Discussion
Further understanding of the commonalities and differences governing the development of upper GI tract intestinal metaplasias and their progression to cancer will lead to improved diagnostic and therapeutic avenues.
Methods
Here, we utilize an upper GI tract patient-derived tissue microarray that encompasses the sequential development of cancer from normal tissues to illustrate the expression of a set of metaplastic markers.
Results
We report that in contrast to gastric intestinal metaplasia, which has traits of both incomplete and complete intestinal metaplasia, Barrett's esophagus (i.e., esophageal intestinal metaplasia) demonstrates hallmarks of incomplete intestinal metaplasia. Specifically, this prevalent incomplete intestinal metaplasia seen in Barrett's esophagus manifests as concurrent development and expression of both gastric and intestinal traits. Additionally, many gastric and esophageal cancers display a loss of or a decrease in these characteristic differentiated cell properties, demonstrating the plasticity of molecular pathways associated with the development of these cancers.