Faculty Opinions recommendation of The topography of mutational processes in breast cancer genomes.

The topography of mutational processes in breast cancer genomes Sandro Morganella1, Ludmil B. Alexandrov2,3,4, Dominik Glodzik2, Xueqing Zou2, Helen Davies2, Johan Staaf5, Anieta M. Sieuwerts6, Arie B. Brinkman7, Sancha Martin2, Manasa Ramakrishna2, Adam Butler2, Hyung-Yong Kim8, Åke Borg5, Christos Sotiriou9, P. Andrew Futreal1,10, Peter J. Campbell2, Paul N. Span11, Steven Van Laere12, Sunil R. Lakhani13,14, Jorunn E. Eyfjord15, Alastair M. Thompson16,17, Hendrik G. Stunnenberg7, Marc J. van de Vijver18, John W.M. Martens6, Anne-Lise Børresen-Dale19,20, Andrea L. Richardson21,22, Gu Kong8, Gilles Thomas23, Julian Sale24, Cristina Rada24, Michael R. Stratton2, Ewan Birney1 & Serena Nik-Zainal2,25

[1]  B. Arcangioli,et al.  Fission yeast switches mating type by a replication–recombination coupled process , 2000, The EMBO journal.

[2]  David M. Gilbert,et al.  Making Sense of Eukaryotic DNA Replication Origins , 2001, Science.

[3]  B. Alberts,et al.  Molecular Biology of the Cell (4th Ed) , 2002 .

[4]  B. Strauss The "A" rule revisited: polymerases as determinants of mutational specificity. , 2002, DNA repair.

[5]  Reuben S Harris,et al.  RNA editing enzyme APOBEC1 and some of its homologs can act as DNA mutators. , 2002, Molecular cell.

[6]  J. Sale,et al.  Rev1 is essential for DNA damage tolerance and non‐templated immunoglobulin gene mutation in a vertebrate cell line , 2003, The EMBO journal.

[7]  J. Dalgaard,et al.  RNase-sensitive DNA modification(s) initiates S. pombe mating-type switching. , 2004, Genes & development.

[8]  J. Nickoloff,et al.  Good Timing in the Cell Cycle for Precise DNA Repair by BRCA1 , 2005, Cell cycle.

[9]  P. Hanawalt,et al.  Transcriptional inhibition by an oxidized abasic site in DNA. , 2006, Chemical research in toxicology.

[10]  N. Rhind,et al.  DNA replication timing: random thoughts about origin firing , 2006, Nature Cell Biology.

[11]  P. Hanawalt,et al.  Transcription arrest at an abasic site in the transcribed strand of template DNA. , 2006, Chemical research in toxicology.

[12]  P. Hanawalt,et al.  Transcription-coupled DNA repair: two decades of progress and surprises , 2008, Nature Reviews Molecular Cell Biology.

[13]  S. Conticello The AID/APOBEC family of nucleic acid mutators , 2008, Genome Biology.

[14]  B. Gómez-González,et al.  Genome instability: a mechanistic view of its causes and consequences , 2008, Nature Reviews Genetics.

[15]  Sumio Sugano,et al.  Chromatin-Associated Periodicity in Genetic Variation Downstream of Transcriptional Start Sites , 2009, Science.

[16]  J. Stamatoyannopoulos,et al.  Human mutation rate associated with DNA replication timing , 2009, Nature Genetics.

[17]  T. Nouspikel Nucleotide excision repair : variations on versatility , 2009 .

[18]  C. Allis,et al.  Decreased replication origin activity in temporal transition regions , 2009, The Journal of cell biology.

[19]  Tom Royce,et al.  A comprehensive catalogue of somatic mutations from a human cancer genome , 2010, Nature.

[20]  E. Kass,et al.  Collaboration and competition between DNA double‐strand break repair pathways , 2010, FEBS letters.

[21]  Alain Arneodo,et al.  Evidence for Sequential and Increasing Activation of Replication Origins along Replication Timing Gradients in the Human Genome , 2011, PLoS Comput. Biol..

[22]  S. De,et al.  DNA replication timing and long-range DNA interactions predict mutational landscapes of cancer genomes , 2011, Nature Biotechnology.

[23]  P. Park,et al.  Impact of chromatin structure on sequence variability in the human genome , 2011, Nature Structural &Molecular Biology.

