成胶质细胞瘤中EGFR靶向治疗耐药机制的研究进展

Resistance mechanisms underlying the EGFR-targeted therapies in glioblastoma

多形性成胶质细胞瘤（GBM）是成人中发病率较高的神经系统恶性肿瘤。研究表明,约40%~60%的胶质瘤有表皮生长因子受体（EGFR）过量表达和基因扩增,其中约40%伴随着EGFR突变,目前已有多个针对EGFR的靶向药物用于临床肿瘤治疗,然而在GBM患者的临床应用中,EGFR靶向治疗却鲜有成效。如何克服靶向治疗过程中出现的原发或继发性耐药,对医学工作者而言仍然是一个巨大挑战。本文将对EGFR靶向药物在GBM中的主要耐药机制进行综述。

Glioblastoma multiforme（GBM）is the most common primary malignant neoplasm of the central nervous system in adults. Previous work has shown that the over-expression of epidermal growth factor receptor（EGFR）and EGFR gene amplification was found in approximately 40-60% of GBM patients,of which about 40% with EGFR mutations. Presently,multiple therapeutic drugs targeting EGFR have been used in clinical trials. However EGFR targeted therapy has limited efficacy in patients with GBM. It remains a haunting challenge to overcome the primary and secondary drug resistance to EGFR-targeted therapy in GBM patients.This review summarizes recent advances in the main resistance mechanisms underlying the EGFR-targeted therapies in glioblastoma.