Open AccessChloroquine SensitizesGNAQ/11-mutated Melanoma to MEK1/2 Inhibition
Author(s) -
Amanda Truong,
Jae Hyuk Yoo,
Michael T. Scherzer,
John Michael S. Sanchez,
Kali J. Dale,
Conan G. Kinsey,
Jackson R. Richards,
Donghan Shin,
Phaedra C. Ghazi,
Michael D. Onken,
Kendall J. Blumer,
Shan J. Odelberg,
Martin McMahon
Publication year - 2020
Publication title -
clinical cancer research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.427
H-Index - 324
eISSN - 1557-3265
pISSN - 1078-0432
DOI - 10.1158/1078-0432.ccr-20-1675
Subject(s) - trametinib , gnaq , autophagy , cancer research , mapk/erk pathway , melanoma , mek inhibitor , programmed cell death , lysosome , biology , bafilomycin , cytotoxicity , pharmacology , microbiology and biotechnology , signal transduction , apoptosis , in vitro , mutation , biochemistry , gene , enzyme
Mutational activation of GNAQ or GNA11 ( GNAQ/11 ), detected in >90% of uveal melanomas, leads to constitutive activation of oncogenic pathways, including MAPK and YAP. To date, chemo- or pathway-targeted therapies, either alone or in combination, have proven ineffective in the treatment of patients with metastatic uveal melanoma.