Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
5658743 | Gastroenterology | 2017 | 49 Pages |
Abstract
In mice, fucosylation deficiency leads to colitis and adenocarcinoma, loss of Notch activation, and down-regulation of Hes1. HES1 loss correlates with the development of human right-sided colorectal tumors with epigenetic loss of MLH1. These findings indicate that carcinogenesis in a subset of colon cancer is consequent to a molecular mechanism driven by fucosylation deficiency and/or HES1-loss.
Keywords
RT-PCRTNFGZMBGranzyme BMLH1GMDSAALIBDSSLSSAmRNAFITCMutL homolog 1messenger RNASessile serrated adenomaAleuria aurantia lectininterferonIFNinterleukinInflammatory bowel diseaseGDPTumorigenesisColorectal cancerColon cancertumor necrosis factorfluorescein isothiocyanateMetabolismwild typeSignal transductionreverse-transcription polymerase chain reactionCRCguanosine diphosphate
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Authors
Yiwei Wang, Dan Huang, Kai-Yuan Chen, Min Cui, Weihuan Wang, Xiaoran Huang, Amad Awadellah, Qing Li, Ann Friedman, William W. Xin, Luca Di Martino, Fabio Cominelli, Alex Miron, Ricky Chan, James G. Fox, Yan Xu, Xiling Shen, Mathew F. Kalady, Lan Zhou,