Myosin light chain kinase inhibition potentiates the anti-tumor effects of avapritinib in PDGFRA D842V-mutant gastrointestinal stromal tumor.

Ferdinando Rossi Mengyuan Liu Andrew D Tieniber Mark S Etherington Andrew N Hanna Gerardo A Vitiello Nesteene J Param Kevin J Do Laura Wang Cristina R Antonescu Shan Zeng Jennifer Q Zhang Ronald P DeMatteo

Published in: Clinical cancer research : an official journal of the American Association for Cancer Research (2023)

MYLK upregulation is a novel mechanism of tumor persistence after tyrosine kinase inhibition. Concomitant MYLK inhibition may enable the use of a lower dose of avapritinib, which is associated with dose-dependent cognitive side effects.

Keyphrases

tyrosine kinase
epidermal growth factor receptor
poor prognosis
signaling pathway
cell proliferation
protein kinase
long non coding rna