TRKing down drug resistance in NTRK fusion-positive cancers

J Pathol. 2024 Oct;264(2):129-131. doi: 10.1002/path.6341. Epub 2024 Jul 29.

Abstract

In a recent issue of The Journal of Pathology, Chen and colleagues established novel patient-derived ex vivo models of NTRK fusion-positive soft tissue sarcoma to characterize resistance mechanisms against targeted therapy with tyrosine kinase inhibitors. Prolonged exposure to escalating concentrations of the tyrosine kinase inhibitor, entrectinib, ultimately led to the occurrence of resistant clones that harbored an inactivating mutation in the NF2 gene, not previously described in this context, accompanied by increased PI3K/AKT/mTOR and Ras/Raf/MEK/ERK signaling. Finally, an inhibitor screen identified, among others, MEK and mTOR inhibitors as potential combination agents. © 2024 The Pathological Society of Great Britain and Ireland.

Keywords: NF2; patient‐derived ex vivo cell model; therapy resistance; tyrosine kinase inhibitor.

Publication types

  • Comment

MeSH terms

  • Antineoplastic Agents / pharmacology
  • Antineoplastic Agents / therapeutic use
  • Benzamides / pharmacology
  • Benzamides / therapeutic use
  • Drug Resistance, Neoplasm* / genetics
  • Humans
  • Indazoles / pharmacology
  • Indazoles / therapeutic use
  • Mutation
  • Neurofibromin 2 / genetics
  • Oncogene Proteins, Fusion / genetics
  • Protein Kinase Inhibitors* / pharmacology
  • Protein Kinase Inhibitors* / therapeutic use
  • Receptor, trkA / genetics
  • Receptor, trkA / metabolism
  • Sarcoma / drug therapy
  • Sarcoma / genetics
  • Sarcoma / pathology
  • Signal Transduction / genetics
  • TOR Serine-Threonine Kinases / genetics
  • TOR Serine-Threonine Kinases / metabolism

Substances

  • Protein Kinase Inhibitors
  • Neurofibromin 2
  • Oncogene Proteins, Fusion
  • entrectinib
  • NF2 protein, human
  • Benzamides
  • Receptor, trkA
  • Indazoles
  • Antineoplastic Agents
  • TOR Serine-Threonine Kinases