In This Issue
Cancer Discov December 1 2018 8 (12) 1494-1497; DOI:10.1158/2159-8290.CD-ITI8-12
RET fusions were detected in patients with EGFR-mutant NSCLC who developed resistance to EGFR inhibition, and targeting RET in combination with EGFR inhibition produced responses in two patients.
IDH1- or IDH2-mutant acute myeloid leukemia and solid tumors can develop resistance to isoform-selective IDH inhibition through mutation of the other IDH isoform.
Comprehensive, multiplatform genomic analyses of malignant pleural mesothelioma characterize a near-haploid molecular subtype, define prognostic molecular subsets, and identify high expression of VISTA in the epithelioid subtype.
An identified MCL1 inhibitor induced apoptosis in AML cells and was safely combined with BCL2 inhibition to overcome BCL2 inhibitor resistance and enhance antitumor activity in mouse models of AML.
Drug discovery and optimization yielded the selective MCL1 inhibitor AMG 176, which induced apoptosis in cells from hematologic malignancies in vitro and in vivo and could be combined with other therapies.
Dual inhibition of MCL1 and MEK induces apoptosis and tumor regression in KRAS-mutant models of NSCLC, and BCL-xL inhibition may enhance sensitivity to MCL1 inhibition.
SYNCRIP and SNHG5 haploinsufficiency increases leukemic-initiating cell activity and drives del(6q) T-ALL progression by reducing the translation efficiency of transcripts involved in mitochondrial respiration.
Somatic loss-of-function mutation of TET2 reduces enhancer hydroxymethylation to suppress genes that promote exit of B-cells from germinal centers and is a driving event in DLBCL.