In This Issue
Cancer Discov October 1 2016 6 (10) 1069-1071; DOI:10.1158/2159-8290.CD-ITI6-10
Venetoclax monotherapy has clinical activity and is generally well tolerated in patients with heavily pretreated AML, and BCL2 dependence and lack of BCL-XL and MCL1 dependence predicted the best response.
Molecular mechanisms of resistance to ALK inhibitors were characterized in ALK-positive lung cancer.
PIM kinases promote resistance to PI3K inhibition in PIK3CA-mutant breast cancer by activating downstream PI3K effectors in an AKT-independent manner.
Integrin-α10 drives high-grade myxofibrosarcoma growth and survival by interacting with TRIO and RICTOR, which are commonly overexpressed in this disease, to activate RAC and AKT signaling.
MLL1 and DOT1L regulate expression of HOX, MEIS1, and FLT3 to suppress differentiation and promote NPM1-mutant leukemogenesis and are potential therapeutic targets.
Inflammatory monocytes in the tumor microenvironment induce a subset of IFNγ-producing IL21+ T helper cells that promote B-cell maturation, which subsequently stimulates protumorigenic macrophage polarization.