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Circulating tumour DNA profiling reveals heterogeneity of EGFR inhibitor resistance mechanisms in lung cancer patients

Author

Listed:
  • Jacob J. Chabon

    (Institute for Stem Cell Biology and Regenerative Medicine, Stanford University
    Stanford Cancer Institute, Stanford University)

  • Andrew D. Simmons

    (Clovis Oncology, Inc.)

  • Alexander F. Lovejoy

    (Institute for Stem Cell Biology and Regenerative Medicine, Stanford University
    Stanford Cancer Institute, Stanford University)

  • Mohammad S. Esfahani

    (Institute for Stem Cell Biology and Regenerative Medicine, Stanford University
    Stanford Cancer Institute, Stanford University)

  • Aaron M. Newman

    (Institute for Stem Cell Biology and Regenerative Medicine, Stanford University
    Stanford Cancer Institute, Stanford University)

  • Henry J. Haringsma

    (Clovis Oncology, Inc.)

  • David M. Kurtz

    (Stanford University
    Stanford University)

  • Henning Stehr

    (Institute for Stem Cell Biology and Regenerative Medicine, Stanford University
    Stanford Cancer Institute, Stanford University)

  • Florian Scherer

    (Stanford Cancer Institute, Stanford University
    Stanford University)

  • Chris A. Karlovich

    (Clovis Oncology, Inc.)

  • Thomas C. Harding

    (Clovis Oncology, Inc.)

  • Kathleen A. Durkin

    (Molecular Graphics and Computation Facility, College of Chemistry, University of California)

  • Gregory A. Otterson

    (The Ohio State University)

  • W. Thomas Purcell

    (University of Colorado School of Medicine)

  • D. Ross Camidge

    (University of Colorado School of Medicine)

  • Jonathan W. Goldman

    (David Geffen School of Medicine, University of California, Los Angeles)

  • Lecia V. Sequist

    (Massachusetts General Hospital & Harvard Medical School)

  • Zofia Piotrowska

    (Massachusetts General Hospital & Harvard Medical School)

  • Heather A. Wakelee

    (Stanford University)

  • Joel W. Neal

    (Stanford University)

  • Ash A. Alizadeh

    (Institute for Stem Cell Biology and Regenerative Medicine, Stanford University
    Stanford Cancer Institute, Stanford University
    Stanford University
    Stanford University)

  • Maximilian Diehn

    (Institute for Stem Cell Biology and Regenerative Medicine, Stanford University
    Stanford Cancer Institute, Stanford University
    Stanford University)

Abstract

Circulating tumour DNA (ctDNA) analysis facilitates studies of tumour heterogeneity. Here we employ CAPP-Seq ctDNA analysis to study resistance mechanisms in 43 non-small cell lung cancer (NSCLC) patients treated with the third-generation epidermal growth factor receptor (EGFR) inhibitor rociletinib. We observe multiple resistance mechanisms in 46% of patients after treatment with first-line inhibitors, indicating frequent intra-patient heterogeneity. Rociletinib resistance recurrently involves MET, EGFR, PIK3CA, ERRB2, KRAS and RB1. We describe a novel EGFR L798I mutation and find that EGFR C797S, which arises in ∼33% of patients after osimertinib treatment, occurs in

Suggested Citation

  • Jacob J. Chabon & Andrew D. Simmons & Alexander F. Lovejoy & Mohammad S. Esfahani & Aaron M. Newman & Henry J. Haringsma & David M. Kurtz & Henning Stehr & Florian Scherer & Chris A. Karlovich & Thoma, 2016. "Circulating tumour DNA profiling reveals heterogeneity of EGFR inhibitor resistance mechanisms in lung cancer patients," Nature Communications, Nature, vol. 7(1), pages 1-15, September.
    • Handle: RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms11815
    DOI: 10.1038/ncomms11815
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    Cited by:

    1. Lavinia Tan & Chris Brown & Antony Mersiades & Chee Khoon Lee & Thomas John & Steven Kao & Genni Newnham & Kenneth O’Byrne & Sagun Parakh & Victoria Bray & Kevin Jasas & Sonia Yip & Stephen Q. Wong & , 2024. "A Phase II trial of alternating osimertinib and gefitinib therapy in advanced EGFR-T790M positive non-small cell lung cancer: OSCILLATE," Nature Communications, Nature, vol. 15(1), pages 1-13, December.

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