Journal
NATURE
Volume 486, Issue 7403, Pages 400-+Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nature11017
Keywords
-
Categories
Funding
- Wellcome Trust [077012/Z/05/Z]
- Breakthrough Breast Cancer
- Wellcome Trust Senior Clinical Research Fellowship [WT088340MA]
- Research Foundation - Flanders (FWO)
- travel grant from the FWO
- International Human Frontier Science Program Organization
- Norwegian Research Council
- Norwegian Cancer Society
- Radium Hospital Foundation
- Health Region SO
- 'Interface INSERM' grant
- Department of Health via the National Institute for Health Research comprehensive Biomedical Research Centre award
- St Thomas' NHS Foundation Trust
- King's College London
- King's College Hospital NHS Foundation Trust
- Cancer Research UK
- National Institute for Health Research
- Welsh Assembly Government
- HSC R&D Office for Northern Ireland and the Chief Scientist Office, Scotland
- MEDIC foundation
- Fonds National de Recherche Scientifique
- Netherlands Genomics Initiative/Netherlands Organization for Scientific Research
- Institut National du Cancer
- Fondation Synergie-Lyon-Cancer
- Canceropole Lyon Auverge Rhone Alpes
- Centre Leon Berard
- Ludwig Institute for Cancer Research
- Dutch Genomics Initiative-Cancer Genomics Center
- BBSRC [BBS/E/T/000PR6193] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [BBS/E/T/000PR6193] Funding Source: researchfish
- Cancer Research UK [10118, 11022] Funding Source: researchfish
- National Institute for Health Research [NF-SI-0611-10154] Funding Source: researchfish
Ask authors/readers for more resources
All cancers carry somatic mutations in their genomes. A subset, known as driver mutations, confer clonal selective advantage on cancer cells and are causally implicated in oncogenesis(1), and the remainder are passenger mutations. The driver mutations and mutational processes operative in breast cancer have not yet been comprehensively explored. Here we examine the genomes of 100 tumours for somatic copy number changes and mutations in the coding exons of protein-coding genes. The number of somatic mutations varied markedly between individual tumours. We found strong correlations between mutation number, age at which cancer was diagnosed and cancer histological grade, and observed multiple mutational signatures, including one present in about ten per cent of tumours characterized by numerous mutations of cytosine at TpC dinucleotides. Driver mutations were identified in several new cancer genes including AKT2, ARID1B, CASP8, CDKN1B, MAP3K1, MAP3K13, NCOR1, SMARCD1 and TBX3. Among the 100 tumours, we found driver mutations in at least 40 cancer genes and 73 different combinations of mutated cancer genes. The results highlight the substantial genetic diversity underlying this common disease.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available