ArticleNucleic acids research2011
Distinct patterns of somatic alterations in a lymphoblastoid and a tumor genome derived from the same individual.
Article in Nucleic acids research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 52 citations in OpenAlex.
- SQUID: transcriptomic structural variation detection from RNA-seq.Genome biology · 2018Article
- Identifying structural variants using linked-read sequencing data.Bioinformatics (Oxford, England) · 2018Article
- Genetic Alterations of TRAF Proteins in Human Cancers.Frontiers in immunology · 2018Review
- Protein domain-level landscape of cancer-type-specific somatic mutations.PLoS computational biology · 2015Article
- Alternative polyadenylation allows differential negative feedback of human miRNA miR-579 on its host gene ZFR.PloS one · 2015Article
- Mutation Screening of 1,237 Cancer Genes across Six Model Cell Lines of Basal-Like Breast Cancer.PloS one · 2015Article
- Modulation of HJURP (Holliday Junction-Recognizing Protein) levels is correlated with glioblastoma cells survival.PloS one · 2013Article
- Gene copy-number polymorphism caused by retrotransposition in humans.PLoS genetics · 2013Article
- nFuse: discovery of complex genomic rearrangements in cancer using high-throughput sequencing.Genome research · 2012Article
- Methods, challenges, and promise of next-generation sequencing in cancer biology.The Yale journal of biology and medicine · 2011Review
- Distribution of copy number variations and rearrangement endpoints in human cancers with a review of literature.Mutation researchReview
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Authors and funding
32 authors at 3 institutions in 1 country.
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Abstract
Although patterns of somatic alterations have been reported for tumor genomes, little is known on how they compare with alterations present in non-tumor genomes. A comparison of the two would be crucial to better characterize the genetic alterations driving tumorigenesis. We sequenced the genomes of a lymphoblastoid (HCC1954BL) and a breast tumor (HCC1954) cell line derived from the same patient and compared the somatic alterations present in both. The lymphoblastoid genome presents a comparable number and similar spectrum of nucleotide substitutions to that found in the tumor genome. However, a significant difference in the ratio of non-synonymous to synonymous substitutions was observed between both genomes (P = 0.031). Protein-protein interaction analysis revealed that mutations in the tumor genome preferentially affect hub-genes (P = 0.0017) and are co-selected to present synergistic functions (P < 0.0001). KEGG analysis showed that in the tumor genome most mutated genes were organized into signaling pathways related to tumorigenesis. No such organization or synergy was observed in the lymphoblastoid genome. Our results indicate that endogenous mutagens and replication errors can generate the overall number of mutations required to drive tumorigenesis and that it is the combination rather than the frequency of mutations that is crucial to complete tumorigenic transformation.
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