How does imatinib work?

Focusing on GIST, the effect of imatinib (Gleevec) is to stop the cell-proliferation actions of the KIT and PDGFRA tyrosine kinases. These are growth factor receptors that initiate a signaling pathway causing the cell to proliferate (reproduce through cell division). When GIST cells divide, the tumor gets larger.

This signaling normally occurs only when KIT or PDGFRA receptors are triggered by molecules called ligands. The ligand for KIT is stem cell factor, and the ligand for PDGFRA is platelet-derived growth factor (PDGF). However, when the genes for these receptors are mutated, then the proteins are abnormally constructed, and they activate signaling without being stimulated by their ligands (constitutive activation).

This abnormal growth signaling causes the GI stromal tumor to develop and keep enlarging. You can refer to our website page Mutation Analysis: KIT and PDGFRA for a more detailed discussion. Imatinib binds the intracellular activation pocket of the receptor in the ...

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