Search for mutations and examination of allelic expression imbalance of the p73 gene at 1p36.33 in human lung cancers.
Search for mutations and examination of allelic expression imbalance of the p73 gene at 1p36.33 in human lung cancers.
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发表时间：
1998-04
期刊：
影响因子：
11.2
通讯作者：
Shuji Nomoto;N. Haruki;M. Kondo;Hiroyuki Konishi;Takao Takahashi;Toshitada Takahashi;Takashi Takahashi
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文献类型：
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作者：
Shuji Nomoto;N. Haruki;M. Kondo;Hiroyuki Konishi;Takao Takahashi;Toshitada Takahashi;Takashi Takahashi
我们研究了61例肺癌病例，以确定p73（一种新的单等位基因表达的p53样分子）的改变是否可能参与肺癌的发病机制。在1p36.33位点p73等位基因缺失的发生率为42%（26例信息丰富的病例中有11例），鳞状细胞癌往往最常携带这种病变。然而，尽管我们进行了广泛的搜索，但p73基因本身的体细胞突变并未被检测到。我们发现正常肺中p73的等位基因表达存在个体间差异，甚至在同一个体中也存在组织间差异，但表达等位基因的优先丢失似乎不太可能是p73失活的机制。因此，这项研究表明，在1p的亚端粒区存在一个或多个尚未确定的肿瘤抑制基因，需要进一步的研究来分离它。
We examined 61 lung cancer cases to determine whether alterations of p73, a novel monoallelically expressed p53-like molecule, may be involved in the pathogenesis of lung cancer. Allelic loss at the p73 locus at 1p36.33 was observed in 42% (11 of 26 informative cases), and squamous cell carcinoma tended to carry this lesion most frequently. Somatic mutations in the p73 gene itself, however, were not detected, despite our extensive search. We found interindividual difference in the allelic expression of p73 in normal lung, as well as intertissue variance, even within the same individual, but preferential loss of the expressed allele appeared to be an unlikely mechanism for p73 inactivation. This study, consequently, suggests the presence of an as yet unidentified tumor suppressor gene or genes within the subtelomeric region of 1p, warranting further studies aimed at its isolation.