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| The first 150 words of the full text of this article appear below. |
Oesophageal adenocarcinoma arises from columnar epithelium called Barrett’s epithelium. The molecular events underlying the metaplasia–dysplasia–adenocarcinoma sequence remain poorly defined, although they are of obvious diagnostic, therapeutic and prognostic importance. One signalling pathway that is often disturbed in gastrointestinal malignancy is the transforming growth factor-ß (TGF-ß) pathway, but its role in Barrett’s epithelium is not understood. TGF-ß is a cytokine that binds cell surface receptors, leading to phosphorylation of intracellular signalling molecules called Smad, which translocate to the nucleus and activate a gene programme. Here it is demonstrated that Smad4 is frequently inactivated by methylation, deletion or protein modification. This prevents TGF-ß suppressing the proliferation of oesophageal epithelial cells.
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H pylori outer membrane proteins (OMPs), which are though to be important for bacterial adherence, are variably expressed in different strains. Previous studies examining genomic variation have yielded
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