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Precancerous neoplastic cells can move through the pancreatic ductal system

Author

Listed:
  • Alvin P. Makohon-Moore

    (Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center)

  • Karen Matsukuma

    (University of California, Davis)

  • Ming Zhang

    (The Johns Hopkins University School of Medicine)

  • Johannes G. Reiter

    (Stanford University School of Medicine
    Harvard University)

  • Jeffrey M. Gerold

    (Harvard University)

  • Yuchen Jiao

    (The Johns Hopkins University School of Medicine)

  • Lisa Sikkema

    (Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center
    VU University Amsterdam, Master’s Oncology Program, VU University Medical Center)

  • Marc A. Attiyeh

    (Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center)

  • Shinichi Yachida

    (Graduate School of Medicine, Osaka University)

  • Corinne Sandone

    (The Johns Hopkins University School of Medicine)

  • Ralph H. Hruban

    (The Johns Hopkins University School of Medicine
    The Johns Hopkins University School of Medicine
    The Johns Hopkins University School of Medicine)

  • David S. Klimstra

    (Memorial Sloan Kettering Cancer Center)

  • Nickolas Papadopoulos

    (The Johns Hopkins University School of Medicine)

  • Martin A. Nowak

    (Harvard University
    Harvard University)

  • Kenneth W. Kinzler

    (The Johns Hopkins University School of Medicine)

  • Bert Vogelstein

    (The Johns Hopkins University School of Medicine
    The Johns Hopkins University School of Medicine
    The Johns Hopkins Kimmel Cancer Center)

  • Christine A. Iacobuzio-Donahue

    (Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center
    Memorial Sloan Kettering Cancer Center)

Abstract

Most adult carcinomas develop from noninvasive precursor lesions, a progression that is supported by genetic analysis. However, the evolutionary and genetic relationships among co-existing lesions are unclear. Here we analysed the somatic variants of pancreatic cancers and precursor lesions sampled from distinct regions of the same pancreas. After inferring evolutionary relationships, we found that the ancestral cell had initiated and clonally expanded to form one or more lesions, and that subsequent driver gene mutations eventually led to invasive pancreatic cancer. We estimate that this multi-step progression generally spans many years. These new data reframe the step-wise progression model of pancreatic cancer by illustrating that independent, high-grade pancreatic precursor lesions observed in a single pancreas often represent a single neoplasm that has colonized the ductal system, accumulating spatial and genetic divergence over time.

Suggested Citation

  • Alvin P. Makohon-Moore & Karen Matsukuma & Ming Zhang & Johannes G. Reiter & Jeffrey M. Gerold & Yuchen Jiao & Lisa Sikkema & Marc A. Attiyeh & Shinichi Yachida & Corinne Sandone & Ralph H. Hruban & D, 2018. "Precancerous neoplastic cells can move through the pancreatic ductal system," Nature, Nature, vol. 561(7722), pages 201-205, September.
    • Handle: RePEc:nat:nature:v:561:y:2018:i:7722:d:10.1038_s41586-018-0481-8
    DOI: 10.1038/s41586-018-0481-8
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    Cited by:

    1. Chung Shing Rex Ha & Martina Müller-Nurasyid & Agnese Petrera & Stefanie M Hauck & Federico Marini & Detlef K Bartsch & Emily P Slater & Konstantin Strauch, 2023. "Proteomics biomarker discovery for individualized prevention of familial pancreatic cancer using statistical learning," PLOS ONE, Public Library of Science, vol. 18(1), pages 1-21, January.
    2. Walid K. Chatila & Henry Walch & Jaclyn F. Hechtman & Sydney M. Moyer & Valeria Sgambati & David M. Faleck & Amitabh Srivastava & Laura Tang & Jamal Benhamida & Dorina Ismailgeci & Carl Campos & Fan W, 2023. "Integrated clinical and genomic analysis identifies driver events and molecular evolution of colitis-associated cancers," Nature Communications, Nature, vol. 14(1), pages 1-13, December.

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