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.
Resources from the same session
3190 - GI101, a novel triple-targeting bispecific CD80-IgG4-IL2variant fusion protein, elicits synergistic anti-tumor effects in preclinical models
Presenter: Jae Chan Park
Session: Poster Display session 3
Resources:
Abstract
4062 - Phase 1b, open-label, dose-escalation study of M9241 (NHS-IL12) plus avelumab in patients (pts) with advanced solid tumors
Presenter: Julius Strauss
Session: Poster Display session 3
Resources:
Abstract
5777 - THOR-707, a novel not-alpha IL-2, promotes all key immune system anti-tumoral actions of IL-2 without eliciting vascular leak syndrome (VLS)
Presenter: Marcos Milla
Session: Poster Display session 3
Resources:
Abstract
5047 - A phase I clinical trial of malignant pleural mesothelioma treated with locally delivered autologous anti-FAP-targeted CAR T-cells
Presenter: Alessandra Curioni
Session: Poster Display session 3
Resources:
Abstract
1679 - HPV16 E6-specific TCR-T armored with checkpoint blockade in the treatment of cervical cancer
Presenter: Paul Bryson
Session: Poster Display session 3
Resources:
Abstract
1133 - the Mutant Neoantigen Specific T Cell Is a Personalized Immunotherapy in Refractory Solid Tumor
Presenter: Qi Song
Session: Poster Display session 3
Resources:
Abstract
3338 - NY-ESO-1 and LAGE1A –an emerging target for cell therapies in solid tumours
Presenter: Ioanna Eleftheriadou
Session: Poster Display session 3
Resources:
Abstract
3089 - Targeting myeloid-derived suppressor cells and T cells: combination treatment with MTL-CEBPA and PD-1 antibody in a mouse syngeneic CT26 model
Presenter: Mikael Sodergren
Session: Poster Display session 3
Resources:
Abstract
5991 - Master Checkpoint Cbl-b Inhibition: Anti-tumor Efficacy in a Murine Colorectal Cancer Model Following siRNA-based Cell Therapy
Presenter: Kathrin Thell
Session: Poster Display session 3
Resources:
Abstract
5007 - Functional systemic CD4 immunity is required for clinical responses to PD-L1/PD-1 blockade therapy
Presenter: Miren Zuazo
Session: Poster Display session 3
Resources:
Abstract