In This Issue
Cancer Discov April 1 2016 6 (4) 331-333; DOI:10.1158/2159-8290.CD-ITI6-4
Mutant CALR alone is sufficient to induce myeloproliferative neoplasia and requires the mutant CALR C-terminus to transform cells via a thrombopoietin receptor–dependent activation of JAK–STAT signaling.
Kinase inhibitors reduce proteolytic shedding of surface receptors to enhance bypass signaling–induced resistance.
Activation of monocyte/macrophage-dependent antifibrotic activity can potentiate gemcitabine efficacy in PDAC, and tumor fibrosis is a bidirectional process that can be reversed by regulating tumor-infiltrating monocytes.
In the absence of STAT5, NK cells secrete elevated levels of the angiogenic factor VEGFA, enhancing angiogenesis and promoting tumor formation.
CBP and p300 exhibit synthetic lethality, whereby the loss or inhibition of the CBP paralog p300 in CBP-deficient cancers leads to cell death via downregulation of MYC.
Monoclonal antibodies against CD96 inhibit metastasis by enhancing cytotoxic NK cell activity and may be used in combination with other immunotherapeutic and chemotherapeutic agents.