作者: Matthias Raggi , Rupert Langer , Markus Feith , Helmut Friess , Matthias Schauer
DOI: 10.1007/S00423-010-0607-4
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摘要: Introduction For the better understanding of pathophysiological events occurring in sequence inflammation–metaplasia–carcinoma esophageal adenocarcinoma, an animal model would be desirable. In past, several rat models have been used yielding conflicting results. Some demonstrated a similar to human situation whereas others failed initiate true adenocarcinoma or even Barrett’s metaplasia. For study molecular involved carcinogenesis carcinoma, mouse much more promising since most genetically altered animals are mice. However, as now no such exists, past predominately due high mortality with surgical procedure create mixed duodenogastric reflux.