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Expression profiling of the adhesion G protein-coupled receptor GPR133 (ADGRD1) in glioma subtypes

BACKGROUND: Glioma is a family of primary brain malignancies with limited treatment options and in need of novel therapies. We previously demonstrated that the adhesion G protein-coupled receptor GPR133 (ADGRD1) is necessary for tumor growth in adult glioblastoma, the most advanced malignancy within...

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Detalles Bibliográficos
Autores principales: Frenster, Joshua D, Kader, Michael, Kamen, Scott, Sun, James, Chiriboga, Luis, Serrano, Jonathan, Bready, Devin, Golub, Danielle, Ravn-Boess, Niklas, Stephan, Gabriele, Chi, Andrew S, Kurz, Sylvia C, Jain, Rajan, Park, Christopher Y, Fenyo, David, Liebscher, Ines, Schöneberg, Torsten, Wiggin, Giselle, Newman, Robert, Barnes, Matt, Dickson, John K, MacNeil, Douglas J, Huang, Xinyan, Shohdy, Nadim, Snuderl, Matija, Zagzag, David, Placantonakis, Dimitris G
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Oxford University Press 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7262742/
https://www.ncbi.nlm.nih.gov/pubmed/32642706
http://dx.doi.org/10.1093/noajnl/vdaa053
Descripción
Sumario:BACKGROUND: Glioma is a family of primary brain malignancies with limited treatment options and in need of novel therapies. We previously demonstrated that the adhesion G protein-coupled receptor GPR133 (ADGRD1) is necessary for tumor growth in adult glioblastoma, the most advanced malignancy within the glioma family. However, the expression pattern of GPR133 in other types of adult glioma is unknown. METHODS: We used immunohistochemistry in tumor specimens and non-neoplastic cadaveric brain tissue to profile GPR133 expression in adult gliomas. RESULTS: We show that GPR133 expression increases as a function of WHO grade and peaks in glioblastoma, where all tumors ubiquitously express it. Importantly, GPR133 is expressed within the tumor bulk, as well as in the brain-infiltrating tumor margin. Furthermore, GPR133 is expressed in both isocitrate dehydrogenase (IDH) wild-type and mutant gliomas, albeit at higher levels in IDH wild-type tumors. CONCLUSION: The fact that GPR133 is absent from non-neoplastic brain tissue but de novo expressed in glioma suggests that it may be exploited therapeutically.