele is the main mechanism of the p16 inactivation, which could be useful techniques for early detection of NSCLC.
【Fund】: 国家“九五”攻关项目基金(编号:96-906-01-14);; 国家重点基础研究发展规划项目基金(“973”课题,编号:G1998
【CateGory Index】: R734.2
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