Pharmacologic Targeting of TFIIH Suppresses KRAS-Mutant Pancreatic Ductal Adenocarcinoma and Synergizes with TRAIL

  • Cancer Res. 2022 Sep 16;82(18):3375-3393. doi: 10.1158/0008-5472.CAN-21-4222.
Russell Moser  1 ,  James Annis  2 ,  Olga Nikolova  3 ,  Cliff Whatcott  4 ,  Kay Gurley  1 ,  Eduardo Mendez  5 ,  Kim Moran-Jones  6 ,  Craig Dorrell  7 ,  Rosalie C Sears  7 ,  Calvin Kuo  8 ,  Haiyong Han  4 ,  Andrew Biankin  4 ,  Carla Grandori  9 ,  Daniel D Von Hoff  4 ,  Christopher J Kemp  1
Affiliations
  • 1. Division of Human Biology, Fred Hutchinson Cancer Research Center, Seattle, Washington.
  • 2. Quellos High Throughput Facility, Institute for Stem Cell and Regenerative Medicine, University of Washington Medicine Research, Seattle, Washington.
  • 3. Department of Computational Biology, Oregon Health and Science University, Portland, Oregon.
  • 4. Translational Genomics Research Institute, Molecular Medicine Division, Phoenix, Arizona.
  • 5. Division of Clinical Research, Fred Hutchinson Cancer Research Center, Seattle, Washington.
  • 6. Wolfson Wohl Cancer Research Centre, Institute of Cancer Sciences, University of Glasgow, Glasgow, United Kingdom.
  • 7. Brenden-Colson Center for Pancreatic Care, Oregon Health and Science University, Portland, Oregon.
  • 8. Department of Medicine, Division of Hematology, Stanford University School of Medicine, Stanford, California.
  • 9. SEngine Precision Medicine, Seattle, Washington.
PMID: 35819261 DOI: 10.1158/0008-5472.CAN-21-4222
Abstract

This study utilizes functional genetic and pharmacological profiling of KRAS-mutant pancreatic adenocarcinoma to identify therapeutic strategies and finds that TFIIH inhibition synergizes with TRAIL to induce Apoptosis in KRAS-driven pancreatic Cancer.

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