Cancer cells are shaped through an evolutionary process of DNA mutation, cell selection and population expansion. Early steps in this process are driven by a set of mutated driver genes and structural alterations to the genome through copy number gains or losses. Oesophageal adenocarcinoma (EAC) and the pre-invasive tissue, Barrett’s oesophagus (BE), provide an ideal example in which to observe and study this evolution. BE displays early genomic instability, specifically in copy number changes that may later be observed in EAC. Furthermore, these early changes result in patterns of progression (that is, ‘born bad’, gradual or catastrophic) that may help to describe the evolution of EAC. As only a small proportion of patients with BE will go on to develop cancer, a better understanding of these patterns and the resulting genomic changes should improve early detection in EAC and may provide clues for the evolution of cancer more broadly.

癌细胞是通过 DNA 突变、细胞选择和种群扩张的进化过程形成的。这个过程的早期步骤是由一组突变的驱动基因和通过拷贝数增加或减少对基因组的结构改变驱动的。食管腺癌 (EAC) 和浸润前组织巴雷特食管 (BE) 为观察和研究这种演变提供了一个理想的例子。BE 表现出早期基因组不稳定性，特别是在稍后可能在 EAC 中观察到的拷贝数变化中。此外，这些早期变化导致的进展模式（即“天生坏”、渐进或灾难性）可能有助于描述 EAC 的演变。由于只有一小部分 BE 患者会继续发展为癌症，