In This Issue
Cancer Discov September 1 2019 9 (9) 1143-1146; DOI:10.1158/2159-8290.CD-ITI9-9
A previously uncharacterized mutation in mitogen-activated protein kinase 1 (MEK1) is activating and resistant to allosteric MEK inhibitors, but sensitive to ATP-competitive inhibitors.
Myeloproliferative neoplasm–associated calreticulin mutations elicit T-cell responses that can be promoted by immune checkpoint blockade with pembrolizumab.
Immune dysfunction associated with age in a mouse model of TNBC leads to lack of response to immune checkpoint blockade treatment that can be rescued by the addition of a STING agonist.
Knockout of the PRC2 component EZH2 and activating NRAS mutations cooperate to cause MPN progression to leukemia by upregulating the BCAA-metabolism enzyme BCAT1.
Glioma stem cells upregulate the polyunsaturated synthesis enzyme ELOVL2, which alters cell-membrane properties and composition to maintain EGFR signaling.
Activating Kras mutations cause upregulation of the mitophagy-promoting protein NIX, which alters mitochondrial function and enhances redox capacity to support progression of pancreatic cancer.
Innate αβ T cells are a significant component of the tumor microenvironment in pancreatic ductal adenocarcinoma and delay tumor growth in mouse and human models.
Efficient repair of DNA double-strand breaks depends on NSD2-mediated dimethylation of PTEN and its interaction with p53-binding protein 1.