Department of Surgery, University of Miami, Miami, FL, United States of America.
Department of Clinical Pathology, University of Miami, Miami, FL, United States of America.
Biochim Biophys Acta Rev Cancer. 2019 Aug;1872(1):37-48. doi: 10.1016/j.bbcan.2019.05.003. Epub 2019 May 30.
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）在美国和许多其他西方国家的发病率上升速度最快之一。EAC 的一个独特危险因素是胃食管反流病（GERD），这是一种慢性消化疾病，胃酸和十二指肠胆汁经常混合进入食管，导致食管组织损伤。在细胞水平上，反流和慢性炎症因子导致的持续 DNA 损伤增加了突变率，促进了基因组不稳定，这是 EAC 进展的基础。尽管在癌症诊断和治疗方面最近取得了成功，但 EAC 仍然是一种难以治疗的疾病。最近的研究揭示了 EAC 进展的分子改变，并揭示了新的治疗选择。这篇综述聚焦于 EAC 的遗传和分子研究。还讨论了正常 Barrett 食管向食管腺癌转化过程中发生的分子变化。
