ReviewCritical reviews in oncology/hematology2020
New therapeutic approaches to overcoming resistant EGFR exon 20 alterations.
Review in Critical reviews in oncology/hematology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed, 19 citations in OpenAlex.
- Anti-CD47 tri-specific killer engager enhances NK cell cytotoxicity against lung cancer.Investigational new drugs · 2025Article
- PD-L1 induces autophagy and primary resistance to EGFR-TKIs in EGFR-mutant lung adenocarcinoma via the MAPK signaling pathway.Cell death & disease · 2024Article
- The Perceived Value of Liquid Biopsy: Results From a Canadian Validation Study of Circulating Tumor DNAJTO clinical and research reports · 2024Article
- EGFR and HER2 exon 20 insertions in solid tumours: from biology to treatment.Nature reviews. Clinical oncology · 2022Review
- Cetuximab in Patients with Non-Small Cell Lung Cancer and EGFR Exon 20 Insertion Alterations.Clinical oncology, case reports · 2022Article
- A Lung Cancer Patient Harboring a Rare Oncogenic EGFR Exon 20 V786M Mutation Responded to a Third-Generation Tyrosine Kinase Inhibitor: Case Report and Review of the Literature.Frontiers in oncology · 2022Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
EGFR exon 20 alterations are rare events seen mainly in non-small cell lung cancer (NSCLC). They include EGFR T790 and C797S mutations (associated with secondary resistance to classic EGFR tyrosine kinase inhibitors (TKIs)), and EGFR exon 20 in-frame insertions (associated with resistance to first- and second-generation EGFR TKIs). In silico modeling of structural changes in aberrant proteins has informed selection of compounds with potential clinical activity: poziotinib (whose smaller size permits access to the restricted kinase pocket created by EGFR and ERBB2 exon 20 insertions); cetuximab (an antibody that attenuates dimerization caused by EGFR exon 20 insertions), and TAK-788 (another EGFR/ERBB2 TKI). Other alterations, such as EGFR T790 M, are responsive to osimertinib, while the EGFR C797S alteration seen in osimertinib resistance demonstrates preclinical sensitivity to combined brigatinib and cetuximab. These observations indicate that clinical resistance can be overcome by utilizing advanced genomic interrogation coupled with computer modeling.
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Registered trials
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