ArticleGenome research2013
Somatic rearrangements across cancer reveal classes of samples with distinct patterns of DNA breakage and rearrangement-induced hypermutability.
Article in Genome research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers, 1 of them a synthesis that pooled it.
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Who cites it
94 citing papers in PubMed, 1 synthesis or guideline pooled it.
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- Double-strand break repair-associated intragenic deletions and tandem duplications suggest the architecture of the repair replication fork.bioRxiv : the preprint server for biology · 2023Article
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- Tangent normalization for somatic copy-number inference in cancer genome analysis.Bioinformatics (Oxford, England) · 2022Article
- Evolution of the ancestral mammalian karyotype and syntenic regions.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Somatic structural variant formation is guided by and influences genome architecture.Genome research · 2022Article
- Implementation of a prostate cancer-specific targeted sequencing panel for credentialing of patient-derived cell lines and genomic characterization of patient samples.The Prostate · 2022Article
- Current status of structural variation studies in plants.Plant biotechnology journal · 2021Review
- CloneSig can jointly infer intra-tumor heterogeneity and mutational signature activity in bulk tumor sequencing data.Nature communications · 2021Article
34 more citing papers are in PubMed but not listed here.
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9 authors.
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Abstract
Whole-genome sequencing using massively parallel sequencing technologies enables accurate detection of somatic rearrangements in cancer. Pinpointing large numbers of rearrangement breakpoints to base-pair resolution allows analysis of rearrangement microhomology and genomic location for every sample. Here we analyze 95 tumor genome sequences from breast, head and neck, colorectal, and prostate carcinomas, and from melanoma, multiple myeloma, and chronic lymphocytic leukemia. We discover three genomic factors that are significantly correlated with the distribution of rearrangements: replication time, transcription rate, and GC content. The correlation is complex, and different patterns are observed between tumor types, within tumor types, and even between different types of rearrangements. Mutations in the APC gene correlate with and, hence, potentially contribute to DNA breakage in late-replicating, low %GC, untranscribed regions of the genome. We show that somatic rearrangements display less microhomology than germline rearrangements, and that breakpoint loci are correlated with local hypermutability with a particular enrichment for transversions.
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