Published online Jul 28, 2017. doi: 10.3748/wjg.v23.i28.5115
Peer-review started: February 8, 2017
First decision: March 16, 2017
Revised: March 31, 2017
Accepted: May 9, 2017
Article in press: May 9, 2017
Published online: July 28, 2017
Processing time: 172 Days and 2.6 Hours
To assess dietary myo-inositol in reducing stem cell activation in colitis, and validate pβ-cateninS552 as a biomarker of recurrent dysplasia.
We examined the effects of dietary myo-inositol treatment on inflammation, pβ-cateninS552 and pAkt levels by histology and western blot in IL-10-/- and dextran sodium sulfate-treated colitic mice. Additionally, we assessed nuclear pβ-cateninS552 in patients treated with myo-inositol in a clinical trial, and in patients with and without a history of colitis-induced dysplasia.
In mice, pβ-cateninS552 staining faithfully reported the effects of myo-inositol in reducing inflammation and intestinal stem cell activation. In a pilot clinical trial of myo-inositol administration in patients with a history of low grade dysplasia (LGD), two patients had reduced numbers of intestinal stem cell activation compared to the placebo control patient. In humans, pβ-cateninS552 staining discriminated ulcerative colitis patients with a history of LGD from those with benign disease.
Enumerating crypts with increased numbers of pβ-cateninS552 - positive cells can be utilized as a biomarker in colitis-associated cancer chemoprevention trials.
Core tip: We report that dietary myo-inositol reduced inflammation and intestinal stem cell activation in both genetic and chemically-induced mouse models of colitis. In a limited clinical trial of colitis patients with a history of recurrent low grade dysplasia (LGD), myo-inositol reduced the number of intestinal crypts with activated stem cells. This study demonstrated for the first time that nuclear pβ-cateninS552 staining discriminates between patients with inflammation and those with a history of LGD, suggesting that nuclear pβ-cateninS552 staining may reflect local expansions of activated stem cells with neoplastic potential. Based on these data, we propose a more extensive clinical trial.