In This Issue
Cancer Discov March 1 2017 7 (3) 235-237; DOI:10.1158/2159-8290.CD-ITI7-3
Patients with FGFR2 fusion–positive ICC develop resistance to the FGFR inhibitor BGJ398 through acquisition of multiple recurrent point mutations in FGFR2 that can be overcome by structurally distinct FGFR inhibitors.
Acquired resistance to immune checkpoint inhibitors is accompanied by elimination of a subset of immunogenic mutation-associated neoantigens.
ESR1 mutations were characterized and assessed for constitutive activity and sensitivity to ER antagonists.
OTX2 is a pioneer transcription factor that occupies the majority of active enhancers in Group 3 medulloblastoma and, in cooperation with NEUROD1, maintains their activation state.
Treatment with the MEK inhibitor trametinib induces an epigenetic upregulation of receptor tyrosine kinases to promote resistance in TNBC cells that can be overcome by inhibition of BRD4 or P-TEFb.
CREBBP regulates germinal center B-cell enhancers for normal B-cell differentiation, and CREBBP haploinsufficiency cooperates with BCL2 dysregulation to promote B-cell lymphoma.