Systemic therapy for advanced gastrointestinal stromal tumors: Beyond imatinib

Edward Kim, Mark M. Zalupski

Research output: Contribution to journalArticle

15 Citations (Scopus)

Abstract

Progression on first-line therapy with imatinib in gastrointestinal stromal tumors (GIST) is caused by either initial resistance or more often a secondary mutation in tyrosine kinases KIT or PDGFR. Therapies in development for imatinib-resistant GIST include agents that target KIT/PDGFR with greater potency or possess broader kinase inhibition profiles including VEGFR. To circumvent secondary mutations in KIT/PDGFR, inhibition of the downstream signaling in PI3K/Akt/mTOR pathway and enhanced degradation of KIT/PDGFR are also under investigation. J. Surg. Oncol. 2011; 104:901-906.

Original languageEnglish (US)
Pages (from-to)901-906
Number of pages6
JournalJournal of Surgical Oncology
Volume104
Issue number8
DOIs
StatePublished - Dec 2011
Externally publishedYes

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Gastrointestinal Stromal Tumors
Mutation
Phosphatidylinositol 3-Kinases
Protein-Tyrosine Kinases
Phosphotransferases
Therapeutics
Imatinib Mesylate

Keywords

  • GIST
  • KIT PDGFR
  • tyrosine kinase inhibitors

ASJC Scopus subject areas

  • Surgery
  • Oncology

Cite this

Systemic therapy for advanced gastrointestinal stromal tumors : Beyond imatinib. / Kim, Edward; Zalupski, Mark M.

In: Journal of Surgical Oncology, Vol. 104, No. 8, 12.2011, p. 901-906.

Research output: Contribution to journalArticle

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