This article discusses the molecular basis of esophageal cancer development and subsequent progression of disease. Differing epidemiologic factors are associated with esophageal adenocarcinoma and squamous cell carcinoma. These 2 different histologic types have differing putative underlying mechanisms of transdifferentiation from normal esophageal mucosa to malignant histologies via gene dysregulation, biochemical modifications, and altered cell signaling pathways. Our developing understanding of the molecular events underlying esophageal cancer is leading to the establishment of identifiable biomarkers and the clinical use of molecularly targeted treatment agents. The identification of driving genetic mutations and altered signaling pathways has also had favorable outcomes.
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