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Whole-genome sequencing reveals novel tandem-duplication hotspots and a prognostic mutational signature in gastric cancer.

Abstract：

:Genome-wide analysis of genomic signatures might reveal novel mechanisms for gastric cancer (GC) tumorigenesis. Here, we analysis structural variations (SVs) and mutational signatures via whole-genome sequencing of 168 GCs. Our data demonstrates diverse models of complex SVs operative in GC, which lead to high-level amplification of oncogenes. We find varying proportion of tandem-duplications (TDs) among individuals and identify 24 TD hotspots involving well-established cancer genes such as CCND1, ERBB2 and MYC. Specifically, we nominate a novel hotspot involving the super-enhancer of ZFP36L2 presents in approximately 10% GCs from different cohorts, the oncogenic role of which is further confirmed by experimental data. In addition, our data reveal a mutational signature, specifically occurring in noncoding region, significantly enriched in tumors with cadherin 1 mutations, and associated with poor prognoses. Collectively, our data suggest that TDs might serve as an important mechanism for cancer gene activation and provide a novel signature for stratification.

journal_name

Nat Commun

journal_title

Nature communications

authors

Xing R,Zhou Y,Yu J,Yu Y,Nie Y,Luo W,Yang C,Xiong T,Wu WKK,Li Z,Bing Y,Lin S,Zhang Y,Hu Y,Li L,Han L,Yang C,Huang S,Huang S,Zhou R,Li J,Wu K,Fan D,Tang G,Dou J,Zhu Z,Ji J,Fang X,Lu Y

doi

10.1038/s41467-019-09644-6

subject

Has Abstract

pub_date

2019-05-02 00:00:00

pages

2037

issue

1

issn

2041-1723

pii

10.1038/s41467-019-09644-6

journal_volume

10

pub_type

杂志文章

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