The biological underpinnings of therapeutic resistance in pancreatic cancer

  1. Diane M. Simeone3,4,8,10
  1. 1Abramson Cancer Center; University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA;
  2. 2Division of Hematology-Oncology, Department of Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA;
  3. 3Department of Surgery, New York University School of Medicine, New York, New York 10016, USA;
  4. 4Perlmutter Cancer Center, New York University Langone Medical Center, New York, New York 10016, USA;
  5. 5Department of Molecular and Integrative Physiology, Division of Gastroenterology and Hepatology, University of Michigan, Ann Arbor, Michigan 48109, USA;
  6. 6Department of Internal Medicine, Division of Gastroenterology and Hepatology, University of Michigan, Ann Arbor, Michigan 48109, USA;
  7. 7Rogel Cancer Center, University of Michigan, Ann Arbor, Michigan 48109, USA;
  8. 8Department of Pathology, New York University School of Medicine, New York, New York 10016, USA
  1. Corresponding authors: diane.simeone{at}nyulangone.org, gregory.beatty{at}pennmedicine.upenn.edu
  1. 9 These authors contributed equally to this work.

  2. 10 These authors contributed equally to this work.

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is a leading cause of cancer-related mortality in the United States and has only recently achieved a 5-yr survival rate of 10%. This dismal prognosis reflects the remarkable capacity of PDAC to effectively adapt to and resist therapeutic intervention. In this review, we discuss recent advances in our understanding of the biological underpinnings of PDAC and their implications as targetable vulnerabilities in this highly lethal disease.

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Footnotes

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