Somatic rearrangements across cancer reveal classes of samples with distinct patterns of DNA breakage and rearrangement-induced hypermutability. - Wikidata - wikimedia - TriplyDB

Somatic rearrangements across cancer reveal classes of samples with distinct patterns of DNA breakage and rearrangement-induced hypermutability.

Somatic rearrangements across cancer reveal classes of samples with distinct patterns of DNA breakage and rearrangement-induced hypermutability.

http://www.wikidata.org/entity/Q36580560

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Emerging Role of Genomic Rearrangements in Breast Cancer: Applying Knowledge from Other Cancers Whole-exome sequencing and clinical interpretation of formalin-fixed, paraffin-embedded tumor samples to guide precision cancer medicine.Molecular mechanism and clinical impact of APOBEC3B-catalyzed mutagenesis in breast cancer Hypermutation in human cancer genomes: footprints and mechanisms Comprehensive red blood cell and platelet antigen prediction from whole genome sequencing: proof of principle An oncogenic MYB feedback loop drives alternate cell fates in adenoid cystic carcinoma.Unraveling the clonal hierarchy of somatic genomic aberrations.Clinical analysis and interpretation of cancer genome data Microhomology-mediated end joining induces hypermutagenesis at breakpoint junctions.Clustered and genome-wide transient mutagenesis in human cancers: Hypermutation without permanent mutators or loss of fitness Evidence for APOBEC3B mutagenesis in multiple human cancers MYB-QKI rearrangements in angiocentric glioma drive tumorigenicity through a tripartite mechanism.Exome and genome sequencing of nasopharynx cancer identifies NF-κB pathway activating mutations Functional chromatin features are associated with structural mutations in cancer Genomic rearrangements in prostate cancer.Oligometastases in prostate cancer: restaging stage IV cancers and new radiotherapy options.Break-induced replication is a source of mutation clusters underlying kataegis Fragile DNA motifs trigger mutagenesis at distant chromosomal loci in saccharomyces cerevisiae.Complementary genomic approaches highlight the PI3K/mTOR pathway as a common vulnerability in osteosarcoma Sporadic hemangioblastomas are characterized by cryptic VHL inactivation.Detecting somatic genetic alterations in tumor specimens by exon capture and massively parallel sequencing.Genetic variation in human DNA replication timing Can we safely target the WNT pathway?Modeling the integration of bacterial rRNA fragments into the human cancer genome An APOBEC3A hypermutation signature is distinguishable from the signature of background mutagenesis by APOBEC3B in human cancers APOBEC-Induced Cancer Mutations Are Uniquely Enriched in Early-Replicating, Gene-Dense, and Active Chromatin Regions Whole-genome sequencing reveals activation-induced cytidine deaminase signatures during indolent chronic lymphocytic leukaemia evolution Transcriptional elongation requires DNA break-induced signalling.Mutation pattern is an influential factor on functional mutation rates in cancer.Targetable genetic features of primary testicular and primary central nervous system lymphomas.DNA replication timing, genome stability and cancer: late and/or delayed DNA replication timing is associated with increased genomic instability.Genetic Effect of Chemotherapy Exposure in Children of Testicular Cancer Survivors.Analyzing Somatic Genome Rearrangements in Human Cancers by Using Whole-Exome Sequencing.Punctuated evolution of prostate cancer genomes.A survey of intragenic breakpoints in glioblastoma identifies a distinct subset associated with poor survival.Translocation and deletion breakpoints in cancer genomes are associated with potential non-B DNA-forming sequences Nuclear Magnetic Resonance Structure of the APOBEC3B Catalytic Domain: Structural Basis for Substrate Binding and DNA Deaminase Activity.Loss of heterozygosity preferentially occurs in early replicating regions in cancer genomes.The topography of mutational processes in breast cancer genomes.An APOBEC cytidine deaminase mutagenesis pattern is widespread in human cancers.

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P2860

Somatic rearrangements across cancer reveal classes of samples with distinct patterns of DNA breakage and rearrangement-induced hypermutability.

http://www.wikidata.org/entity/Q36580560

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Chip Stewart

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A role for the Adenomatous Polyposis Coli protein in chromosome segregation

Melanoma genome sequencing reveals frequent PREX2 mutations

Mapping copy number variation by population-scale genome sequencing

The genomic complexity of primary human prostate cancer

Mutational processes molding the genomes of 21 breast cancers

Initial genome sequencing and analysis of multiple myeloma

Comprehensive molecular characterization of human colon and rectal cancer

Massive genomic rearrangement acquired in a single catastrophic event during cancer development

Complex landscapes of somatic rearrangement in human breast cancer genomes.

Mapping short DNA sequencing reads and calling variants using mapping quality scores

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