EMR is useful in the management of type 1 gastric carcinoids as classified by Rindi (hypergastrinemia; tumor diameter of 10 mm or less).

In patients with m3 or sm1 SEC, tumors that have lymphatic invasion, larger superficial size, and wider LMM invasion are associated with a high risk for lymph-node metastasis. EMR might be indicated for the treatment of patients with m3 or sm1 SECs without these characteristics.

Background and Aims: The frequency of benign stenosis in ulcerative colitis (UC) is low, reported as being 3.2–11.2%, with fibrosis in the submucosa or deeper pointed out as one of the causes. The aim of the present study was to assess stenosis in UC cases using immunostaining and to analyze differences between stenotic and nonstenotic cases, focusing on basic-fibroblast growth factor (b-FGF) expression and myofibroblasts. Methods: Totals of 9 stenotic and 17 nonstenotic UC cases were histopathologically examined and immunohistochemically stained for b-FGF, α-smooth muscle actin (α-SMA), CD34, CD68 and IL-6. To identify b-FGF-positive cells, double immunostaining for b-FGF and myeloperoxidase or CD68 was performed. Results: In addition to submucosal fibrosis, a significant increase of b-FGF-positive inflammatory cells and myofibroblasts was observed in stenotic portions. Most b-FGF-positive cells were also positive for myeloperoxidase, and a correlation between b-FGF-positive and total neutrophil counts was found. Conclusions: One of the major causes of stenosis in long-standing UC is fibrosis in the bowel wall, possibly induced by infiltrating inflammatory neutrophils producing b-FGF.