Esophageal adenocarcinoma (EAC) has one of the fastest rising incidence rates in the U.S. and many other Western countries. One of the unique risk factors for EAC is gastroesophageal reflux disease (GERD), a chronic digestive condition in which acidic contents from the stomach, frequently mixed with duodenal bile, enter the esophagus resulting in esophageal tissue injury. At the cellular level, progression to EAC is underlined by continuous DNA damage caused by reflux and chronic inflammatory factors that increase the mutation rate and promote genomic instability. Despite recent successes in cancer diagnostics and treatment, EAC remains a poorly treatable disease. Recent research has shed new light on molecular alterations underlying progression to EAC and revealed novel treatment options. This review focuses on the genetic and molecular studies of EAC. The molecular changes that occur during the transformation of normal Barrett’s esophagus to esophageal adenocarcinoma are also discussed.

食管腺癌（EAC）是美国和许多其他西方国家发病率上升最快的癌症之一。EAC 的独特危险因素之一是胃食管反流病 (GERD)，这是一种慢性消化系统疾病，胃中的酸性物质经常与十二指肠胆汁混合，进入食管，导致食管组织损伤。在细胞水平上，反流和慢性炎症因素引起的持续 DNA 损伤强调了 EAC 的进展，这些损伤增加了突变率并促进基因组不稳定。尽管最近在癌症诊断和治疗方面取得了成功，但 EAC 仍然是一种难以治疗的疾病。最近的研究为 EAC 进展的分子改变提供了新的线索，并揭示了新的治疗方案。本综述重点关注 EAC 的遗传和分子研究。还讨论了正常巴雷特食管向食管腺癌转化过程中发生的分子变化。