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Michael R. Stratton
Wellcome Trust Sanger Institute
CancerMutationBreast cancerGeneticsBiology
480Publications
139H-index
99.6kCitations
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Publications 483
Newest
#1Ludmil B. Alexandrov (UCSD: University of California, San Diego)H-Index: 45
#2Jaegil Kim (Broad Institute)H-Index: 40
Last. Erik N. Bergstrom (UCSD: University of California, San Diego)H-Index: 1
view all 21 authors...
Somatic mutations in cancer genomes are caused by multiple mutational processes, each of which generates a characteristic mutational signature1. Here, as part of the Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium2 of the International Cancer Genome Consortium (ICGC) and The Cancer Genome Atlas (TCGA), we characterized mutational signatures using 84,729,690 somatic mutations from 4,645 whole-genome and 19,184 exome sequences that encompass most types of cancer. We identified 49 single-ba...
21 CitationsSource
#1Kenichi Yoshida (Wellcome Trust Sanger Institute)H-Index: 1
#2Kate H.C. Gowers (UCL: University College London)H-Index: 4
Last. Elizabeth Anderson (Wellcome Trust Sanger Institute)H-Index: 9
view all 21 authors...
Tobacco smoking causes lung cancer1–3, a process that is driven by more than 60 carcinogens in cigarette smoke that directly damage and mutate DNA4,5. The profound effects of tobacco on the genome of lung cancer cells are well-documented6–10, but equivalent data for normal bronchial cells are lacking. Here we sequenced whole genomes of 632 colonies derived from single bronchial epithelial cells across 16 subjects. Tobacco smoking was the major influence on mutational burden, typically adding fro...
6 CitationsSource
#1Sigurgeir Olafsson (Wellcome Trust Sanger Institute)H-Index: 1
#2Rebecca E McIntyre (Wellcome Trust Sanger Institute)H-Index: 15
Last. Carl A. Anderson (Wellcome Trust Sanger Institute)H-Index: 39
view all 18 authors...
Source
#1Ayesha Noorani (University of Cambridge)H-Index: 11
#2Xiaodun Li (University of Cambridge)H-Index: 6
Last. Rebecca C. Fitzgerald (University of Cambridge)H-Index: 36
view all 26 authors...
The poor outcomes in esophageal adenocarcinoma (EAC) prompted us to interrogate the pattern and timing of metastatic spread. Whole-genome sequencing and phylogenetic analysis of 388 samples across 18 individuals with EAC showed, in 90% of patients, that multiple subclones from the primary tumor spread very rapidly from the primary site to form multiple metastases, including lymph nodes and distant tissues—a mode of dissemination that we term ‘clonal diaspora’. Metastatic subclones at autopsy wer...
1 CitationsSource
#1Tim H. H. CoorensH-Index: 2
#2Taryn D Treger (University of Cambridge)H-Index: 2
Last. Sam Behjati (University of Cambridge)H-Index: 22
view all 41 authors...
Adult cancers often arise from premalignant clonal expansions. Whether the same is true of childhood tumors has been unclear. To investigate whether Wilms tumor (nephroblastoma; a childhood kidney cancer) develops from a premalignant background, we examined the phylogenetic relationship between tumors and corresponding normal tissues. In 14 of 23 cases studied (61%), we found premalignant clonal expansions in morphologically normal kidney tissues that preceded tumor development. These clonal exp...
1 CitationsSource
#1Jiqiu Cheng (Katholieke Universiteit Leuven)H-Index: 6
#2Jonas Demeulemeester (Katholieke Universiteit Leuven)H-Index: 20
Last. Peter Van Loo (Katholieke Universiteit Leuven)H-Index: 48
view all 18 authors...
Source
#1Sigurgeir Olafsson (Wellcome Trust Sanger Institute)H-Index: 1
#2Rebecca E McIntyre (Wellcome Trust Sanger Institute)H-Index: 15
Last. Carl A. Anderson (Wellcome Trust Sanger Institute)H-Index: 39
view all 18 authors...
Inflammatory bowel disease (IBD) is a chronic inflammatory disease associated with increased risk of gastrointestinal cancers but our understanding of the effects of IBD on the mutational profile and clonal structure of the colon is limited. Here, we isolated and whole-genome sequenced 370 colonic crypts from 45 IBD patients, and compared these to 413 crypts from 41 non-IBD controls. We estimated the base substitution rate of affected colonic epithelial cells to be doubled after IBD onset. This ...
Source
#1Simon F. Brunner (Wellcome Trust Sanger Institute)H-Index: 2
#2Nicola D. Roberts (Wellcome Trust Sanger Institute)H-Index: 9
Last. Peter J. Campbell (University of Cambridge)H-Index: 95
view all 15 authors...
The most common causes of chronic liver disease are excess alcohol intake, viral hepatitis and non-alcoholic fatty liver disease, with the clinical spectrum ranging in severity from hepatic inflammation to cirrhosis, liver failure or hepatocellular carcinoma (HCC). The genome of HCC exhibits diverse mutational signatures, resulting in recurrent mutations across more than 30 cancer genes1–7. Stem cells from normal livers have a low mutational burden and limited diversity of signatures8, which sug...
12 CitationsSource
#1Erik N. Bergstrom (UCLA: University of California, Los Angeles)H-Index: 1
#2Mi Ni Huang (NUS: National University of Singapore)H-Index: 7
Last. Ludmil B. Alexandrov (UCLA: University of California, Los Angeles)H-Index: 45
view all 7 authors...
Cancer genomes are peppered with somatic mutations imprinted by different mutational processes. The mutational pattern of a cancer genome can be used to identify and understand the etiology of the underlying mutational processes. A plethora of prior research has focused on examining mutational signatures and mutational patterns from single base substitutions and their immediate sequencing context. We recently demonstrated that further classification of small mutational events (including substitu...
1 CitationsSource
#1Henry Lee-SixH-Index: 5
#2Sigurgeir OlafssonH-Index: 1
Last. Michael R. StrattonH-Index: 139
view all 22 authors...
The colorectal adenoma–carcinoma sequence has provided a paradigmatic framework for understanding the successive somatic genetic changes and consequent clonal expansions that lead to cancer1. However, our understanding of the earliest phases of colorectal neoplastic changes—which may occur in morphologically normal tissue—is comparatively limited, as for most cancer types. Here we use whole-genome sequencing to analyse hundreds of normal crypts from 42 individuals. Signatures of multiple mutatio...
21 CitationsSource
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