期刊
EXPERT OPINION ON BIOLOGICAL THERAPY
卷 9, 期 8, 页码 1087-1098出版社
TAYLOR & FRANCIS LTD
DOI: 10.1517/14712590903124346
关键词
antigens; CDX-110; central nervous system neoplasms; EGFR; immunotherapy; PEPvIII-KLH
资金
- NCI NIH HHS [P50 CA108786-050003, R01 CA097222, P50 CA108786, R01 CA097222-05, R01 CA235612] Funding Source: Medline
Conventional therapies for glioblastoma multiforme (GBM) fail to target tumor cells exclusively, resulting in non-specific toxicity. Immune targeting of tumor-specific mutations may allow for more precise eradication of neoplastic cells. EGFR variant III (EGFRvIII) is a tumor-specific mutation that is widely expressed in GBM and other neoplasms and its expression enhances tumorigenicity. This in-frame deletion mutation splits a codon, resulting in a novel glycine at the fusion junction producing a tumor-specific epitope target for cellular or humoral immunotherapy. We have previously shown that vaccination with a peptide that spans the EGFRvIII fusion junction (PEPvIII-KLH/CDX-110) is an efficacious immunotherapy in syngeneic murine models. In this review, we summarize our results in GBM patients targeting this mutation in multiple, multi-institutional Phase II immunotherapy trials. These trials demonstrated that a selected population of GBM patients who received vaccines targeting EGFRvIII had an unexpectedly long survival time. Further therapeutic strategies and potential pitfalls of using this approach are discussed.
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