In This Issue
Cancer Discov January 1 2016 6 (1) 1-3; DOI:10.1158/2159-8290.CD-ITI6-1
Analyses of liquid biopsies and xenotransplanted patient tumors identify point mutations in the catalytic domain of TRKA as a mechanism of acquired resistance to the pan-TRK kinase inhibitor entrectinib.
The MECP2 oncogene is amplified in multiple tumor types, promotes transformation by binding to epigenetically modified cytosines, and has functional redundancy with oncogenic KRAS.
Dual treatment with an mTORC1 inhibitor and rDNA transcription inhibitor induces apoptosis via distinct mechanisms and is more effective than single-agent therapy in MYC-driven lymphoma.
BATF3 is essential for dendritic cell cross-priming of CD8+ T cells and synergizes with anti-CD137 and anti-PD1 monoclonal antibodies for effective immunostimulatory immunotherapy.
YAP1 activation in prostate cancer cells promotes MDSC infiltration and tumor progression via upregulation of the CXCL5–CXCR2 axis.
The ALK inhibitor PF-06463922 is more potent as a single agent than crizotinib against ALK variants in neuroblastoma.