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Title: Genomic Evolution of Breast Cancer Metastasis and Relapse

Abstract

Patterns of genomic evolution between primary and metastatic breast cancer have not been studied in large numbers, despite patients with metastatic breast cancer having dismal survival. We sequenced whole genomes or a panel of 365 genes on 299 samples from 170 patients with locally relapsed or metastatic breast cancer. Several lines of analysis indicate that clones seeding metastasis or relapse disseminate late from primary tumors, but continue to acquire mutations, mostly accessing the same mutational processes active in the primary tumor. Most distant metastases acquired driver mutations not seen in the primary tumor, drawing from a wider repertoire of cancer genes than early drivers. Lastly, these include a number of clinically actionable alterations and mutations inactivating SWI-SNF and JAK2-STAT3 pathways.

Authors:
 [1];  [2];  [3];  [4];  [5];  [6];  [7];  [8];  [9];  [9];  [10];  [5];  [10];  [11];  [6];  [6];  [6];  [6];  [6];  [12] more »;  [13];  [13];  [6];  [14];  [4];  [15];  [16];  [17];  [2];  [6] « less
+ Show Author Affiliations
  1. Wellcome Trust Sanger Inst., Hinxton (United Kingdom); English National Health Service (NHS), London (United Kingdom). Guys and St Thomas' NHS Trust, Dept. of Clinical Oncology
  2. Univ. of Bergen (Norway). Section of Oncology, Dept. of Clinical Science; Haukeland University Hospital, Bergen (Norway). Dept. of Clinical Science
  3. Wellcome Trust Sanger Inst., Hinxton (United Kingdom); Univ. of Oxford (United Kingdom). Big Data Inst.
  4. Univ. of Cambridge (United Kingdom). Cancer Research UK Cambridge Inst.
  5. Wellcome Trust Sanger Inst., Hinxton (United Kingdom); European Bioinformatics Inst. EMBL-EBI, Hinxton (United Kingdom)
  6. Wellcome Trust Sanger Inst., Hinxton (United Kingdom)
  7. Los Alamos National Lab. (LANL), Los Alamos, NM (United States); Univ. of New Mexico Comprehensive Cancer Center, Albuquerque, NM (United States)
  8. Francis Crick Inst., London (United Kingdom); Univ. of Leuven (Belgium)
  9. Haukeland Univ. Hospital, Bergen (Norway). Dept. of Pathology; Univ. of Bergen, Bergen (Norway). Gade Lab. for Pathology, Dept. of Clinical Medicine
  10. Wellcome Trust Sanger Inst., Hinxton (United Kingdom); Memorial Sloan Kettering Cancer Inst., New York, NY (United States). Computational Oncology, Epidemiology and Biostatistics
  11. King's College London (United Kingdom). Division of Cancer Studies
  12. English National Health Service (NHS), London (United Kingdom). Guys and St Thomas' NHS Trust, Dept. of Clinical Oncology; King's College London (United Kingdom). Division of Cancer Studies
  13. Univ. Libre de Bruxelles, Brussels (Belgium). Breast Cancer Translational Research Lab.
  14. Erasmus Univ. Medical Center, Rotterdam (Netherlands). Erasmus MC Cancer Inst. and Cancer Genomics Netherlands
  15. Erasmus Univ. Medical Center, Rotterdam (Netherlands). Erasmus MC Cancer Inst. and Cancer Genomics Netherlands
  16. Brigham and Women's Hospital (Harvard Medical School), Boston, MA (United States). Dept. of Pathology; Dana-Farber Cancer Inst., Boston, MA (United States)
  17. King's College Lo Division of Cancer Studies; King's College London (United Kingdom). Breast Cancer Now Research Unit; Inst. of Cancer Research, London (United Kingdom). Breast Cancer Now Toby Robins Research Centre
Publication Date:
Research Org.:
Los Alamos National Laboratory (LANL), Los Alamos, NM (United States)
Sponsoring Org.:
USDOE Laboratory Directed Research and Development (LDRD) Program; USDOE National Nuclear Security Administration (NNSA); Wellcome Trust; Bergen Research Foundation; Norwegian Cancer Society; Norwegian Research Council
OSTI Identifier:
1392804
Report Number(s):
LA-UR-16-27672
Journal ID: ISSN 1535-6108
Grant/Contract Number:  
AC52-06NA25396
Resource Type:
Accepted Manuscript
Journal Name:
Cancer Cell
Additional Journal Information:
Journal Volume: 32; Journal Issue: 2; Journal ID: ISSN 1535-6108
Publisher:
Elsevier
Country of Publication:
United States
Language:
English
Subject:
59 BASIC BIOLOGICAL SCIENCES; 60 APPLIED LIFE SCIENCES; Biological Science; breast cancer; metastasis; relapse; genomics; somatic mutation

