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Genomic and Molecular Landscape of DNA Damage Repair Deficiency across The Cancer Genome Atlas
Journal article   Open access   Peer reviewed

Genomic and Molecular Landscape of DNA Damage Repair Deficiency across The Cancer Genome Atlas

Theo A Knijnenburg, Linghua Wang, Michael T Zimmermann, Nyasha Chambwe, Galen F Gao, Andrew D Cherniack, Huihui Fan, Hui Shen, Gregory P Way, Casey S Greene, …
Cell reports (Cambridge), Vol.23(1), pp.239-254.e6
04/03/2018
DOI: 10.1016/j.celrep.2018.03.076
PMCID: PMC5961503
PMID: 29617664
url
https://doi.org/10.1016/j.celrep.2018.03.076View
Published (Version of record) Open Access

Abstract

DNA damage repair (DDR) pathways modulate cancer risk, progression, and therapeutic response. We systematically analyzed somatic alterations to provide a comprehensive view of DDR deficiency across 33 cancer types. Mutations with accompanying loss of heterozygosity were observed in over 1/3 of DDR genes, including TP53 and BRCA1/2. Other prevalent alterations included epigenetic silencing of the direct repair genes EXO5, MGMT, and ALKBH3 in ∼20% of samples. Homologous recombination deficiency (HRD) was present at varying frequency in many cancer types, most notably ovarian cancer. However, in contrast to ovarian cancer, HRD was associated with worse outcomes in several other cancers. Protein structure-based analyses allowed us to predict functional consequences of rare, recurrent DDR mutations. A new machine-learning-based classifier developed from gene expression data allowed us to identify alterations that phenocopy deleterious TP53 mutations. These frequent DDR gene alterations in many human cancers have functional consequences that may determine cancer progression and guide therapy.
Machine Learning Mutation Cell Line, Tumor DNA Damage Gene Silencing Genome, Human Humans Loss of Heterozygosity Neoplasms - classification Neoplasms - genetics Recombinational DNA Repair Tumor Suppressor Proteins - genetics Tumor Suppressor Proteins - metabolism

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