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Background  Intratumor heterogeneity has been demonstrated in several cancer types, following a model of branched evolution. It is unknown to which extent intratumor heterogeneity is applicable to esophageal adenocarcinoma. Therefore the aim of this study was to characterise intratumor heterogeneity in esophageal adenocarcinoma.    Methods  Multiregional targeted sequencing of four commonly altered genes was performed on 19 tumor regions collected from five esophageal adenocarcinomas. Alterations were classified as homogeneous or heterogeneous based on mutational and loss of heterozygosity analysis.    Results  Identical  TP53  mutations and homogeneously loss of heterozygosity of the  TP53  locus were identified in all separated tumor regions in each of five adenocarcinomas, and in the corresponding Barrett’s esophagus and tumor positive lymph node of one primary tumor. Loss of heterozygosity of the  P16  locus was homogeneous among all tumor regions in four adenocarcinomas, and an identical pattern of loss of heterozygosity was present in the Barrett’s esophagus. Loss of heterozygosity of the  SMAD4  and  APC  loci was observed in a heterogeneous pattern.    Conclusions  Known driver alterations, such as  TP53  and  P16  are homogeneously present within each adenocarcinoma, and therefore occur early during carcinogenesis and subsequently clonally expand throughout the entire tumor. However, loss of heterozygosity of the  SMAD4  and  APC  loci shows a heterogeneous pattern, indicating intratumor heterogeneity of esophageal adenocarcinoma.

Molecular clonality analysis of esophageal adenocarcinoma by multiregion sequencing of tumor samples