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The Origins and Consequences of Localized and Global Somatic Hypermutation

https://doi.org/10.1101/287839
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What this work says

Outgoing claims: the papers this work cites, builds on, or argues with.

inferredcites →https://doi.org/10.1002/gcc.2870080102openalex-snapshot
Preferential clustering of chromosomal breakpoints in Burkitt's lymphomas and L3 type acute lymphoblastic leukemias with a t(8;14) translocation
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Activation-induced cytidine deaminase (AID) linking immunity, chronic inflammation, and cancer
inferredcites →https://doi.org/10.1016/j.ccr.2014.07.014openalex-snapshot
The Somatic Genomic Landscape of Chromophobe Renal Cell Carcinoma
inferredcites →https://doi.org/10.1016/j.cell.2011.02.013openalex-snapshot
Hallmarks of Cancer: The Next Generation
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Mutational Processes Molding the Genomes of 21 Breast Cancers
inferredcites →https://doi.org/10.1016/j.cell.2012.06.024openalex-snapshot
A Landscape of Driver Mutations in Melanoma
inferredcites →https://doi.org/10.1016/j.cell.2014.06.049openalex-snapshot
Multiplatform Analysis of 12 Cancer Types Reveals Molecular Classification within and across Tissues of Origin
inferredcites →https://doi.org/10.1016/j.cell.2014.11.013openalex-snapshot
B Cell Super-Enhancers and Regulatory Clusters Recruit AID Tumorigenic Activity
inferredcites →https://doi.org/10.1016/j.cell.2015.12.050openalex-snapshot
Mutational Strand Asymmetries in Cancer Genomes Reveal Mechanisms of DNA Damage and Repair
inferredcites →https://doi.org/10.1016/j.celrep.2014.03.003openalex-snapshot
Recurrent Somatic Structural Variations Contribute to Tumorigenesis in Pediatric Osteosarcoma
inferredcites →https://doi.org/10.1016/j.celrep.2016.06.026openalex-snapshot
Kataegis Expression Signature in Breast Cancer Is Associated with Late Onset, Better Prognosis, and Higher HER2 Levels
inferredcites →https://doi.org/10.1016/j.compbiolchem.2014.08.012openalex-snapshot
Evidence of a cancer type-specific distribution for consecutive somatic mutation distances
inferredcites →https://doi.org/10.1016/j.dnarep.2014.11.006openalex-snapshot
AID expression in B-cell lymphomas causes accumulation of genomic uracil and a distinct AID mutational signature
inferredcites →https://doi.org/10.1016/j.jhep.2018.02.029openalex-snapshot
Spatial and temporal clonal evolution of intrahepatic cholangiocarcinoma
inferredcites →https://doi.org/10.1016/s0092-8674(00)81683-9openalex-snapshot
The Hallmarks of Cancer
inferredcites →https://doi.org/10.1016/s1470-2045(14)71021-6openalex-snapshot
Tumour genomic and microenvironmental heterogeneity for integrated prediction of 5-year biochemical recurrence of prostate cancer: a retrospective cohort study
inferredcites →https://doi.org/10.1038/nature05610openalex-snapshot
Patterns of somatic mutation in human cancer genomes
inferredcites →https://doi.org/10.1038/nature12213openalex-snapshot
Mutational heterogeneity in cancer and the search for new cancer-associated genes
inferredcites →https://doi.org/10.1038/nature12477openalex-snapshot
Signatures of mutational processes in human cancer
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Comprehensive molecular profiling of lung adenocarcinoma
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Comprehensive molecular characterization of gastric adenocarcinoma
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The evolutionary history of lethal metastatic prostate cancer
inferredcites →https://doi.org/10.1038/nature17661openalex-snapshot
Nucleotide excision repair is impaired by binding of transcription factors to DNA
inferredcites →https://doi.org/10.1038/nature20788openalex-snapshot
Genomic hallmarks of localized, non-indolent prostate cancer
inferredcites →https://doi.org/10.1038/nature23302openalex-snapshot
Role of stem-cell divisions in cancer risk
inferredcites →https://doi.org/10.1038/ncomms12605openalex-snapshot
Mutational signatures of ionizing radiation in second malignancies
inferredcites →https://doi.org/10.1038/ncomms3997openalex-snapshot
Heterogeneity of genomic evolution and mutational profiles in multiple myeloma
