{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Michaelsen SR"],"funding":["Novo Nordisk","The Danish Cancer Society","Torben & Alice Frimodts","Danish Cancer Society","Novo Nordisk Fonden"],"pagination":["1462-1474"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6176801"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["20(11)"],"pubmed_abstract":["Background:Glioblastoma ranks among the most lethal cancers, with current therapies offering only palliation. Paracrine vascular endothelial growth factor (VEGF) signaling has been targeted using anti-angiogenic agents, whereas autocrine VEGF/VEGF receptor 2 (VEGFR2) signaling is poorly understood. Bevacizumab resistance of VEGFR2-expressing glioblastoma cells prompted interrogation of autocrine VEGF-C/VEGFR2 signaling in glioblastoma. Methods:Autocrine VEGF-C/VEGFR2 signaling was functionally investigated using RNA interference and exogenous ligands in patient-derived xenograft lines and primary glioblastoma cell cultures in vitro and in vivo. VEGF-C expression and interaction with VEGFR2 in a matched pre- and post-bevacizumab treatment cohort were analyzed by immunohistochemistry and pro"],"journal":["Neuro-oncology"],"pubmed_title":["VEGF-C sustains VEGFR2 activation under bevacizumab therapy and promotes glioblastoma maintenance."],"pmcid":["PMC6176801"],"funding_grant_id":["R148-A10151","R146-A9511","NNF17OC0026056","NNF16OC0023146"],"pubmed_authors":["Pedersen H","Nedergaard MK","Lassen U","Urup T","Broholm H","Meulengracht C","Hamerlik P","Poulsen HS","Majewski W","Brennum J","Staberg M","Skjoth-Rasmussen J","Kjær A","Lukacova S","Stockhausen MT","Jensen KE","Michaelsen SR","Villingshoj M"],"additional_accession":[]},"is_claimable":false,"name":"VEGF-C sustains VEGFR2 activation under bevacizumab therapy and promotes glioblastoma maintenance.","description":"Background:Glioblastoma ranks among the most lethal cancers, with current therapies offering only palliation. Paracrine vascular endothelial growth factor (VEGF) signaling has been targeted using anti-angiogenic agents, whereas autocrine VEGF/VEGF receptor 2 (VEGFR2) signaling is poorly understood. Bevacizumab resistance of VEGFR2-expressing glioblastoma cells prompted interrogation of autocrine VEGF-C/VEGFR2 signaling in glioblastoma. Methods:Autocrine VEGF-C/VEGFR2 signaling was functionally investigated using RNA interference and exogenous ligands in patient-derived xenograft lines and primary glioblastoma cell cultures in vitro and in vivo. VEGF-C expression and interaction with VEGFR2 in a matched pre- and post-bevacizumab treatment cohort were analyzed by immunohistochemistry and pro","dates":{"release":"2018-01-01T00:00:00Z","publication":"2018 Oct","modification":"2025-04-18T16:10:43.161Z","creation":"2019-03-27T00:02:24Z"},"accession":"S-EPMC6176801","cross_references":{"pubmed":["29939339"],"doi":["10.1093/neuonc/noy103"]}}