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Epidermal growth factor receptor (EGFR) variant III (vIII) is the most common oncogenic rearrangement in glioblastoma (GBM), generated by deletion of exons 2 to 7 of EGFR. The proximal breakpoints occur in variable positions within the 123-kb intron 1, presenting significant challenges in terms of polymerase chain reaction (PCR)-based mapping. Molecular mechanisms underlying these deletions remain unclear.

Mapping of genomic EGFRvIII deletions in glioblastoma: insight into rearrangement mechanisms and biomarker development