The incidence of esophageal adenocarcinoma has increased dramatically in the United States and Europe since the 1970s without apparent cause. Although specific host factors can affect risk of disease, such a rapid increase in incidence must be predominantly environmental. In the stomach, infection with Helicobacter pylori has been linked to chronic atrophic gastritis, an inflammatory precursor of gastric adenocarcinoma. However, the role of H. pylori in the development of esophageal adenocarcinoma is not well established. Meanwhile, several studies have established that a complex microbiome in the distal esophagus might play a more direct role. Transformation of the microbiome in precursor states to esophageal adenocarcinoma—reflux esophagitis and Barrett metaplasia—from a predominance of gram-positive bacteria to mostly gram-negative bacteria raises the possibility that dysbiosis is contributing to pathogenesis. However, knowledge of the microbiome in esophageal adenocarcinoma itself is lacking. Microbiome studies open a new avenue to the understanding of the etiology and pathogenesis of reflux disorders.
From the *Department of Medicine, New York University School of Medicine, New York, NY; and †Department of Veterans Affairs New York Harbor Healthcare System, New York, NY 10010; Departments of Medicine and Pathology, New York University School of Medicine, New York, NY.
This work was supported in part by grants U01CA18237, UH3CA140233, R03CA159414, and R01CA159036 from the National Cancer Institute and NIH Human Microbiome Project and by the Department of Veterans Affairs, Veterans Health Administration, Office of Research and Development.
The authors report no conflict of interest.
Reprints: Zhiheng Pei, MD, PhD, FASCP, Departments of Medicine and Pathology, New York University School of Medicine, 423 East 23rd Street, Room 6001W, New York, NY 10010. E-mail: email@example.com.