inferredcites →https://doi.org/10.1038/ng.2702openalex-snapshot
An APOBEC cytidine deaminase mutagenesis pattern is widespread in human cancers
inferredcites →https://doi.org/10.1038/ng.2762openalex-snapshot
Emerging landscape of oncogenic signatures across human cancers
inferredcites →https://doi.org/10.1038/ng.2764openalex-snapshot
The Cancer Genome Atlas Pan-Cancer analysis project
inferredcites →https://doi.org/10.1038/nmeth.1311openalex-snapshot
Amplification-free Illumina sequencing-library preparation facilitates improved mapping and assembly of (G+C)-biased genomes
inferredcites →https://doi.org/10.1038/nrc.2017.52openalex-snapshot
Fragile sites in cancer: more than meets the eye
inferredcites →https://doi.org/10.1038/sj.leu.2403661openalex-snapshot
Concurrent translocation of BCL2 and MYC with a single immunoglobulin locus in high-grade B-cell lymphomas
inferredcites →https://doi.org/10.1038/sj.leu.2404457openalex-snapshot
ERIC recommendations on IGHV gene mutational status analysis in chronic lymphocytic leukemia
inferredcites →https://doi.org/10.1038/sj.leu.2404529openalex-snapshot
Mapping of MYC breakpoints in 8q24 rearrangements involving non-immunoglobulin partners in B-cell lymphomas
inferredcites →https://doi.org/10.1056/nejmoa1113205openalex-snapshot
Intratumor Heterogeneity and Branched Evolution Revealed by Multiregion Sequencing
inferredcites →https://doi.org/10.1084/jem.20030802openalex-snapshot
The Balance Between Pax5 and Id2 Activities Is the Key to AID Gene Expression
inferredcites →https://doi.org/10.1084/jem.20070884openalex-snapshot
A role for AID in chromosome translocations between c-myc and the IgH variable region
inferredcites →https://doi.org/10.1093/jnci/djx033openalex-snapshot
Spatio-Temporal Genomic Heterogeneity, Phylogeny, and Metastatic Evolution in Salivary Adenoid Cystic Carcinoma
inferredcites →https://doi.org/10.1093/nar/gkr223openalex-snapshot
How does DNA break during chromosomal translocations?
inferredcites →https://doi.org/10.1093/nar/gkw199openalex-snapshot
g:Profiler—a web server for functional interpretation of gene lists (2016 update)
inferredcites →https://doi.org/10.1101/161562openalex-snapshot
The evolutionary history of 2,658 cancers
inferredcites →https://doi.org/10.1101/162784openalex-snapshot
Pan-cancer analysis of whole genomes
inferredcites →https://doi.org/10.1101/237313openalex-snapshot
Discovery and characterization of coding and non-coding driver mutations in more than 2,500 whole cancer genomes
inferredcites →https://doi.org/10.1101/322859openalex-snapshot
The Repertoire of Mutational Signatures in Human Cancer
inferredcites →https://doi.org/10.1101/gad.200014.112openalex-snapshot
Regulation of AID, the B-cell genome mutator
inferredcites →https://doi.org/10.1101/gr.141382.112openalex-snapshot
Somatic rearrangements across cancer reveal classes of samples with distinct patterns of DNA breakage and rearrangement-induced hypermutability
inferredcites →https://doi.org/10.1101/gr.161026.113openalex-snapshot
Genomic and transcriptomic plasticity in treatment-naïve ovarian cancer
inferredcites →https://doi.org/10.1126/science.1260825openalex-snapshot
Variation in cancer risk among tissues can be explained by the number of stem cell divisions
inferredcites →https://doi.org/10.1126/science.aaf9011openalex-snapshot
Stem cell divisions, somatic mutations, cancer etiology, and cancer prevention
inferredcites →https://doi.org/10.1182/blood.v94.6.1840openalex-snapshot
Ig V Gene Mutation Status and CD38 Expression As Novel Prognostic Indicators in Chronic Lymphocytic Leukemia
inferredcites →https://doi.org/10.1182/blood.v94.6.1848openalex-snapshot
Unmutated Ig VH Genes Are Associated With a More Aggressive Form of Chronic Lymphocytic Leukemia
inferredcites →https://doi.org/10.1186/1745-6150-7-47openalex-snapshot
AID/APOBEC cytosine deaminase induces genome-wide kataegis
inferredcites →https://doi.org/10.1186/gb-2011-12-2-r18openalex-snapshot
Analyzing and minimizing PCR amplification bias in Illumina sequencing libraries
inferredcites →https://doi.org/10.18632/oncotarget.653openalex-snapshot
Recurrent targets of aberrant somatic hypermutation in lymphoma
inferredcites →https://doi.org/10.3390/ijms130911974openalex-snapshot
Common Fragile Sites: Genomic Hotspots of DNA Damage and Carcinogenesis

