Journal article

Activation of ERBB4 in Glioblastoma Can Contribute to Increased Tumorigenicity and Influence Therapeutic Response

Jacqueline F Donoghue, Lauren T Kerr, Naomi W Alexander, Sameer A Greenall, Anthony B Longano, Nicholas G Gottardo, Rong Wang, Viviane Tabar, Timothy E Adams, Paul S Mischel, Terrance G Johns

CANCERS | MDPI | Published : 2018

Abstract

Glioblastoma (GBM) is often resistant to conventional and targeted therapeutics. ErbB2 Receptor Tyrosine Kinase 4 (ERBB4) is expressed throughout normal brain and is an oncogene in several pediatric brain cancers; therefore, we investigated ERBB4 as a prognostic marker and therapeutic target in GBM. Using RT-qPCR, we quantified mRNA encoding total ERBB4 and known ERBB4 variants in GBM and non-neoplastic normal brain (NNB) samples. Using immunohistochemistry, we characterized the localization of total and phosphorylated ERBB4 (p-ERBB4) and EGFR protein in archived GBM samples and assessed their association with patient survival. Furthermore, we evaluated the effect of ERBB4 phosphorylation on..

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Grants

Funding Acknowledgements

This work was supported by funding from the Victorian Cancer Agency (J.F.D.) and the Victorian Government's Operational Infrastructure Support Program. J.F.D. and T.G.J. are members of the Brain Cancer Discovery Collaborative, which is supported by Cure Brain Cancer Foundation. Panitumumab was supplied by Amgen, and dacomitinib was supplied by Pfizer through a grant-in-aid. TGJ is a Principal Research Fellow with the National Health and Medical Research Council of Australia.