Insights Into the Pathophysiology of Esophageal Adenocarcinoma

Gastroenterology. 2018 Jan;154(2):406-420. doi: 10.1053/j.gastro.2017.09.046. Epub 2017 Oct 14.

Abstract

Although researchers have identified genetic alterations that contribute to development of esophageal adenocarcinoma, we know little about features of patients or environmental factors that mediate progression of chronic acid biliary reflux to Barrett's esophagus and cancer. Increasing our understanding of the mechanisms by which normal squamous epithelium progresses to early-stage invasive cancer will help formulate rational surveillance guidelines and allow us to divest resources away from patients at low risk of malignancy. We review the cellular and genetic alterations that occur during progression of Barrett's esophagus, based on findings from clinical studies and mouse models of disease. We review the features of the luminal and mucosal microenvironment of Barrett's esophagus that promote, in a small proportion of patients, development of esophageal adenocarcinoma. Markers of clonal evolution can be used to determine patient risk for cancer and set surveillance intervals.

Keywords: BE; Biomarker; EAC; Metaplasia.

Publication types

  • Review

MeSH terms

  • Adenocarcinoma / epidemiology
  • Adenocarcinoma / etiology*
  • Adenocarcinoma / pathology
  • Animals
  • Barrett Esophagus / etiology*
  • Barrett Esophagus / pathology
  • Carcinogenesis / pathology*
  • Cell Transformation, Neoplastic / pathology
  • Disease Models, Animal
  • Disease Progression
  • Environmental Exposure / adverse effects
  • Esophageal Mucosa / pathology
  • Esophageal Neoplasms / epidemiology
  • Esophageal Neoplasms / etiology*
  • Esophageal Neoplasms / pathology
  • Gastroesophageal Reflux / etiology*
  • Gastroesophageal Reflux / pathology
  • Gastrointestinal Microbiome
  • Genes, Tumor Suppressor
  • Helicobacter Infections / epidemiology
  • Helicobacter Infections / microbiology
  • Humans
  • Incidence
  • Interleukins / metabolism
  • Mice
  • Mucins / metabolism
  • Tumor Microenvironment*

Substances

  • Interleukins
  • Mucins

Supplementary concepts

  • Adenocarcinoma Of Esophagus