The epidermal growth factor receptor (EGFR) is activated through corresponding gene amplification, and/or mutation in approximately 40% of glioblastomas, and the large subgroup of glioblastoma patients whose tumors have this molecular characteristic are thought to be excellent candidates for benefitting from EGFR-targeted therapy. However, available EGFR inhibitors have shown poor activity in treating glioblastoma patients, in large part due to poor CNS penetration. In this report, Yoshida and colleagues show that NT113, a novel pan-ERBB inhibitor, has excellent CNS penetration and activity against glioblastoma xenografts with activated EGFR, thereby supporting the clinical development of NT113 for treating this cancer.

Clinical resistance to BRAF and MEK inhibitors demonstrates the need for further drug combination approaches in melanoma. The use of AT13387, an HSP90 inhibitor currently in clinical trials, to tackle resistance was investigated. AT13387 was effective in melanoma models with acquired resistance to BRAF and MEK inhibitors, and also delayed the...

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