Nomoto S, Haruki N, Kondo M, Konishi H, Takahashi T, Takahashi T, Takahashi T
Laboratory of Ultrastructure Research, Aichi Cancer Center Research Institute, Nagoya, Japan.
Cancer Res. 1998 Apr 1;58(7):1380-3.
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.
我们检测了61例肺癌病例,以确定新型单等位基因表达的p53样分子p73的改变是否可能参与肺癌的发病机制。在1p36.33的p73基因座处观察到42%(26例信息充分的病例中有11例)出现等位基因缺失,鳞状细胞癌最常出现这种病变。然而,尽管我们进行了广泛搜索,但未检测到p73基因本身的体细胞突变。我们发现正常肺组织中p73的等位基因表达存在个体差异,以及同一人体内不同组织间的差异,但是表达等位基因的优先缺失似乎不太可能是p73失活的机制。因此,本研究提示在1p亚端粒区域内存在一个或多个尚未确定的肿瘤抑制基因,值得进一步开展旨在分离该基因的研究。