Molecular analysis of the FHIT gene at 3p14.2 in lung cancer cell lines.
Molecular analysis of the FHIT gene at 3p14.2 in lung cancer cell lines.
复制标题
肺癌细胞系 3p14.2 处 FHIT 基因的分子分析。
作者：
K. Yanagisawa;M. Kondo;H. Osada;K. Uchida;K. Takagi;A. Masuda;Toshitada Takahashi;Takashi Takahashi
染色体3 p在各种癌症中经常缺失，包括肺癌的例子。最近从3p14.2的脆性位点分离出一个新的基因，称为FHIT，在肺癌肿瘤标本中有异常转录本的报道。为了避免忽略由于原发肿瘤中污染正常细胞而导致的肿瘤特异性改变的转录物，本研究在41个肺癌细胞系中检查了FHIT改变。在24例非小细胞肺癌中有7例（29%）观察到异常剪接转录物缺乏可检测的表达或排他性表达，通常伴有基因内纯合缺失，但在17例小细胞肺癌中没有观察到异常剪接转录物（0%）。广泛的逆转录-PCR-单链构象多态性分析显示多态性和选择性剪接，但未能确定点突变。这些结果表明，不同的机制FHIT改变在肺肿瘤的发生和进一步研究这个有趣的基因是必要的。
Chromosome 3p is frequently deleted in various cancers including examples in the lung. A novel gene, termed FHIT, was recently isolated from the fragile site at 3p14.2, with aberrant transcripts being reported in lung cancer tumor specimens. To avoid overlooking tumor-specific altered transcripts due to contaminating normal cells in primary tumors, FHIT alterations were examined in 41 lung cancer cell lines in the present study. Lack of detectable expression or exclusive expression of aberrantly spliced transcripts, often accompanied by intragenic homozygous deletions, were observed in 7 of 24 non-small cell lung cancers (29%) but in 0 of 17 small cell lung cancers (0%). Extensive reverse transcription-PCR-single-strand conformation polymorphism analysis revealed polymorphisms and alternative splicing but failed to identify point mutations. These results suggest distinct mechanisms for FHIT alterations in lung tumorigenesis and that further studies of this interesting gene are warranted.
DOI：
10.1073/pnas.93.9.4120
发表时间：
1996-04-30
影响因子：
11.1
作者：
Sekido, Y;Bader, S;Minna, JD
通讯作者：
Minna, JD
影响因子：
56.9
作者：
KAMB, A;GRUIS, NA;SKOLNICK, MH
通讯作者：
SKOLNICK, MH
小细胞肺癌细胞系 3 号染色体上的纯合缺失与肿瘤抑制活性区域相关。
影响因子：
8
作者：
Daly,MC;Xiang,RH;Buchhagen,D;Hensel,CH;Garcia,DK;Killary,AM;Minna,JD;Naylor,SL
通讯作者：
Naylor,SL