Journal
SCIENCE
Volume 362, Issue 6413, Pages 420-+Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.aav1898
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Funding
- National Cancer Institute, NIH [R35-CA209919, P50-HG007735]
- Parker Institute for Cancer Immunotherapy
- NIH [K99-AG059918]
- NIH Genomic Data Analysis Networks [1U24CA210974-01, 1U24CA210949-01, 1U24CA210978-01, 1U24CA210952-01, 1U24CA210989-01, 1U24CA210990-01, 1U24CA210950-01, 1U24CA210969-01, 1U24CA210988-01]
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We present the genome-wide chromatin accessibility profiles of 410 tumor samples spanning 23 cancer types from The Cancer Genome Atlas (TCGA). We identify 562,709 transposase-accessible DNA elements that substantially extend the compendium of known cis-regulatory elements. Integration of ATAC-seq (the assay for transposase-accessible chromatin using sequencing) with TCGA multi-omic data identifies a large number of putative distal enhancers that distinguish molecular subtypes of cancers, uncovers specific driving transcription factors via protein-DNA footprints, and nominates long-range gene-regulatory interactions in cancer. These data reveal genetic risk loci of cancer predisposition as active DNA regulatory elements in cancer, identify gene-regulatory interactions underlying cancer immune evasion, and pinpoint noncoding mutations that drive enhancer activation and may affect patient survival. These results suggest a systematic approach to understanding the noncoding genome in cancer to advance diagnosis and therapy.
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