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The cancer genome

Author

Listed:
  • Michael R. Stratton

    (Cancer Genome Project, Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1SA, UK
    Institute of Cancer Research, 15 Cotswold Road, Sutton, Surrey SM2 5NG, UK)

  • Peter J. Campbell

    (Cancer Genome Project, Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1SA, UK
    University of Cambridge)

  • P. Andrew Futreal

    (Cancer Genome Project, Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1SA, UK)

Abstract

The cancer genomics era Since the discovery in 1982 of the link between HRAS gene mutations and bladder cancer, about 100,000 abnormal genes have been identified in cancer patients. As a result, much has been learned about the development of cancer, but with so many distinct cancer and tissue types, there is much more to be learned. Now with the development of massively parallel DNA sequencing, hundreds of millions of cancer-related mutations will soon be revealed. In a broad-ranging review, Michael Stratton, Peter Campbell and Andrew Futreal look back at the achievements of cancer genomics, and forward to the prospect that the complete DNA sequencing of large numbers of cancers will help us move towards a deeper understanding of how to treat cancers.

Suggested Citation

  • Michael R. Stratton & Peter J. Campbell & P. Andrew Futreal, 2009. "The cancer genome," Nature, Nature, vol. 458(7239), pages 719-724, April.
  • Handle: RePEc:nat:nature:v:458:y:2009:i:7239:d:10.1038_nature07943
    DOI: 10.1038/nature07943
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    Cited by:

    1. Ronglai Shen & Qianxing Mo & Nikolaus Schultz & Venkatraman E Seshan & Adam B Olshen & Jason Huse & Marc Ladanyi & Chris Sander, 2012. "Integrative Subtype Discovery in Glioblastoma Using iCluster," PLOS ONE, Public Library of Science, vol. 7(4), pages 1-9, April.
    2. van Wieringen Wessel N. & van de Wiel Mark A., 2014. "Penalized differential pathway analysis of integrative oncogenomics studies," Statistical Applications in Genetics and Molecular Biology, De Gruyter, vol. 13(2), pages 141-158, April.
    3. Yi-Yu Chen & Jing-Yu Ge & Si-Yuan Zhu & Zhi-Ming Shao & Ke-Da Yu, 2022. "Copy number amplification of ENSA promotes the progression of triple-negative breast cancer via cholesterol biosynthesis," Nature Communications, Nature, vol. 13(1), pages 1-16, December.
    4. Tommaso Rondelli & Margherita Berardi & Benedetta Peruzzi & Luca Boni & Roberto Caporale & Piero Dolara & Rosario Notaro & Lucio Luzzatto, 2013. "The Frequency of Granulocytes with Spontaneous Somatic Mutations: A Wide Distribution in a Normal Human Population," PLOS ONE, Public Library of Science, vol. 8(1), pages 1-7, January.
    5. Tingting Lin & Peng Lyu, 2019. "The Application of Next Generation Sequencing in Cancer Precision Diagnosis and Target Therapy Selection," Biomedical Journal of Scientific & Technical Research, Biomedical Research Network+, LLC, vol. 20(1), pages 14809-14812, July.
    6. Eva G. Álvarez & Jonas Demeulemeester & Paula Otero & Clemency Jolly & Daniel García-Souto & Ana Pequeño-Valtierra & Jorge Zamora & Marta Tojo & Javier Temes & Adrian Baez-Ortega & Bernardo Rodriguez-, 2021. "Aberrant integration of Hepatitis B virus DNA promotes major restructuring of human hepatocellular carcinoma genome architecture," Nature Communications, Nature, vol. 12(1), pages 1-12, December.
    7. Michael Mak & Cynthia A Reinhart-King & David Erickson, 2011. "Microfabricated Physical Spatial Gradients for Investigating Cell Migration and Invasion Dynamics," PLOS ONE, Public Library of Science, vol. 6(6), pages 1-8, June.
    8. Manako Yamaguchi & Hirofumi Nakaoka & Kazuaki Suda & Kosuke Yoshihara & Tatsuya Ishiguro & Nozomi Yachida & Kyota Saito & Haruka Ueda & Kentaro Sugino & Yutaro Mori & Kaoru Yamawaki & Ryo Tamura & Sun, 2022. "Spatiotemporal dynamics of clonal selection and diversification in normal endometrial epithelium," Nature Communications, Nature, vol. 13(1), pages 1-18, December.
    9. Yukinari Haraoka & Yuki Akieda & Yuri Nagai & Chihiro Mogi & Tohru Ishitani, 2022. "Zebrafish imaging reveals TP53 mutation switching oncogene-induced senescence from suppressor to driver in primary tumorigenesis," Nature Communications, Nature, vol. 13(1), pages 1-15, December.

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