In This Issue
Cancer Discov May 1 2013 3 (5) 471-473; DOI:10.1158/2159-8290.CD-ITI13-05
Histone variant H3.3 glycine-34 mutations induce differential genome-wide histone H3 lysine 36 trimethylation and lead to upregulation of MYCN in the developing forebrain.
Lineage-specific HER3 upregulation and ligand-dependent HER2/HER3 activation confer resistance to MAPK pathway inhibitors in BRAF-mutant thyroid cancer cells.
Transcriptional derepression of PDGFRβ in response to EGFR inhibition renders EGFR-mutant glioblastomas dependent on PDGFRβ for survival.
KRAS-mutant NSCLC cells are selectively sensitive to inhibition of IGF1R, which is required for KRAS-mediated activation of PI3K signaling.
Activation of tyrosine kinase 2 (TYK2) by mutation or autocrine interleukin-10 signaling promotes T-ALL cell survival through activation of STAT1 and upregulation of BCL2.
Metastasis-incompetent tumors systemically reprogram bone marrow–derived myeloid cells in the premetastatic niche to produce TSP-1 to suppress metastatic outgrowth.