ArticleMolecular genetics & genomic medicine2020
Oncogenic mutations within the β3-αC loop of EGFR/ERBB2/BRAF/MAP2K1 predict response to therapies.
Article in Molecular genetics & genomic medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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7 citing papers in PubMed, 8 citations in OpenAlex.
- Expert consensus on the diagnosis and treatment of solid tumors with BRAF mutations.Innovation (Cambridge (Mass.)) · 2024Review
- A phase 1 study of triple-targeted therapy with BRAF, MEK, and AKT inhibitors for patients with BRAF-mutated cancers.Cancer · 2024Article
- Architecture of the MKK6-p38α complex defines the basis of MAPK specificity and activation.Science (New York, N.Y.) · 2023Article
- BRAFScience advances · 2023Article
- Prediction of Amino Acid Substitutions in ABL1 Protein Leading to Tumor Drug Resistance Based on "Structure-Property" Relationship Classification Models.Life (Basel, Switzerland) · 2023Article
- Oncogenic mutations within the β3-αC loop of EGFR/ERBB2/BRAF/MAP2K1 predict response to therapies.Molecular genetics & genomic medicine · 2020Article
- Prediction for Intravenous Immunoglobulin Resistance Combining Genetic Risk Loci Identified From Next Generation Sequencing and Laboratory Data in Kawasaki Disease.Frontiers in pediatrics · 2020Article
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Authors and funding
15 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundβ3-αC loop is a highly conserved structural domain across oncogene families, which is a switch for kinase activity. There have been numerous researches on mutations within β3-αC loop in EGFR, but relatively less in ERBB2, BRAF, and MAP2K1. In addition, previous studies mainly focus on β3-αC deletion in EGFR, which is the most common type affecting kinase activity and driving lung cancer. Other mutation types are not well studied.
methodsHere we analyzed the profile of β3-αC loop mutations in a total of 10,000 tumor biopsy and/or ctDNA patient samples using hybridization capture-based next-generation sequencing.
resultsWe identified 1616 mutations within β3-αC loop in this cohort. Most mutations were located in EGFR, with less percentage in ERBB2, BRAF, and MAP2K1. EGFR β3-αC deletions occurred at a high percentage of 96.7% and were all drug-relevant. We also detected rare EGFR β3-αC insertions and point mutations, most of which were related to EGFR TKIs resistance. ERBB2 β3-αC deletions were only found in breast cancers and sensitive to EGFR/ERBB2 inhibitor. Moreover, BRAF and MAP2K1 mutations within β3-αC loop also demonstrated drugs relevance.
conclusionOur study showed that oncogenic mutations within the β3-αC loop of ERBB2, MAP2K1, and BRAF are analogous to that of EGFR, which have profound effect on drug response. Understanding the mutation profile within the β3-αC loop is critical for targeted therapies.
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