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The distinction between high grade dysplasia and intramucosal carcinoma is not easily made by expert pathologists, with little improvement even after agreeing on uniform criteria for the use of
The rapidly rising incidence of oesophageal adenocarcinoma in the Western world has stimulated considerable experimental and clinical research in recent years. After a long period of uncertainty, it is now generally held that the majority, if not all, of these cancers arise on a background of intestinal metaplasia (Barrett’s oesophagus), secondary to chronic gastro-oesophageal reflux. While there has been much debate on the risk of cancer development, it is again accepted that in a proportion of patients, this metaplastic epithelium becomes unstable, leading to a sequential progression through dysplasia to carcinoma. Considerable effort has gone into characterising the changes which seem to occur at the molecular level 1.
In this issue, Ormsby and colleagues2 suggest that it may be important to distinguish high grade dysplasia (HGD) from intramucosal carcinoma (IMC) in order to reach a decision about endoscopic surveillance and how this might influence the nature and timing of subsequent therapy [see page 671]. They show that the distinction between HGD and IMC is not easily …
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- Gastrointestinal cancer