Konishi H, Takahashi T, Kozaki K, Yatabe Y, Mitsudomi T, Fujii Y, Sugiura T, Matsuda H, Takahashi T, Takahashi T
Laboratory of Ultrastructure Research, Aichi Cancer Center Research Institute, Nagoya, Japan.
Oncogene. 1998 Oct 22;17(16):2095-100. doi: 10.1038/sj.onc.1202128.
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.
17号染色体短臂是肺癌中最常受影响的染色体区域之一，同时有确凿证据表明位于17p13.1的p53基因是17p频繁缺失的靶点。在本研究中，我们通过参照每100例原发性肺癌病例中的p53基因状态，对17p上的最小缺失区域进行详细分析，重新评估了肺癌中的17p缺失情况。除了17p13.1处的p53基因座外，还在17p13.3处鉴定出一个独立的、常见的缺失区域。此外，17p13.3处的杂合性缺失（LOH）比17p13.1处更为常见，并且似乎在没有p53突变和/或17p13.1缺失的情况下发生。这些结果表明，除了17p13.1处的p53基因外，位于17p13.3的一个尚未确定的肿瘤抑制基因可能在肺癌发生过程中发挥作用，可能比p53基因更早发挥作用。这将有必要开展进一步研究以鉴定17p13.3处的假定肿瘤抑制基因，从而更好地了解这种致命疾病的分子发病机制。
