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| Content Provider | PubMed Central |
|---|---|
| Author | Roberts, Callie Chagoya, Gustavo Nanni, Cory Madan, Kwatra |
| Copyright Year | 2014 |
| Abstract | Amplification of the EGFR gene and subsequent overexpression of EGFR is seen in about 40% of glioblastomas. Over 50% of these glioblastomas with overexpressed EGFR also contain a variant of EGFR, known as EGFRvIII, which lacks amino acids 30-297 in its extracellular domain. Key features of EGFRvIII include a lack of binding to EGF and constitutive tyrosine kinase activity. Because EGFRvIII occurs in more than 20% of glioblastoma patients and is not present in normal brain cells, extensive efforts are being made to understand how EGFRvIII functions. Toward this goal, we recently characterized a panel of twenty patient-derived xenografts (PDGX) using a proteomics approach. This analysis revealed that seven out of the twenty PDGX expressed activated EGFR. Among those seven, three were EGFRvIII positive. A comparison of the proteomic profile of the four PDGX with activated EGFR that was not EGFRvIII with the proteomic profile of the three PDGX that expressed EGFRvIII revealed several differences. The most notable difference was the upregulation of beta-catenin. This discovery provides a novel target against EGFRvIII positive glioblastoma. |
| Related Links | http://dx.doi.org/10.1093/neuonc/nou265.27 |
| Starting Page | 164 |
| File Format | |
| ISSN | 15228517 |
| e-ISSN | 15235866 |
| Journal | Neuro-Oncology |
| Issue Number | Suppl 5 |
| Volume Number | 16 |
| Language | English |
| Publisher | Oxford University Press |
| Publisher Date | 2014-11-01 |
| Access Restriction | Open |
| Rights Holder | Oxford University Press |
| Subject Keyword | Cancer Research Oncology Clinical Neurology Research in Higher Education |
| Content Type | Text |
| Resource Type | Article |
| Subject | Cancer Research Neurology (clinical) Oncology |
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