Combined hereditary and somatic mutations of replication error repair genes result in rapid onset of ultra-hypermutated cancers View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2015-03

AUTHORS

Adam Shlien, Brittany B Campbell, Richard de Borja, Ludmil B Alexandrov, Daniele Merico, David Wedge, Peter Van Loo, Patrick S Tarpey, Paul Coupland, Sam Behjati, Aaron Pollett, Tatiana Lipman, Abolfazl Heidari, Shriya Deshmukh, Na'ama Avitzur, Bettina Meier, Moritz Gerstung, Ye Hong, Diana M Merino, Manasa Ramakrishna, Marc Remke, Roland Arnold, Gagan B Panigrahi, Neha P Thakkar, Karl P Hodel, Erin E Henninger, A Yasemin Göksenin, Doua Bakry, George S Charames, Harriet Druker, Jordan Lerner-Ellis, Matthew Mistry, Rina Dvir, Ronald Grant, Ronit Elhasid, Roula Farah, Glenn P Taylor, Paul C Nathan, Sarah Alexander, Shay Ben-Shachar, Simon C Ling, Steven Gallinger, Shlomi Constantini, Peter Dirks, Annie Huang, Stephen W Scherer, Richard G Grundy, Carol Durno, Melyssa Aronson, Anton Gartner, M Stephen Meyn, Michael D Taylor, Zachary F Pursell, Christopher E Pearson, David Malkin, P Andrew Futreal, Michael R Stratton, Eric Bouffet, Cynthia Hawkins, Peter J Campbell, Uri Tabori, Biallelic Mismatch Repair Deficiency Consortium

ABSTRACT

DNA replication-associated mutations are repaired by two components: polymerase proofreading and mismatch repair. The mutation consequences of disruption to both repair components in humans are not well studied. We sequenced cancer genomes from children with inherited biallelic mismatch repair deficiency (bMMRD). High-grade bMMRD brain tumors exhibited massive numbers of substitution mutations (>250/Mb), which was greater than all childhood and most cancers (>7,000 analyzed). All ultra-hypermutated bMMRD cancers acquired early somatic driver mutations in DNA polymerase ɛ or δ. The ensuing mutation signatures and numbers are unique and diagnostic of childhood germ-line bMMRD (P < 10(-13)). Sequential tumor biopsy analysis revealed that bMMRD/polymerase-mutant cancers rapidly amass an excess of simultaneous mutations (∼600 mutations/cell division), reaching but not exceeding ∼20,000 exonic mutations in <6 months. This implies a threshold compatible with cancer-cell survival. We suggest a new mechanism of cancer progression in which mutations develop in a rapid burst after ablation of replication repair. More... »

PAGES

257-262

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/ng.3202

DOI

http://dx.doi.org/10.1038/ng.3202

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1041610044

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/25642631


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