肠化生作为胃癌的癌前病变,其病理过程并未完全阐明。新近研究表明,肠化生的发生涉及到了尾型同源盒转录因子1、尾型同源盒转录因子2、OCT-1及Erk通路成分的异位表达,以及胃特异性转录因子性别决定区Y框蛋白2、Sonichedgehog信号通路、RUNT相关转录因子3等抑癌基因的表达受抑。宿主生长因子、细胞因子、环氧合酶2等的表达增强也参与了肠化生的发生。本文就上述研究进展进行了综述。
Intestinal Metaplasia (IM) is generally considered to be the precancerous lesion of gastric cancer, however, its pathological process has yet to be clarified in detail. Recent investigations suggest that the molecular mechanisms of IM include the ectopic expressions of CDX1, CDX2, OCT-1 and members of the Erk signal pathway. Suppression of the expression of specific transcription factors such as SOX2, genes that are involved in the Sonic hedgehog signal pathway, and tumor suppressor genes such as RUNX3, could be additional relevant alterations. Host factors such as increased expression of growth factors, cytokines and COX-2 have been also reported to play roles in the development of IM. This review summarizes the above research developments