Abstract 2115
Background
Epithelial Growth Factor Receptor (EGFR), a type of the ERBB receptor tyrosine kinase, associated with cell survival and proliferation has properties to activate tumorigenesis and metastasis in cancer. Normally, EGFR is expressed in normal tissues such like other tyrosine kinase receptors especially in epithelial cell type tissues. In various cancer types, EGFR amplification or overexpression is commonly detected in cancer cells compared with normal epithelial tissues, and so known as a still promising therapeutic biomarker for cancer therapy in colorectal cancer, Lung cancer, gastric cancer and glioblastoma. However, several EGFR targeted therapy failed in clinical trial for cancer patients include glioblastoma and hard to find responder group in cancer patients.
Methods
To figure out clinical criteria for cancer patients, we tested a novel EGFR targeted antibody (GC1118) in glioblastoma patient-derived xenograft (PDX) models and patient-derived cell (PDC) with its genomic data.
Results
Through Xeno Trial, a method using a small scale of mice per treatment to enable the investigation of efficacy in substantially larger panels of PDX models, and it implies that therapeutic response is expected to be evident in EGFR amplification in brain tumors, in addition to efficacy was also observed in patients with EGFR amplification via High Throughput Screening (HTS). Through High Throughput Screening using glioblastoma patient-derived cells shown that cell growth inhibition in EGFR amplify cases by GC1118. In Xeno trail, inhibitory effects of tumor growth observed in EGFR amplification PDX models by GC1118 treatment as well.
Conclusions
Overall, this study results suggest that EGFR amplification status is still one of the important criteria to find responder group in glioblastoma patients.
Clinical trial identification
Editorial acknowledgement
Legal entity responsible for the study
The authors.
Funding
The Korea Health Technology R&D Project through the Korea Health Industry Development Institute (KHIDI), funded by the Ministry of Health & Welfare, Republic of Korea. (HI14C3418).
Disclosure
All authors have declared no conflicts of interest.
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