Response to imatinib mesylate of a gastrointestinal stromal tumor with very low expression of KIT

Sebastian Bauer, Christopher L. Corless, Michael C. Heinrich, Olaf Dirsch, Gerald Antoch, Jörg Kanja, Siegfried Seeber, Jochen Schütte

Research output: Contribution to journalArticlepeer-review

77 Scopus citations


More than 90% of gastrointestinal stromal tumors (GISTs) express the receptor tyrosine kinase KIT, and activating mutations of the KIT gene are detectable in the vast majority of these tumors. Imatinib mesylate (formerly STI571) is a potent inhibitor of KIT kinase activity and has been proven to be highly active in patients with unresectable or metastatic GIST expressing immunohistochemically detectable KIT protein. Here we report a patient with metastatic GIST who responded well to imatinib mesylate treatment despite the near absence of KIT expression in two different samples of his tumor. The tumor was morphologically typical for a GIST, stained positively for CD34, and harbored an in-frame deletion (WK 557-558) in KIT exon 11 that is common in GISTs. Our experience with this patient suggests that even GISTs with very low levels of KIT expression may respond to imatinib mesylate therapy.

Original languageEnglish (US)
Pages (from-to)261-265
Number of pages5
JournalCancer Chemotherapy and Pharmacology
Issue number3
StatePublished - Mar 1 2003


  • GIST
  • Gastrointestinal stromal tumor
  • Imatinib
  • KIT immunonegativity

ASJC Scopus subject areas

  • Oncology
  • Toxicology
  • Pharmacology
  • Cancer Research
  • Pharmacology (medical)


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