An in Vivo shRNA-Drug Screen to Identify Novel Targeted Therapy Combinations for KRAS Mutant Cancers

Abstract

KRAS mutations occur in ~90% of all pancreatic cancers and in ~20% of all human cancers, but no effective therapies targeting KRAS have been developed. We proposed a functional genomic screen to identify gene targets that, when inhibited, cooperate with MEK inhibitors (which block signaling through the MAPK pathway, a key KRAS effector) to kill KRAS mutant pancreatic cancer cells in order to develop novel therapeutic combinations for these cancers. Our efforts identified several components within the MAPK pathway that can lead to feedback reactivation of MAPK signaling despite the presence of MEK inhibitors, creating a key vulnerability of MEK inhibitors that can lead to resistance. Importantly, we found that ERK inhibitors (which block downstream of MEK inhibitors) could overcome MAPK reactivation and produced enhanced efficacy. Our efforts also identified multiple members of a metabolic and autophagy-regulating pathway, suggesting that autophagy inhibitors (currently in clinical trials for pancreatic cancer) in combination with MAPK inhibitors may be a promising approach. We expect these data to drive new clinical trials for pancreatic cancer patients.

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Document Details

Document Type
Technical Report
Publication Date
Dec 01, 2014
Accession Number
ADA620992

Entities

People

  • Ryan B. Corcoran

Organizations

  • Massachusetts General Hospital

Tags

DTIC Thesaurus Topics

  • Autophagy
  • Biomedical Research
  • Cancer
  • Cell Line
  • Cells
  • Clinical Trials
  • Feedback
  • Health Services
  • Inhibition
  • Inhibitors
  • Mutations
  • Neoplasms
  • Resistance
  • Standards
  • Targeting
  • Targets
  • Therapy

Fields of Study

  • Biology
  • Medicine

Readers

  • Cellular and Molecular Pathways of Apoptosis.
  • Oncology