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Mutational Strand Asymmetries in Cancer Genomes Reveal Mechanisms of DNA Damage and Repair.

Mutational Strand Asymmetries in Cancer Genomes Reveal Mechanisms of DNA Damage and Repair.

http://www.wikidata.org/entity/Q36578527

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New insights into the generation and role of de novo mutations in health and disease APOBEC3A and APOBEC3B Preferentially Deaminate the Lagging Strand Template during DNA Replication Whole-genome analysis of papillary kidney cancer finds significant noncoding alterations Insertions and Deletions Target Lineage-Defining Genes in Human Cancers.Mutation Processes in 293-Based Clones Overexpressing the DNA Cytosine Deaminase APOBEC3B.Mutational Biases Drive Elevated Rates of Substitution at Regulatory Sites across Cancer Types Activation induced deaminase mutational signature overlaps with CpG methylation sites in follicular lymphoma and other cancers.Strand-biased cytosine deamination at the replication fork causes cytosine to thymine mutations in Escherichia coli.Genome-wide kinetics of DNA excision repair in relation to chromatin state and mutagenesis APOBEC3A damages the cellular genome during DNA replication Functional Upregulation of the DNA Cytosine Deaminase APOBEC3B by Polyomaviruses.Somatic ERCC2 mutations are associated with a distinct genomic signature in urothelial tumors.When Genome Maintenance Goes Badly Awry.Merkel Cell Polyomavirus Exhibits Dominant Control of the Tumor Genome and Transcriptome in Virus-Associated Merkel Cell Carcinoma.Risks at the DNA Replication Fork: Effects upon Carcinogenesis and Tumor Heterogeneity Genomic landscape of high-grade meningiomas.Elevated APOBEC3B expression drives a kataegic-like mutation signature and replication stress-related therapeutic vulnerabilities in p53-defective cells.From Mutational Mechanisms in Single Cells to Mutational Patterns in Cancer Genomes.The Nonbulky DNA Lesions Spiroiminodihydantoin and 5-Guanidinohydantoin Significantly Block Human RNA Polymerase II Elongation in Vitro.Human mismatch repair system balances mutation rates between strands by removing more mismatches from the lagging strand.Molecular classification of pulmonary sarcomatoid carcinomas suggests new therapeutic opportunities.Understanding mutagenesis through delineation of mutational signatures in human cancer.DNA Polymerases Divide the Labor of Genome Replication.APOBEC3B cytidine deaminase targets the non-transcribed strand of tRNA genes in yeast.Functions and Malfunctions of Mammalian DNA-Cytosine Deaminases HBXIP, a binding protein of HBx, regulates maintenance of the G2/M phase checkpoint induced by DNA damage and enhances sensitivity to doxorubicin-induced cytotoxicity.APOBEC3A/B-induced mutagenesis is responsible for 20% of heritable mutations in the TpCpW context.Mutational Signatures in Breast Cancer: The Problem at the DNA Level Perturbations in the Replication Program Contribute to Genomic Instability in Cancer.Nucleotide excision repair is impaired by binding of transcription factors to DNA.Single-cell whole-genome analyses by Linear Amplification via Transposon Insertion (LIANTI).Global genome nucleotide excision repair is organized into domains that promote efficient DNA repair in chromatin.Avoidance of APOBEC3B-induced mutation by error-free lesion bypass Mutational signatures reveal the dynamic interplay of risk factors and cellular processes during liver tumorigenesis.Reduced mutation rate in exons due to differential mismatch repair.Universal Patterns of Selection in Cancer and Somatic Tissues.Global unleashing of transcription elongation waves in response to genotoxic stress restricts somatic mutation rate.Enzyme cycling contributes to efficient induction of genome mutagenesis by the cytidine deaminase APOBEC3B.Detecting presence of mutational signatures in cancer with confidence.Mismatch repair prefers exons.

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Mutational Strand Asymmetries in Cancer Genomes Reveal Mechanisms of DNA Damage and Repair.

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Amnon Koren

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Atanas Kamburov

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David A Wheeler

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Esther Rheinbay

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Eve Shinbrot

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Jaegil Kim

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Julian M Hess

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Kyle R Covington

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Lior Z Braunstein

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Michael S Lawrence

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P2860

The major roles of DNA polymerases epsilon and delta at the eukaryotic replication fork are evolutionarily conserved

A small-cell lung cancer genome with complex signatures of tobacco exposure

Mutational heterogeneity in cancer and the search for new cancer-associated genes

Mutational processes molding the genomes of 21 breast cancers

A comprehensive catalogue of somatic mutations from a human cancer genome

Initial genome sequencing and analysis of multiple myeloma

Somatic mutations in aging, cancer and neurodegeneration

Exonuclease mutations in DNA polymerase epsilon reveal replication strand specific mutation patterns and human origins of replication

A Major Role of DNA Polymerase δ in Replication of Both the Leading and Lagging DNA Strands

Reconsidering DNA Polymerases at the Replication Fork in Eukaryotes

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