[24]  Wen-Hsiung Li,et al.  DNA replication timing and selection shape the landscape of nucleotide variation in cancer genomes , 2012, Nature Communications.

[25]  A. Børresen-Dale,et al.  The Life History of 21 Breast Cancers , 2012, Cell.

[26]  B. Schuster-Böckler,et al.  Chromatin organization is a major influence on regional mutation rates in human cancer cells , 2012, Nature.

[27]  Paz Polak,et al.  Differential relationship of DNA replication timing to different forms of human mutation and variation. , 2012, American journal of human genetics.

[28]  ENCODEConsortium,et al.  An Integrated Encyclopedia of DNA Elements in the Human Genome , 2012, Nature.

[29]  Daniel J. Gaffney,et al.  Controls of Nucleosome Positioning in the Human Genome , 2012, PLoS genetics.

[30]  Maxwell W. Libbrecht,et al.  Ubiquitous heterogeneity and asymmetry of the chromatin environment at regulatory elements , 2012, Genome research.

[31]  G. Almouzni,et al.  Interplay between mismatch repair and chromatin assembly , 2012, Proceedings of the National Academy of Sciences.

[32]  J. Jiricny,et al.  Mammalian mismatch repair: error-free or error-prone? , 2012, Trends in biochemical sciences.

[33]  A. Børresen-Dale,et al.  Mutational Processes Molding the Genomes of 21 Breast Cancers , 2012, Cell.

[34]  A. Gronenborn,et al.  NMR structure of human restriction factor APOBEC3A reveals substrate binding and enzyme specificity , 2013, Nature Communications.

[35]  L. M. Mansky,et al.  APOBEC3G cytosine deamination hotspots are defined by both sequence context and single-stranded DNA secondary structure , 2013, Nucleic acids research.

[36]  David T. W. Jones,et al.  Signatures of mutational processes in human cancer , 2013, Nature.

[37]  B. Stillman,et al.  Principles and concepts of DNA replication in bacteria, archaea, and eukarya. , 2013, Cold Spring Harbor perspectives in biology.

[38]  A. Carr,et al.  Replication stress-induced genome instability: the dark side of replication maintenance by homologous recombination. , 2013, Journal of molecular biology.

[39]  S. De,et al.  DNA replication timing and higher-order nuclear organization determine single nucleotide substitution patterns in cancer genomes , 2013, Nature Communications.

[40]  M. Stratton,et al.  Deciphering Signatures of Mutational Processes Operative in Human Cancer , 2013, Cell reports.

[41]  S. Gabriel,et al.  Somatic rearrangements across cancer reveal classes of samples with distinct patterns of DNA breakage and rearrangement-induced hypermutability , 2012, Genome research.

[42]  Serena Nik-Zainal,et al.  Mechanisms underlying mutational signatures in human cancers , 2014, Nature Reviews Genetics.

[43]  Adam P Butler,et al.  Association of a germline copy number polymorphism of APOBEC3A and APOBEC3B with burden of putative APOBEC-dependent mutations in breast cancer , 2014, Nature Genetics.

[44]  T. Kunkel,et al.  Heterogeneous polymerase fidelity and mismatch repair bias genome variation and composition , 2014, Genome research.

[45]  George Iliakis,et al.  Break-Induced Replication Repair of Damaged Forks Induces Genomic Duplications in Human Cells , 2014, Science.

[46]  Ben Lehner,et al.  Differential DNA mismatch repair underlies mutation rate variation across the human genome , 2015, Nature.

[47]  Paz Polak,et al.  Cell-of-origin chromatin organization shapes the mutational landscape of cancer , 2015, Nature.

[48]  M. Méchali,et al.  DNA replication origin activation in space and time , 2015, Nature Reviews Molecular Cell Biology.

[49]  Kyle M. Miller,et al.  Mammalian polymerase θ promotes alternative NHEJ and suppresses recombination , 2015, Nature.

[50]  Paul Nurse,et al.  The spatial and temporal organization of origin firing during the S-phase of fission yeast , 2015, Genome research.

[51]  P. Nurse,et al.  Molecular Combing of Single DNA Molecules on the 10 Megabase Scale , 2016, Scientific Reports.

[52]  David C. Jones,et al.  Landscape of somatic mutations in 560 breast cancer whole genome sequences , 2016, Nature.