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Dis Esophagus. 2003;16(3):214-7.

K-ras codon 12 mutations of the super-minute dysplasia in Barrett's esophagus by DNA extraction using a microdissection method.

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The Department of Pathology, Juntendo Izunagaoka Hospital of Juntendo University School of Medicine, Kawagoe, Japan.


The aim of this study was to clarify the histogenesis of Barrett's cancer. First, 28 lesions of the super-minute dysplasia <or= 1 mm in diameter were detected by pathological examinations for Barrett's esophagus. Secondly, the K-ras codon 12 mutations in these super-minute neoplasias of the Barrett's esophagus were examined by DNA extraction using a microdissection. It was found that seven of 28 (25%) super-minute dysplasia lesions in the Barrett's esophagus showed K-ras mutation, and were a single mutation, with AGT being detected in three lesions and GAT being detected in four lesions. Also, these dysplasia lesions could be divided into two groups according to p53-LI. Two among three lesions with p53-LI over 90%, which were considered to be morphologically high grade dysplasia or intramucosal adenocarcinoma, showed K-ras mutations (both lesions: GGT-->AGT), and 5 among 25 lesions with an average p53-LI of 58%, which were considered to be morphologically low grade dysplasia, showed K-ras mutation (four lesions: GGT-->GAT, 1 lesion: GGT-->AGT). This current study shows that some dysplasia lesions have K-ras mutations in their initial condition, whether these atypical tubule lesions are low grade dysplasia or high grade dysplasia (intramucosal adenocarcinoma), and supports the dysplasia-carcinoma sequence in the histogenesis of Barrett's cancer and synchronously suggests that there is a different route to it.

[Indexed for MEDLINE]

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