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Germline BRCA2 mutations drive prostate cancers with distinct evolutionary trajectories

Author

Listed:
  • Renea A. Taylor

    (Monash Partners Comprehensive Cancer Consortium and Cancer Program, Biomedicine Discovery Institute, Monash University)

  • Michael Fraser

    (Princess Margaret Cancer Centre, University Health Network)

  • Julie Livingstone

    (Informatics & Biocomputing Program, Ontario Institute for Cancer Research)

  • Shadrielle Melijah G. Espiritu

    (Informatics & Biocomputing Program, Ontario Institute for Cancer Research)

  • Heather Thorne

    (kConFab, Peter MacCallum Cancer Centre
    The Sir Peter MacCallum Department of Oncology University of Melbourne)

  • Vincent Huang

    (Informatics & Biocomputing Program, Ontario Institute for Cancer Research)

  • Winnie Lo

    (Princess Margaret Cancer Centre, University Health Network)

  • Yu-Jia Shiah

    (Informatics & Biocomputing Program, Ontario Institute for Cancer Research)

  • Takafumi N. Yamaguchi

    (Informatics & Biocomputing Program, Ontario Institute for Cancer Research)

  • Ania Sliwinski

    (The Sir Peter MacCallum Department of Oncology University of Melbourne
    University of Melbourne, Austin Hospital)

  • Sheri Horsburgh

    (Princess Margaret Cancer Centre, University Health Network)

  • Alice Meng

    (Princess Margaret Cancer Centre, University Health Network)

  • Lawrence E. Heisler

    (Informatics & Biocomputing Program, Ontario Institute for Cancer Research)

  • Nancy Yu

    (Informatics & Biocomputing Program, Ontario Institute for Cancer Research)

  • Fouad Yousif

    (Informatics & Biocomputing Program, Ontario Institute for Cancer Research)

  • Melissa Papargiris

    (Monash Partners Comprehensive Cancer Consortium and Cancer Program Biomedicine Discovery Institute, Monash University)

  • Mitchell G. Lawrence

    (Monash Partners Comprehensive Cancer Consortium and Cancer Program Biomedicine Discovery Institute, Monash University)

  • Lee Timms

    (Genome Technologies Program, Ontario Institute for Cancer Research)

  • Declan G. Murphy

    (Peter MacCallum Cancer Centre)

  • Mark Frydenberg

    (Monash Partners Comprehensive Cancer Consortium and Cancer Program Biomedicine Discovery Institute, Monash University)

  • Julia F. Hopkins

    (Informatics & Biocomputing Program, Ontario Institute for Cancer Research)

  • Damien Bolton

    (Monash Partners Comprehensive Cancer Consortium and Cancer Program Biomedicine Discovery Institute, Monash University)

  • David Clouston

    (Urological Pathology, Tissupath)

  • John D. McPherson

    (Genome Technologies Program, Ontario Institute for Cancer Research)

  • Theodorus van der Kwast

    (Princess Margaret Cancer Centre, University Health Network)

  • Paul C. Boutros

    (Informatics & Biocomputing Program, Ontario Institute for Cancer Research
    University of Toronto
    University of Toronto)

  • Gail P. Risbridger

    (Monash Partners Comprehensive Cancer Consortium and Cancer Program Biomedicine Discovery Institute, Monash University)

  • Robert G. Bristow

    (Princess Margaret Cancer Centre, University Health Network
    University of Toronto)

Abstract

Germline mutations in the BRCA2 tumour suppressor are associated with both an increased lifetime risk of developing prostate cancer (PCa) and increased risk of aggressive disease. To understand this aggression, here we profile the genomes and methylomes of localized PCa from 14 carriers of deleterious germline BRCA2 mutations (BRCA2-mutant PCa). We show that BRCA2-mutant PCa harbour increased genomic instability and a mutational profile that more closely resembles metastastic than localized disease. BRCA2-mutant PCa shows genomic and epigenomic dysregulation of the MED12L/MED12 axis, which is frequently dysregulated in metastatic castration-resistant prostate cancer (mCRPC). This dysregulation is enriched in BRCA2-mutant PCa harbouring intraductal carcinoma (IDC). Microdissection and sequencing of IDC and juxtaposed adjacent non-IDC invasive carcinoma in 10 patients demonstrates a common ancestor to both histopathologies. Overall we show that localized castration-sensitive BRCA2-mutant tumours are uniquely aggressive, due to de novo aberration in genes usually associated with metastatic disease, justifying aggressive initial treatment.

Suggested Citation

  • Renea A. Taylor & Michael Fraser & Julie Livingstone & Shadrielle Melijah G. Espiritu & Heather Thorne & Vincent Huang & Winnie Lo & Yu-Jia Shiah & Takafumi N. Yamaguchi & Ania Sliwinski & Sheri Horsb, 2017. "Germline BRCA2 mutations drive prostate cancers with distinct evolutionary trajectories," Nature Communications, Nature, vol. 8(1), pages 1-10, April.
  • Handle: RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_ncomms13671
    DOI: 10.1038/ncomms13671
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    Cited by:

    1. Hong Yuen Wong & Quanhu Sheng & Amanda B. Hesterberg & Sarah Croessmann & Brenda L. Rios & Khem Giri & Jorgen Jackson & Adam X. Miranda & Evan Watkins & Kerry R. Schaffer & Meredith Donahue & Elizabet, 2022. "Single cell analysis of cribriform prostate cancer reveals cell intrinsic and tumor microenvironmental pathways of aggressive disease," Nature Communications, Nature, vol. 13(1), pages 1-21, December.
    2. Michael Fraser & Julie Livingstone & Jeffrey L. Wrana & Antonio Finelli & Housheng Hansen He & Theodorus van der Kwast & Alexandre R. Zlotta & Robert G. Bristow & Paul C. Boutros, 2021. "Somatic driver mutation prevalence in 1844 prostate cancers identifies ZNRF3 loss as a predictor of metastatic relapse," Nature Communications, Nature, vol. 12(1), pages 1-15, December.

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