The current study tests the hypothesis that chronic atrophic gastritis from hypochlorhydria in the gastrindeficient mouse predisposes the stomach to gastric cancer. Gross morphology and histology of 12-month-old wildtype (WT), gastrin-deficient (GÀ/À) and somatostatindeficient (SOMÀ/À) mice were examined. Parietal and G cells, Ki67, TUNEL, villin and MUC2 expression were analysed by immunohistochemistry. RUNX3 and STAT3 expression was analysed by Western blot. Anchorageindependent growth was determined by cell cluster formation in soft agar. Compared to the WT and SOMÀ/À mice, hypochlorhydric GÀ/À mice developed parietal cell atrophy, significant antral inflammation and intestinal metaplasia. Areas of metaplasia within the GÀ/ À mouse stomach showed decreased RUNX3 expression with elevated MUC2 and villin expression. Cells isolated from the tumor grew in soft agar. However, the cells isolated from WT, nontransformed GÀ/À and SOMÀ/À gastric tissue did not form colonies in soft agar. Consistent with elevated antral proliferation, tumor tissue isolated from the GÀ/À mice showed elevated phosphorylated STAT3 expression. We then examined the mechanism by which STAT3 was constitutively expressed in the tumor tissue of the GÀ/À mice. We found that IFNc expression was also significantly higher in the tumor tissue of GÀ/À mice compared to WT and SOMÀ/À animals. To determine whether STAT3 was regulated by IFNc, MKN45 cells were cocultured with IFNc or gastrin. IFNc significantly stimulated phosphorylation of STAT3 in the MKN45 cell line, but not gastrin. Therefore, we show here that in the hypochlorhydric mouse stomach, the chronic gastritis, atrophy, metaplasia, dysplasia paradigm can be recapitulated in mice. Moreover, neoplastic transformation of the antral gastric mucosa does not require gastrin.

Persistent colonic inflammation increases risk for cancer, but mucosal appearance on conventional endoscopy correlates poorly with histology. Here we demonstrate the use of a flexible silver halide fiber to collect mid-infrared absorption spectra and an interval model to distinguish colitis from normal mucosa in dextran sulfate sodium treated mice. The spectral regime between 950 and 1800 cm−1 was collected from excised colonic specimens and compared with histology. Our model identified 3 sub-ranges that optimize the classification results, and the performance for detecting inflammation resulted in a sensitivity, specificity, accuracy, and positive predictive value of 92%, 88%, 90%, and 88%, respectively.

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INTRODUCTION: Esophagitis dissecans superficialis (EDS) was first described in 1892. It is a rare and benign desquamative disorder characterized by sloughing of the esophageal mucosa. EDS has been linked to coronary artery disease, chronic kidney disease, autoimmune conditions (celiac disease and pemphigus vulgaris) and medications known to damage the gastrointestinal tract. However, most cases are idiopathic. CASE DESCRIPTION/METHODS: A 48-year-old male with a PMH of GERD presented to the Gastroenterology clinic with a 6-month history of esophageal dysphagia to solid foods. He denies any nausea, vomit, abdominal pain, hematemesis or episodes of melena. Esophagogram revealed delay of the barium tablet (Figure 1). The patient underwent an EGD showing sloughing of the mucosa in the entire esophagus along with LA grade C esophagitis (Figure 2). Biopsies were taken from the proximal and distal esophagus with findings compatible with esophagitis dissecans superficialis (Figure 3). Ranitidine and PPI were continued and he was scheduled for a follow appointment in 6 weeks. DISCUSSION: EDS is typically seen in middle aged women, and is commonly misdiagnosed due to the lack of diagnostic or histologic criteria. Endoscopic features consist of esophageal mucosa with multiple columns of strips that have whitish/pearly appearance andsloughs which are > 2 cm in length, and lack of ulcers in the surrounding mucosa. These findings can be mistaken with esophageal candidiasis, eosinophilic esophagitis, lichen planus and even squamous cell carcinoma. For this reason, the diagnosis is made through histopathologic findings such as parakeratosis and intraepithelial splitting above the basal layer. As in our patient, dysphagia is frequently reported, but nonspecific symptoms like nausea, vomiting or heartburn are also found. There are no specific treatment guidelines. Nevertheless, acid suppressants can be started to aid mucosa healing. Some patients can present with esophageal strictures, but this entity mainly follows a benign course as it shows self-resolution from 8 weeks to 4 months of diagnosis. This case shows the importance of recognizing EDS not only as an underreported cause for dysphagia, but also as an important differential diagnosis for esophageal diseases. It is important to obtain mucosal biopsies in order to get a proper diagnosis and avoid unnecessary treatments.