Citation Formats

Yates, Lucy R., Knappskog, Stian, Wedge, David, Farmery, James H. R., Gonzalez, Santiago, Martincorena, Inigo, Alexandrov, Ludmil B., Van Loo, Peter, Haugland, Hans Kristian, Lilleng, Peer Kaare, Gundem, Gunes, Gerstung, Moritz, Pappaemmanuil, Elli, Gazinska, Patrycja, Bhosle, Shriram G., Jones, David, Raine, Keiran, Mudie, Laura, Latimer, Calli, Sawyer, Elinor, Desmedt, Christine, Sotiriou, Christos, Stratton, Michael R., Sieuwerts, Anieta M., Lynch, Andy G., Martens, John W., Richardson, Andrea L., Tutt, Andrew, Lønning, Per Eystein, and Campbell, Peter J. Genomic Evolution of Breast Cancer Metastasis and Relapse. United States: N. p., 2017. Web. doi:10.1016/j.ccell.2017.07.005.
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Yates, Lucy R., Knappskog, Stian, Wedge, David, Farmery, James H. R., Gonzalez, Santiago, Martincorena, Inigo, Alexandrov, Ludmil B., Van Loo, Peter, Haugland, Hans Kristian, Lilleng, Peer Kaare, Gundem, Gunes, Gerstung, Moritz, Pappaemmanuil, Elli, Gazinska, Patrycja, Bhosle, Shriram G., Jones, David, Raine, Keiran, Mudie, Laura, Latimer, Calli, Sawyer, Elinor, Desmedt, Christine, Sotiriou, Christos, Stratton, Michael R., Sieuwerts, Anieta M., Lynch, Andy G., Martens, John W., Richardson, Andrea L., Tutt, Andrew, Lønning, Per Eystein, & Campbell, Peter J. Genomic Evolution of Breast Cancer Metastasis and Relapse. United States. https://doi.org/10.1016/j.ccell.2017.07.005
Copy to clipboard
Yates, Lucy R., Knappskog, Stian, Wedge, David, Farmery, James H. R., Gonzalez, Santiago, Martincorena, Inigo, Alexandrov, Ludmil B., Van Loo, Peter, Haugland, Hans Kristian, Lilleng, Peer Kaare, Gundem, Gunes, Gerstung, Moritz, Pappaemmanuil, Elli, Gazinska, Patrycja, Bhosle, Shriram G., Jones, David, Raine, Keiran, Mudie, Laura, Latimer, Calli, Sawyer, Elinor, Desmedt, Christine, Sotiriou, Christos, Stratton, Michael R., Sieuwerts, Anieta M., Lynch, Andy G., Martens, John W., Richardson, Andrea L., Tutt, Andrew, Lønning, Per Eystein, and Campbell, Peter J. Mon . "Genomic Evolution of Breast Cancer Metastasis and Relapse". United States. https://doi.org/10.1016/j.ccell.2017.07.005. https://www.osti.gov/servlets/purl/1392804.
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@article{osti_1392804,
title = {Genomic Evolution of Breast Cancer Metastasis and Relapse},
author = {Yates, Lucy R. and Knappskog, Stian and Wedge, David and Farmery, James H. R. and Gonzalez, Santiago and Martincorena, Inigo and Alexandrov, Ludmil B. and Van Loo, Peter and Haugland, Hans Kristian and Lilleng, Peer Kaare and Gundem, Gunes and Gerstung, Moritz and Pappaemmanuil, Elli and Gazinska, Patrycja and Bhosle, Shriram G. and Jones, David and Raine, Keiran and Mudie, Laura and Latimer, Calli and Sawyer, Elinor and Desmedt, Christine and Sotiriou, Christos and Stratton, Michael R. and Sieuwerts, Anieta M. and Lynch, Andy G. and Martens, John W. and Richardson, Andrea L. and Tutt, Andrew and Lønning, Per Eystein and Campbell, Peter J.},
abstractNote = {Patterns of genomic evolution between primary and metastatic breast cancer have not been studied in large numbers, despite patients with metastatic breast cancer having dismal survival. We sequenced whole genomes or a panel of 365 genes on 299 samples from 170 patients with locally relapsed or metastatic breast cancer. Several lines of analysis indicate that clones seeding metastasis or relapse disseminate late from primary tumors, but continue to acquire mutations, mostly accessing the same mutational processes active in the primary tumor. Most distant metastases acquired driver mutations not seen in the primary tumor, drawing from a wider repertoire of cancer genes than early drivers. Lastly, these include a number of clinically actionable alterations and mutations inactivating SWI-SNF and JAK2-STAT3 pathways.},
doi = {10.1016/j.ccell.2017.07.005},
journal = {Cancer Cell},
number = 2,
volume = 32,
place = {United States},
year = {Mon Aug 14 00:00:00 EDT 2017},
month = {Mon Aug 14 00:00:00 EDT 2017}
}
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https://doi.org/10.1016/j.ccell.2017.07.005
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    Molecular Biology and Evolution of Cancer: From Discovery to Action
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    Cooperation among Tumor Cell Subpopulations Leads to Intratumor Heterogeneity
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    The role of poly(ADP-ribose) polymerase inhibitors in the treatment of cancer and methods to overcome resistance: a review
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    Pan-cancer inference of intra-tumor heterogeneity reveals associations with different forms of genomic instability
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    Constitutional Mosaic Epimutations – a hidden cause of cancer?
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    ‘Omics Approaches to Explore the Breast Cancer Landscape
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    Landscape of CDKN1B Mutations in Luminal Breast Cancer and Other Hormone-Driven Human Tumors
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    BCMA (TNFRSF17) Induces APRIL and BAFF Mediated Breast Cancer Cell Stemness
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    Novel and Alternative Targets Against Breast Cancer Stemness to Combat Chemoresistance
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    Targeting of the Eukaryotic Translation Initiation Factor 4A Against Breast Cancer Stemness
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    STAT3 in Breast Cancer Onset and Progression: A Matter of Time and Context
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    Targeting Genome Stability in Melanoma—A New Approach to an Old Field
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    Ampelopsin E Reduces the Invasiveness of the Triple Negative Breast Cancer Cell Line, MDA-MB-231
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    A proteomic analysis of chemoresistance development via sequential treatment with doxorubicin reveals novel players in MCF‑7 breast cancer cells
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    Outcome of Omani Women with Breast Cancer-associated Brain Metastases Experience from a University Hospital
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    • Zahid, Khawaja F.; Kumar, Shiyam; Al-Bimani, Khalid
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    Phase I/II clinical trial of everolimus combined with gemcitabine/cisplatin for metastatic triple-negative breast cancer
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    • Journal of Cancer, Vol. 9, Issue 7
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