COMMENTARY

Oesophageal adenocarcinogenesis

Open questions in oesophageal adenocarcinogenesis

Carlo C Maley

Correspondence to:
Correspondence to:
Dr C C Maley
Molecular and Cellular Oncogenesis Program, The Wistar Institute, 3601 Spruce Street, Philadelphia, PA 19104, USA; cmaley@wistar.org

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Transition from GORD to Barrett’s oesophagus, and possibility of a reversal mechanism

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The first 150 words of the full text of this article appear below.

Barrett’s oesophagus develops as a complication of chronic gastro-oesophageal reflux disease (GORD), and is the only known precursor to oesophageal adenocarcinoma (EA). Barrett’s oesophagus is an ideal model for studying neoplastic progression, because it can be studied longitudinally in vivo, with protocols that allow for safe, reproducible sampling by endoscopy biopsies.¹ Furthermore, the major genetic events that characterise progression in Barrett’s oesophagus are some of the most common genetic events across human neoplasms, including inactivation of the tumour suppressor genes p16 (CDKN2A/INK4A)^2,3 and p53 (TP53),^4,5 with the subsequent development of tetraploidy and aneuploidy.^6,7,8,9,10

There are important open questions at all stages of progression from GORD to EA. Little is known about the transition from GORD to Barrett’s oesophagus. What is the cell of origin for Barrett’s oesophagus? And why do only a minority of patients with GORD undergo that transition? The presence of p16, p53 and ploidy lesions . . . [Full text of this article]

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• Fitzgerald, R. C (2008). Dissecting out the genetic origins of Barrett's oesophagus. Gut 57: 1033-1034 [Full Text]