Overexpression and activation of epidermal growth factor receptor in hemangioblastomas |
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Authors: | Gregory J Chen Matthias A Karajannis Elizabeth W Newcomb " target="_blank">David Zagzag |
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Institution: | (1) Department of Pathology, New York University School of Medicine, New York, NY, USA;(2) Department of Pediatrics, New York University School of Medicine, New York, NY, USA;(3) New York University Cancer Institute, New York University School of Medicine, New York, NY, USA;(4) Microvascular and Molecular Neuro-Oncology Laboratory, New York University School of Medicine, New York, NY, USA;(5) Division of Neuropathology, New York University School of Medicine, New York, NY, USA; |
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Abstract: | Hemangioblastomas frequently develop in patients with von Hippel-Lindau (VHL) disease, an autosomal dominant genetic disorder.
The tumors are characterized by a dense network of blood capillaries, often in association with cysts. Although activation
of receptor tyrosine kinase (RTK) signaling, including epidermal growth factor receptor (EGFR) has been implicated in the
development of malignant brain tumors such as high-grade gliomas, little is known about the role of RTK signaling in hemangioblastomas.
To address this issue, we examined hemangioblastoma tumor specimens using receptor tyrosine kinase (RTK) activation profiling
and immunohistochemistry. Six human hemangioblastomas were analyzed with a phospho-RTK antibody array, revealing EGFR phosphorylation
in all tumors. EGFR expression was confirmed by immunohistochemistry in all tumors analyzed and downstream effector pathway
activation was demonstrated by positive staining for phospho-AKT. Our findings suggest that, in primary hemangioblastomas,
RTK upregulation and signaling predominantly involves EGFR, providing an attractive molecular target for therapeutic intervention. |
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