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BIOMARKER:

EGFR R521K

i
Entrez ID:
over2years
EGFR R521K Polymorphism Is Not a Major Determinant of Clinical Cetuximab Resistance in Head and Neck Cancer. (PubMed, Cancers (Basel))
Our results suggest that EGFR R521K, unlike reported previously, is unable to cause cetuximab resistance in HNSCC patients; therefore, its screening before therapy selection is not justifiable.
Journal
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EGFR (Epidermal growth factor receptor)
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EGFR R521K
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Erbitux (cetuximab)
over3years
EGFR Alterations Influence the Cetuximab Treatment Response and c-MET Tyrosine-Kinase Inhibitor Sensitivity in Experimental Head and Neck Squamous Cell Carcinomas. (PubMed, Pathol Oncol Res)
Interestingly, the cetuximab-resistant R521K tumors were successfully treated with c-MET tyrosine kinase inhibitor SU11274. Our results suggest that HNSCC cell line expressing the R521K mutant form of EGFR does not respond well to cetuximab treatment in vitro or in vivo, but hopefully might be targeted by c-MET tyrosine kinase inhibitor treatment.
Journal
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EGFR (Epidermal growth factor receptor) • MET (MET proto-oncogene, receptor tyrosine kinase)
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EGFR R521K
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Erbitux (cetuximab) • SU11274
over3years
Consequences of extracellular alterations of EGFR on cetuximab therapy in HNSCC (PubMed, Magy Onkol)
This selectivity was not reflected in immunophenotype or survival data of HNSCC patients, suggesting a more complex mechanism behind. Interestingly, c-Met inhibitor SU11274 was more effective in cetuximab-resistant, EGFR R521K heterozygous cells and xenografts, raising the possible importance of simultaneous targeting of the two receptors.
Journal
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EGFR (Epidermal growth factor receptor)
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EGFR R521K
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Erbitux (cetuximab) • SU11274
over3years
Genetic variants of the EGFR ligand-binding domain and their association with structural alterations in Arab cancer patients. (PubMed, BMC Res Notes)
Computational analysis of the genetic variants revealed a reduction in the stabilization of the EGFR tethered form for both V550M and the common R521K variant with low energetic state (- ∆∆G). Molecular interactions analysis suggested that these mutations might affect the receptor's function and promote tumorigenesis.
Clinical • Journal
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EGFR (Epidermal growth factor receptor)
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EGFR R521K
over4years
[VIRTUAL] Comparison of circulating tumor cell (CTC) derived DNA and circulating cell-free DNA (cfDNA) from simultaneous blood sampling of patients with metastatic breast cancer (MBC) (AACR-II 2020)
It is feasible to isolate high quality CTCs and cfDNA from the same blood collection tube to perform targeted sequencing; this streamlines specimen processing, decreases overall costs, and minimizes required blood volumes. Importantly, there is overlap in the majority of mutations identified in CTC-DNA and cfDNA, but actionable mutations (e.g., PIK3CA, EGFR) were detected in CTC-DNA only. The clinical and theranostic relevance of these findings is unclear and warrants further investigation.
Clinical • Circulating Tumor Cells • BRCA Biomarker
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EGFR (Epidermal growth factor receptor) • HER-2 (Human epidermal growth factor receptor 2) • TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • BRCA2 (Breast cancer 2, early onset) • PTEN (Phosphatase and tensin homolog) • DNMT3A (DNA methyltransferase 1) • SMAD4 (SMAD family member 4)
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BRCA2 mutation • PIK3CA mutation • EGFR T790M • PIK3CA H1047R • PTEN mutation • PIK3CA E545K • PIK3CA E542K • EGFR R521K