期刊
CANCER
卷 106, 期 5, 页码 1117-1122出版社
JOHN WILEY & SONS INC
DOI: 10.1002/cncr.21705
关键词
Rad9; cell cycle control; DNA damage check-point pathway; nonsmall cell lung carcinoma; adenocarcinoma; nonsynonymous single nucleotide polymorphism
类别
BACKGROUND. It was previously reported that a functional human (h) Rad9 protein accumulated in the nuclei of nonsmall cell lung carcinoma (NSCLC) cells. Those experiments, however, did not examine whether the hRad9 gene was mutated in those cells. The sequence of the HRAD9 gene in NSCLC cells was investigated. METHODS. The sequence of the HRAD9 was examined in tumor and peripheral normal lung tissues obtained from 50 lung adenocarcinoma patients during surgery. The expression of its mRNA using reverse transcription polymerase chain reaction (RT-PCR) was also examined. RESULTS. No sequence alterations were detected in the HRAD9 gene, which was found to be normally transcribed in surgically resected king carcinoma cells. However, in eight (16.0%) cases a single nucleotide polymorphism (SNP) was observed at the second position of codon 239 (His/Arg heterozygous variant) of the gene. This frequency was significantly higher than that found in the nornial population. CONCLUSIONS. whereas the capacity to produce a functional hRad9 Protein was intact in lung adenocarcinoma cells, a nonsynonymous SNP of HRAD9 was detected that might be associated with the development of lung adenocarcinoma.
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