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

Russell Moser¹, James Annis², Olga Nikolova³, Cliff Whatcott⁴, Kay Gurley¹, Eduardo Mendez⁵, Kim Moran-Jones⁶, Craig Dorrell⁷, Rosalie C Sears⁷, Calvin Kuo⁸, Haiyong Han⁴, Andrew Biankin⁴, Carla Grandori⁹, Daniel D Von Hoff⁴, Christopher J Kemp¹

¹Division of Human Biology, Fred Hutchinson Cancer Research Center, Seattle, Washington.

²Quellos High Throughput Facility, Institute for Stem Cell and Regenerative Medicine, University of Washington Medicine Research, Seattle, Washington.

³Department of Computational Biology, Oregon Health and Science University, Portland, Oregon.

⁴Translational Genomics Research Institute, Molecular Medicine Division, Phoenix, Arizona.

⁵Division of Clinical Research, Fred Hutchinson Cancer Research Center, Seattle, Washington.

⁶Wolfson Wohl Cancer Research Centre, Institute of Cancer Sciences, University of Glasgow, Glasgow, United Kingdom.

⁷Brenden-Colson Center for Pancreatic Care, Oregon Health and Science University, Portland, Oregon.

⁸Department of Medicine, Division of Hematology, Stanford University School of Medicine, Stanford, California.

⁹SEngine Precision Medicine, Seattle, Washington.

PubMed PMC DOI PDF

Abstract

Pancreatic ductal adenocarcinoma (PDAC) typically presents as metastatic disease at diagnosis and remains refractory to treatment. Next-generation sequencing efforts have described the genomic landscape, classified molecular subtypes, and confirmed frequent alterations in major driver genes, with coexistent alterations in KRAS and TP53 correlating with the highest metastatic burden and poorest out…

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