Chronic acid-biliary reflux and Helicobacter pylori infection are instrumental environmental drivers of cancer initiation and progression in the upper gastrointestinal tract. Remarkably, although these environmental carcinogens are quite dissimilar, the tumour progression cascade these carcinogens engender is highly comparable. For this reason, studies of malignant progression occurring at the anatomic borderland between the oesophagus and the stomach have traditionally lumped junctional adenocarcinomas with either oesophageal adenocarcinoma or gastric adenocarcinoma. Whilst studies have revealed remarkable epidemiological and genetic similarities of these cancers and their associated premalignant conditions, these works have also revealed some key differences. This highlights that further scientific effort demands a dedicated focus on the understanding of the cell-cell interaction between the epithelium and the local microenvironment in this anatomic region. We here review available evidence with regards to tumour progression occurring at the gastro-oesophageal junction and contrast it with available data on cancer evolution in the metaplastic oesophagus and distal stomach.

慢性胆汁反流和幽门螺杆菌感染是癌症在上消化道中发生和发展的重要环境驱动因素。值得注意的是，尽管这些环境致癌物完全不同，但这些致癌物引起的肿瘤级联反应却具有高度的可比性。由于这个原因，在食道和胃之间的解剖边界发生恶性进展的研究通常具有结节性结节性腺癌，并伴有食道腺癌或胃腺癌。尽管研究表明这些癌症及其相关的恶变前状况在流行病学和遗传学上有惊人的相似性，但这些工作也揭示了一些关键的差异。这突显了进一步的科学努力需要专注于了解该解剖区域中上皮与局部微环境之间的细胞间相互作用。我们在这里回顾有关胃食管连接处发生的肿瘤进展的可用证据，并将其与化生食道和胃远端癌变的可用数据进行对比。