High-coverage whole-genome analysis of 1220 cancers reveals hundreds of genes deregulated by rearrangement-mediated cis-regulatory alterations.

TitleHigh-coverage whole-genome analysis of 1220 cancers reveals hundreds of genes deregulated by rearrangement-mediated cis-regulatory alterations.
Publication TypeJournal Article
Year of Publication2020
AuthorsZhang, Y, Chen, F, Fonseca, NA, He, Y, Fujita, M, Nakagawa, H, Zhang, Z, Brazma, A, Creighton, CJ
Corporate AuthorsPCAWG Transcriptome Working Group, PCAWG Structural Variation Working Group, PCAWG Consortium
JournalNat Commun
Volume11
Issue1
Pagination736
Date Published2020 Feb 05
ISSN2041-1723
KeywordsDatabases, Genetic, DNA Methylation, Enhancer Elements, Genetic, Gene Expression Regulation, Neoplastic, Genes, Tumor Suppressor, Genomic Structural Variation, Humans, Neoplasms, Oncogenes, Regulatory Sequences, Nucleic Acid, Whole Genome Sequencing
Abstract

The impact of somatic structural variants (SVs) on gene expression in cancer is largely unknown. Here, as part of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium, which aggregated whole-genome sequencing data and RNA sequencing from a common set of 1220 cancer cases, we report hundreds of genes for which the presence within 100 kb of an SV breakpoint associates with altered expression. For the majority of these genes, expression increases rather than decreases with corresponding breakpoint events. Up-regulated cancer-associated genes impacted by this phenomenon include TERT, MDM2, CDK4, ERBB2, CD274, PDCD1LG2, and IGF2. TERT-associated breakpoints involve ~3% of cases, most frequently in liver biliary, melanoma, sarcoma, stomach, and kidney cancers. SVs associated with up-regulation of PD1 and PDL1 genes involve ~1% of non-amplified cases. For many genes, SVs are significantly associated with increased numbers or greater proximity of enhancer regulatory elements near the gene. DNA methylation near the promoter is often increased with nearby SV breakpoint, which may involve inactivation of repressor elements.

DOI10.1038/s41467-019-13885-w
Alternate JournalNat Commun
PubMed ID32024823
PubMed Central IDPMC7002524
Grant ListP30 CA016672 / CA / NCI NIH HHS / United States
P30 CA125123 / CA / NCI NIH HHS / United States
R01 CA218112 / CA / NCI NIH HHS / United States
R35 GM127029 / GM / NIGMS NIH HHS / United States

Similar Publications