EGFRvIII--a stable target for anti-EGFRvIII therapy.

BACKGROUND

Epidermal growth factor receptor (EGFR) gene alterations play important roles in pathogenesis of glioblastoma. Antibodies against EGFRvIII have been recently developed. Their efficacy depends on numerous factors, including the co-existence of EGFRvIII with other genetic alterations, and especially with point mutations of EGFR.

MATERIALS AND METHODS

We examined 91 patients diagnosed with glioblastoma in order to determine the prevalence and mutual relationships between EGFR alterations. Real-time polymerase chain reaction (real-time PCR), fluorescent in situ hybridization (FISH), and sequencing were used to analyze prevalence of the amplification of EGFR gene, polysomy of chromosome 7, EGFRvIII mutation, and point mutations in exons 7-8 and 15 of EGFR.

RESULTS

We revealed that all these alterations can occur independently from each other. Nevertheless, the co-existence of EGFRvIII mutation and excessive copies of EGFR gene was observed in most cases (10/14). Similarly, the point mutations in exons 7-8 and 15 co-existed with an excessive number of EGFR copies in nearly all cases.

CONCLUSION

EGFRvIII is a reliable and stable target for anti-EGFRvIII therapy.