KRAS drives immune evasion in a genetic model of pancreatic cancer

Irene Ischenko; Stephen D’Amico; Manisha Rao; Jinyu Li; Michael J. Hayman; Scott Powers; Oleksi Petrenko; Nancy C. Reich

doi:10.1038/s41467-021-21736-w

Nature Communications (Mar 2021)

KRAS drives immune evasion in a genetic model of pancreatic cancer

Irene Ischenko,
Stephen D’Amico,
Manisha Rao,
Jinyu Li,
Michael J. Hayman,
Scott Powers,
Oleksi Petrenko,
Nancy C. Reich

Affiliations

Irene Ischenko: Department of Molecular Genetics and Microbiology, Stony Brook University
Stephen D’Amico: Department of Molecular Genetics and Microbiology, Stony Brook University
Manisha Rao: Department of Pathology, Stony Brook University
Jinyu Li: Department of Pathology, Stony Brook University
Michael J. Hayman: Department of Molecular Genetics and Microbiology, Stony Brook University
Scott Powers: Department of Pathology, Stony Brook University
Oleksi Petrenko: Department of Molecular Genetics and Microbiology, Stony Brook University
Nancy C. Reich: Department of Molecular Genetics and Microbiology, Stony Brook University

DOI: https://doi.org/10.1038/s41467-021-21736-w
Journal volume & issue: Vol. 12, no. 1
pp. 1 – 15

Abstract

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Oncogenic KRAS signalling is required for tumor initiation; however KRAS-dependency at advanced stages is less understood. Here, the authors show that, in established KRAS-driven pancreatic cancer, KRAS-ablation does not affect intrinsic tumorigenic capacity but elicits antitumor immune response, highlighting the importance of KRAS-driven immune suppression in tumor maintenance.

Published in Nature Communications

ISSN: 2041-1723 (Online)
Publisher: Nature Portfolio
Country of publisher: United Kingdom
LCC subjects: Science
Website: https://www.nature.com/ncomms/

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