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目的研究肺癌组织和转移性肺门淋巴结中脆性组氨酸三联体基因（ｆｒａｇｉｌｅｈｉｓｔｉｄｉｎｅｔｒｉａｄ，ＦＨＩＴ）和ｐ１６基因的改变。方法采用ＲＴＰＣＲ（逆转录ＰＣＲ）和ＲＴＰＣＲＳＳＣＰ（单链构像多态性分析）方法对４９例肺癌组织和１６例相应的转移性肺门淋巴结进行ｐ１６基因和ＦＨＩＴ基因检测，其中２例肺癌组织仅行ｐ１６基因检测。结果３２例（６８．１％）肺癌原发灶（包括２例肺鳞状细胞原位癌）和１５例（９３．８％）转移性肺门淋巴结出现ＦＨＩＴ转录本缺失，二者缺失率相比，差异有显著性（Ｐ＜０．０５）。ＦＨＩＴ基因转录本丢失主要发生于编码区。１４例（２９．８％）肺癌原发灶与９例（５６．３％）转移性肺门淋巴结出现ＦＨＩＴ基因转录本外显子１～４缺失，二者缺失率差异有显著性（Ｐ＜０．０５）。肺癌原发灶和转移性肺门淋巴结ｐ１６基因外显子２～３转录本缺失率分别为３６．７％（１８／４９例）和５６．３％（９／１６例），二者差异无显著性。ＲＴＰＣＲＳＳＣＰ分析未发现突变。结论（１）在肺癌组织中ＦＨＩＴ基因转录本缺失是频发事件，且可能为早期事件；ｐ１６基因表达缺失可能晚发于ＦＨＩＴ基因异常之后。（２）肺癌组织中ＦＨＩＴ和ｐ１?
Objective To investigate the changes of fragilhistidine triad (FHIT) and p16 genes in lung cancer tissues and metastatic hilar lymph nodes. Methods RT-PCR (reverse transcription PCR) and RTPCRSSCP (single strand conformation polymorphism analysis) methods were used to detect p16 gene and FHIT gene in 49 lung cancer tissues and 16 corresponding metastatic hilar lymph nodes. Two cases of lung cancer only performed p16 gene detection. Results FHIT transcript deletion occurred in 32 (68.1%) lung cancer primary tumors (including 2 lung squamous cell carcinoma in situ) and 15 (93.8%) metastatic hilar lymph nodes. Ratio, the difference was significant (P <0.05). The loss of FHIT gene transcripts occurs mainly in the coding region. In 14 cases (29.8%) of lung cancer primary tumors and 9 cases (56.3%) of metastatic hilar lymph nodes, there was a deletion of FHIT gene transcript exons 1-4, and the difference between the two rates was significant (P < 0.05). The transcript deletion rate of exon 2～3 of p16 gene in lung cancer primary metastases and metastatic hilar lymph nodes were 36.7% (18/49) and 56.3% (9/16) respectively. Significant. RT-PCR-SSCP analysis found no mutations. Conclusions (1) FHIT gene transcript deletion in lung cancer is a frequent event and may be an early event; deletion of p16 gene may occur late in the FHIT gene anomaly. (2) FHIT and p1 in lung cancer?