Cardiac mucosa, Barrett's oesophagus and cancer of the gastro-oesophageal junction: what's in a name?

The pathogenesis of adenocarcinoma of the oesophagus is assumed to start with GORD that damages the oesophageal squamous epithelium while also inducing genetic reprogramming of progenitor cells that proliferate to repair the damage.1 Presumably, this GORD-induced reprogramming of developmental transcription factors causes the progenitors to differentiate into columnar cells with intestinal features, resulting in the squamous-to-columnar metaplasia of Barrett's oesophagus. Barrett's metaplasia, in an environment of oxidative and nitrosative stress from ongoing GORD, is predisposed to develop further genetic alterations resulting in dysplasia and, ultimately, cancer. Thus, oesophageal adenocarcinoma is widely regarded as a consequence of GORD and Barrett's oesophagus in most, if not all cases.

A number of observations have been difficult to reconcile with this popular concept of oesophageal carcinogenesis. Most notably, many patients with oesophageal adenocarcinoma have no evidence of antecedent GORD or Barrett's metaplasia.23 Rather than abandoning the...

http://ift.tt/2u56moJ