Secondary C-kit mutation is a cause of acquired resistance to imatinib in gastrointestinal stromal tumor

Scand J Gastroenterol. 2009;44(6):760-3. doi: 10.1080/00365520802647459.

Abstract

C-kit gene gain of function mutations are important in the pathogenesis of gastrointestinal stromal tumors (GISTs). Imatinib is a selective tyrosine kinase inhibitor of KIT and achieves a partial response or stable disease in most patients with metastatic GIST, but there is increasing evidence of acquired resistance. We report a case of GIST with acquired resistance to imatinib during therapy and secondary c-kit mutation besides the primary mutation.

Publication types

  • Case Reports

MeSH terms

  • Aged
  • Benzamides
  • Drug Resistance, Neoplasm / genetics*
  • Gastrointestinal Stromal Tumors / drug therapy*
  • Humans
  • Imatinib Mesylate
  • Male
  • Mutation
  • Piperazines / pharmacology*
  • Protein Kinase Inhibitors / pharmacology*
  • Proto-Oncogene Proteins c-kit / genetics*
  • Pyrimidines / pharmacology*

Substances

  • Benzamides
  • Piperazines
  • Protein Kinase Inhibitors
  • Pyrimidines
  • Imatinib Mesylate
  • Proto-Oncogene Proteins c-kit