Imatinib Inhibits GH Secretion From Somatotropinomas.

摘要: Background: Imatinib, a tyrosine kinase inhibitor, causes growth failure in children with chronic myeloid leukemia probably by targeting the hormone (GH)/insulin like factor-1 (IGF-1) axis. We aim to explore imatinib targets expression pituitary adenomas and study effect of on GH secretion somatotropinoma cells GH3 cell line. Materials Methods: The pattern imatinib's (c-kit, VEGF, PDGFR-α/β) was studied using immunohistochemistry immunoblotting 157 giant (≥4 cm) (121 non-functioning adenomas, 32 somatotropinomas, four prolactinomas) compared normal (n = 4) obtained at autopsy. secretion, viability, immunohistochemistry, electron microscopy, apoptosis primary culture human somatotropinomas 20) rat somato-mammotroph cell-line. A receptor array applied samples identify altered pathways. Results: Somatotropinomas showed significantly higher immunopositivity for c-kit platelet-derived factor receptor-β (PDGFR-β; P < 0.009 0.001, respectively), while staining receptor-α (PDGFR-α) vascular endothelial (VEGF) revealed weaker (P 0.001) pituitary. Imatinib inhibited from both 0.01) 0.001), it did not affect viability apoptosis. that inhibits signaling via PDGFR-β pathway. Conclusion: without affecting may be used as an adjunct therapy treating secreting adenomas.