Rerouting the drug response: overcoming metabolic adaptation in KRAS-mutant cancers

Deborah Y. Moss, Christopher McCann, Emma M. Kerr*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

2 Citations (Scopus)

Abstract

Mutations in guanosine triphosphatase KRAS are common in lung, colorectal, and pancreatic cancers. The constitutive activity of mutant KRAS and its downstream signaling pathways induces metabolic rewiring in tumor cells that can promote resistance to existing therapeutics. In this review, we discuss the metabolic pathways that are altered in response to treatment and those that can, in turn, alter treatment efficacy, as well as the role of metabolism in the tumor microenvironment (TME) in dictating the therapeutic response in KRAS-driven cancers. We highlight metabolic targets that may provide clinical opportunities to overcome therapeutic resistance and improve survival in patients with these aggressive cancers.

Original languageEnglish
Article numbereabj3490
JournalScience Signaling
Volume15
Issue number756
DOIs
Publication statusPublished - 18 Oct 2022

Keywords

  • Tumor Microenvironment - genetics
  • Proto-Oncogene Proteins p21(ras) - genetics - metabolism
  • Guanosine
  • Mutation
  • Cell Line, Tumor
  • Pancreatic Neoplasms - drug therapy - genetics - metabolism
  • Humans
  • Signal Transduction

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