Increased Epithelial Membrane Protein 2 (EMP2) Expression in Glioblastoma After Treatment With Bevacizumab. (16th November 2020)

• Record Type: Journal Article
• Authors: Patel, Kunal S; Kejriwal, Sameer; Duong, Courtney; Yang, Isaac; Wadehra, Madhuri
• Is Part Of: Neurosurgery. Volume 67(2010)Supplement 1
• Publication Date: 2020-11-16
• Subjects: Nervous system -- Surgery -- Periodicals; 617.48005
• DOI: 10.1093/neuros/nyaa447_870
• Languages: English
• ISSNs: 0148-396X

Abstract

Abstract: INTRODUCTION: Anti-angiogenic therapy with bevacizumab has failed to provide substantial gains in overall survival. Epithelial membrane protein 2 (EMP2) is a cell surface protein associated with angiogenesis in glioblastoma in cell line experiments. The relationship between bevacizumab, the VEGF pathway, and EMP2 is not clear. METHODS: Tumor samples were obtained 12 patients with newly diagnosed glioblastoma at two time points: 1) at initial surgery 2) at subsequent surgery for recurrent tumor after bevacizumab treatment. Tumor samples were stained for EMP2 expression. Clinical characteristics and survival data from these patients were collected. The IVY glioblastoma atlas project database was used to evaluate EMP2 expression levels in 270 samples by differing histological areas of tumor. RESULTS: Patients with high EMP2 staining at initial diagnosis had decreased progression free and overall survival after bevacizumab [median progression free survival 4.6 months vs. 5.9 months; Log-Rank P = .076 & overall survival 7.7 months vs. 14.4 months; Log-Rank P = .011]. There was increased EMP2 staining in samples obtained after bevacizumab treatment in both unpaired [Mean H-score 2.31 vs 1.76; P = .006] and paired analyses [Mean difference 0.571; P = .019]. This expression increase correlated with length of bevacizumab therapy [R 2 = 0.449; Pearson P = .024]. CONCLUSION: Elevations in EMP2 levels are associated with decreases in survival with bevacizumab therapy. After bevacizumab treatment, EMP2 protein expression increases. We hypothesize a role of EMP2 in clinical bevacizumab resistance and potential anti-angiogenic therapeutic target in glioblastoma.