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A histological study has helped our understanding of gastric cancer by showing that changes in the mesenchyme occur in tandem with those of the gastric epithelium in the progression to cancer.
The mesenchymal sheath—called the pericryptal fibroblast sheath (PCFS)—underlies the epithelium and is closely associated with it, enveloping the normal intestine. Together the epithelium and PCFS act as a unit whose cell turnover seems to be regulated in parallel to ensure normal structure, maintenance, and function of the crypts of Lieberkühn.
This arrangement was found to be confined to gastrointestinal metaplasia in the stomach of humans and the Cdx2 transgenic mouse but did not appear in human intestinal-type gastric adenocarcinoma, nor normal human or mouse gastric mucosa, stained histochemically for α-smooth muscle actin to locate PCFS. It was present in normal human and Cdx2 mouse large and small intestinal mucosa.
The precursors to human intestinal-type gastric cancer are gastric atrophy and transformation of normal gastric mucosa to intestinal metaplasia, mainly owing to chronic gastric infection with Helicobacter pylori. Human gastric intestinal metaplastic cells express Cdx2—a transcription factor specific to intestinal cells. Transgenic Cdx2 mice have gastric metaplasia throughout their stomachs and are therefore a suitable model for this form of human cancer.
Until now, changes in only gastric epithelial cells had been reported, and it was useful to know whether these changes also affected the mesenchymal sheath.