Paired exome analysis of Barrett's esophagus and adenocarcinoma View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2015-09

AUTHORS

Matthew D Stachler, Amaro Taylor-Weiner, Shouyong Peng, Aaron McKenna, Agoston T Agoston, Robert D Odze, Jon M Davison, Katie S Nason, Massimo Loda, Ignaty Leshchiner, Chip Stewart, Petar Stojanov, Sara Seepo, Michael S Lawrence, Daysha Ferrer-Torres, Jules Lin, Andrew C Chang, Stacey B Gabriel, Eric S Lander, David G Beer, Gad Getz, Scott L Carter, Adam J Bass

ABSTRACT

Barrett's esophagus is thought to progress to esophageal adenocarcinoma (EAC) through a stepwise progression with loss of CDKN2A followed by TP53 inactivation and aneuploidy. Here we present whole-exome sequencing from 25 pairs of EAC and Barrett's esophagus and from 5 patients whose Barrett's esophagus and tumor were extensively sampled. Our analysis showed that oncogene amplification typically occurred as a late event and that TP53 mutations often occurred early in Barrett's esophagus progression, including in non-dysplastic epithelium. Reanalysis of additional EAC exome data showed that the majority (62.5%) of EACs emerged following genome doubling and that tumors with genomic doubling had different patterns of genomic alterations, with more frequent oncogenic amplification and less frequent inactivation of tumor suppressors, including CDKN2A. These data suggest that many EACs emerge not through the gradual accumulation of tumor-suppressor alterations but rather through a more direct path whereby a TP53-mutant cell undergoes genome doubling, followed by the acquisition of oncogenic amplifications. More... »

PAGES

1047-1055

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/ng.3343

    DOI

    http://dx.doi.org/10.1038/ng.3343

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1019888748

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/26192918


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