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Braking the cell’s cycle and invigorating T-cell immunity against pancreatic cancer
  1. Gregory B Lesinski
  1. Hematology and Medical Oncolgy, Emory University, Atlanta, Georgia, USA
  1. Correspondence to Dr Gregory B Lesinski, Hematology and Medical Oncolgy, Emory University, Atlanta GA 30322, Georgia, USA; gregory.b.lesinski{at}emory.edu

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Pancreatic cancer has been an elusive target for immunotherapy. Redundant mechanisms of immune suppression have plagued efforts to elicit vigorous T-cell responses to this disease. Similar frustrations are evident in pancreatic cancer when considering efforts at targeting prominent oncogenic pathways. For example, cyclin-dependent kinase inhibitor 2A is very frequently mutated, suggesting that inhibition of cyclin-dependent kinase 4/6 (CDK4/6) may be a viable strategy against these aggressive tumours.1 Unfortunately, resistance to targeting single oncogenic pathways typically prevails, necessitating a need for combination therapy. The choice of optimal combination approaches, however, is not a simple one. Of course, decisions must be carefully metered by preclinical efficacy data, on-target and off-target toxicities, patient selection and insight into mechanisms of action. These considerations may be even more relevant when combining tumour-directed, small molecule inhibitors with immunotherapy.

The article by Knudsen et al2 addresses these issues by employing a data-driven approach to identify novel combinatorial therapies for pancreatic cancer. Their strategy was to systematically define other agents that cooperate with CDK4/6 inhibitors using a live cell imaging-based in …

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Footnotes

  • Twitter @LesinskiLab

  • Contributors GBL wrote the manuscript.

  • Funding This study was supported by National Institutes of Health (NIH) grants R01CA208253, R01CA228406 and P30CA138292. The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH.

  • Competing interests GBL has consulted for ProDa Biotech, LLC, and received compensation. The terms of this arrangement have been reviewed and approved by Emory University in accordance with its conflict of interest policies. GBL has received research funding through a sponsored research agreement between Emory University and Merck and Co, Bristol-Myers Squibb, Boerhinger-Ingelheim and Vaccinex.

  • Patient and public involvement Patients and/or the public were not involved in the design, conduct, reporting or dissemination plans of this research.

  • Patient consent for publication Not required.

  • Provenance and peer review Commissioned; internally peer reviewed.

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