What points at this work

Incoming claims: where this work appears in other papers’ reference lists and arguments.

inferred← citeshttps://doi.org/10.1016/j.ccell.2019.02.005openalex-snapshot
The Proteogenomic Landscape of Curable Prostate Cancer
inferred← citeshttps://doi.org/10.1038/s41467-019-14052-xopenalex-snapshot
Divergent mutational processes distinguish hypoxic and normoxic tumours
inferred← citeshttps://doi.org/10.1038/s41467-021-24812-3openalex-snapshot
The genomic landscape of 85 advanced neuroendocrine neoplasms reveals subtype-heterogeneity and potential therapeutic targets
inferred← citeshttps://doi.org/10.1038/s41467-023-38891-xopenalex-snapshot
Multi-omic features of oesophageal adenocarcinoma in patients treated with preoperative neoadjuvant therapy
inferred← citeshttps://doi.org/10.1038/s41467-024-53821-1openalex-snapshot
Genomic and transcriptomic landscape of human gastrointestinal stromal tumors
inferred← citeshttps://doi.org/10.1038/s41588-020-0667-5openalex-snapshot
APOBEC3-dependent kataegis and TREX1-driven chromothripsis during telomere crisis
inferred← citeshttps://doi.org/10.1101/2022.09.05.503899openalex-snapshot
The cytidine deaminase APOBEC3G drives cancer mutagenesis and clonal evolution in bladder cancer
inferred← citeshttps://doi.org/10.1101/515460openalex-snapshot
A stress response that allows highly mutated eukaryotic cells to survive and proliferate
inferred← citeshttps://doi.org/10.1158/0008-5472.c.6514373openalex-snapshot
Data from The Cytidine Deaminase APOBEC3G Contributes to Cancer Mutagenesis and Clonal Evolution in Bladder Cancer
inferred← citeshttps://doi.org/10.1158/2159-8290.cd-25-0761openalex-snapshot
The Landscape of Prostate Tumor Methylation
inferred← citeshttps://doi.org/10.1186/s12885-022-09387-6openalex-snapshot
Longitudinal profiling of circulating tumour DNA for tracking tumour dynamics in pancreatic cancer
inferred← citeshttps://doi.org/10.1186/s13073-025-01525-6openalex-snapshot
Replication-associated mechanisms contribute to an increased CpG > TpG mutation burden in mismatch repair-deficient cancers
inferred← citeshttps://doi.org/10.32614/cran.package.seqkatopenalex-snapshot
SeqKat: Detection of Kataegis
inferred← citeshttps://doi.org/10.3410/f.737316896.793571305openalex-snapshot
Faculty Opinions recommendation of Divergent mutational processes distinguish hypoxic and normoxic tumours.
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