Detailed deletion mapping suggests the involvement of a tumor suppressor gene at 17p13.3, distal to p53, in the pathogenesis of lung cancers

被引:53
作者
Konishi, H
Takahashi, T
Kozaki, K
Yatabe, Y
Mitsudomi, T
Fujii, Y
Sugiura, T
Matsuda, H
Takahashi, T
Takahashi, T
机构
[1] Aichi Canc Ctr, Res Inst, Ultrastruct Res Lab, Chikusa Ku, Nagoya, Aichi 464, Japan
[2] Aichi Canc Ctr, Res Inst, Pathophysiol Unit, Chikusa Ku, Nagoya, Aichi 464, Japan
[3] Aichi Canc Ctr, Res Inst, Immunol Lab, Chikusa Ku, Nagoya, Aichi 464, Japan
[4] Aichi Canc Ctr Hosp, Dept Pathol & Clin Labs, Chikusa Ku, Nagoya, Aichi 464, Japan
[5] Aichi Canc Ctr Hosp, Dept Thorac Surg, Chikusa Ku, Nagoya, Aichi 464, Japan
[6] Aichi Canc Ctr Hosp, Dept Internal Med, Chikusa Ku, Nagoya, Aichi 464, Japan
[7] Osaka Univ, Sch Med, Dept Surg 1, Suita, Osaka 565, Japan
[8] Gifu Univ, Sch Med, Dept Surg 2, Gifu 500, Japan
[9] Nagoya City Univ, Sch Med, Dept Surg 2, Mizuho Ku, Nagoya, Aichi 467, Japan
关键词
17p13.3; LOH; p53; tumor suppressor gene; lung cancer;
D O I
10.1038/sj.onc.1202128
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The short arm of chromosome 17 is one of the most frequently affected chromosomal regions in lung cancers, while there is solid evidence that the p53 gene at 17p13.1 is a target for frequent 17p deletions. In the present study, we re-evaluated 17p deletions in lung cancers by conducting a detailed analysis of the minimum deleted region(s) on 17p with reference to the p53 gene status in each 100 primary lung cancer cases. In addition to the p53 locus at 17p13.1, the presence of an independent, commonly deleted region(s) at 17p13.3 was identified, Furthermore, loss of heterozygosity (LOH) at 17p13.3 was shown to be even more frequent than that at 17p13.1 and it appeared to occur in the absence of p53 mutation and/or 17p13.1 deletion. These results suggest that in addition to the p53 gene at 17p13.1, an as yet unidentified tumor suppressor gene(s) residing at 17p13.3 might play a role in lung carcinogenesis possibly in an earlier phase than the p53 gene. This would warrant future studies to identify the putative tumor suppressor gene at 17p13.3 in order to gain a better understanding of the molecular pathogenesis of this fatal disease.
引用
收藏
页码:2095 / 2100
页数:6
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