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Although slow transit constipation (STC) may not be a congenital disease, the frequent onset in adolescence and strong female predominance suggest that STC could be a result of a sex modified multifactorial disorder of the gastrointestinal tract with a genetic basis. Several genes such as RET proto-oncogene and the neurturin gene have been analysed in STC. Unfortunately, few mutations were found to be associated with STC.1,2 Our previous studies described a decrease in volume in interstitial cells of Cajal (ICC) in patients with STC, and downregulation of c-kit mRNA and c-kit protein expression in the colonic tissues of STC patients.3,4 At present, we do not know why ICCs are lost from colonic tissues of patients with STC. Evidence suggests that the c-kit/SCF signal pathway plays a crucial role in ICC development and maintenance …
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Conflict of interest: None declared.