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http://purl.uniprot.org/citations/23530240http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/23530240http://www.w3.org/2000/01/rdf-schema#comment"Granulocyte-colony stimulating factor (G-CSF) promotes mobilization of CD11b(+)Gr1(+) myeloid cells and has been implicated in resistance to anti-VEGF therapy in mouse models. High G-CSF production has been associated with a poor prognosis in cancer patients. Here we show that activation of the RAS/MEK/ERK pathway regulates G-CSF expression through the Ets transcription factor. Several growth factors induced G-CSF expression by a MEK-dependent mechanism. Inhibition of G-CSF release with a MEK inhibitor markedly reduced G-CSF production in vitro and synergized with anti-VEGF antibodies to reduce CD11b(+)Ly6G(+) neutrophil mobilization and tumor growth and led to increased survival in animal models of cancer, including a genetically engineered mouse model of pancreatic adenocarcinoma. Analysis of biopsies from pancreatic cancer patients revealed increased phospho-MEK, G-CSF, and Ets expression and enhanced neutrophil recruitment compared with normal pancreata. These results provide insights into G-CSF regulation and on the mechanism of action of MEK inhibitors and point to unique anticancer strategies."xsd:string
http://purl.uniprot.org/citations/23530240http://purl.org/dc/terms/identifier"doi:10.1073/pnas.1303302110"xsd:string
http://purl.uniprot.org/citations/23530240http://purl.uniprot.org/core/author"Song Q."xsd:string
http://purl.uniprot.org/citations/23530240http://purl.uniprot.org/core/author"Tan M."xsd:string
http://purl.uniprot.org/citations/23530240http://purl.uniprot.org/core/author"Wu X."xsd:string
http://purl.uniprot.org/citations/23530240http://purl.uniprot.org/core/author"Zhuang G."xsd:string
http://purl.uniprot.org/citations/23530240http://purl.uniprot.org/core/author"Meng Y.G."xsd:string
http://purl.uniprot.org/citations/23530240http://purl.uniprot.org/core/author"Ferrara N."xsd:string
http://purl.uniprot.org/citations/23530240http://purl.uniprot.org/core/author"Chung A.S."xsd:string
http://purl.uniprot.org/citations/23530240http://purl.uniprot.org/core/author"Junttila M.R."xsd:string
http://purl.uniprot.org/citations/23530240http://purl.uniprot.org/core/author"Tran C."xsd:string
http://purl.uniprot.org/citations/23530240http://purl.uniprot.org/core/author"Cheng J.H."xsd:string
http://purl.uniprot.org/citations/23530240http://purl.uniprot.org/core/author"Kowanetz M."xsd:string
http://purl.uniprot.org/citations/23530240http://purl.uniprot.org/core/author"Peale F.V."xsd:string
http://purl.uniprot.org/citations/23530240http://purl.uniprot.org/core/author"Phan V.T."xsd:string
http://purl.uniprot.org/citations/23530240http://purl.uniprot.org/core/author"Jackson E.L."xsd:string
http://purl.uniprot.org/citations/23530240http://purl.uniprot.org/core/author"Sambrone A."xsd:string
http://purl.uniprot.org/citations/23530240http://purl.uniprot.org/core/author"Sheng R.X."xsd:string
http://purl.uniprot.org/citations/23530240http://purl.uniprot.org/core/date"2013"xsd:gYear
http://purl.uniprot.org/citations/23530240http://purl.uniprot.org/core/name"Proc Natl Acad Sci U S A"xsd:string
http://purl.uniprot.org/citations/23530240http://purl.uniprot.org/core/pages"6079-6084"xsd:string
http://purl.uniprot.org/citations/23530240http://purl.uniprot.org/core/title"Oncogenic RAS pathway activation promotes resistance to anti-VEGF therapy through G-CSF-induced neutrophil recruitment."xsd:string
http://purl.uniprot.org/citations/23530240http://purl.uniprot.org/core/volume"110"xsd:string
http://purl.uniprot.org/citations/23530240http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/23530240