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在肿瘤的形成和发展过程中往往伴随着染色体的缺失,染色体缺失机制可能与脆性位点有关。脆性组氨酸三联体(FHIT)基因于1996年被Ohta等[1]用定位克隆技术及外显子捕获法确定。大量相关文献表明,在多种原发恶性肿瘤以及肿瘤细胞株中存在FHIT基因表达异常,在食管癌早期即可出现FHIT基因异常变异率增高,提示FHIT基因与食管癌的发生发展有密切关系。现就FHIT基因与食管癌关系研究进展综述如下。
In the process of tumor formation and development are often accompanied by the lack of chromosomes, chromosomal deletion may be related to the fragile sites. The fragile histidine triad (FHIT) gene was identified by Ohta et al. [1] in 1996 using both positional cloning and exon capture. A large number of relevant literatures show that there are abnormal expression of FHIT gene in many kinds of primary malignant tumors and tumor cell lines, and the abnormal mutation rate of FHIT gene may appear in the early stage of esophageal cancer, suggesting that FHIT gene is closely related to the occurrence and development of esophageal cancer. Now on the FHIT gene and esophageal cancer research progress are summarized below.