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|Ref Type||Journal Article|
|Authors||Gautschi O, Peters S, Zoete V, Aebersold-Keller F, Strobel K, Schwizer B, Hirschmann A, Michielin O, Diebold J|
|Title||Lung adenocarcinoma with BRAF G469L mutation refractory to vemurafenib.|
|Journal||Lung cancer (Amsterdam, Netherlands)|
|Abstract Text||BRAF V600E is an emerging drug target in lung cancer, but the clinical significance of non-V600 BRAF mutations in lung cancer and other malignancies is less clear. Here, we report the case of a patient with metastatic lung adenocarcinoma with BRAF G469L mutation refractory to vemurafenib. We calculated a structure model of this very rare type of mutated BRAF kinase to explain the molecular mechanism of drug resistance. This information may help to develop effective targeted therapies for cancers with non-V600 BRAF mutations.|
|Molecular Profile||Treatment Approach|
|Gene Name||Source||Synonyms||Protein Domains||Gene Description||Gene Role|
|Therapy Name||Drugs||Efficacy Evidence||Clinical Trials|
|Drug Name||Trade Name||Synonyms||Drug Classes||Drug Description|
|Gene||Variant||Impact||Protein Effect||Variant Description||Associated with drug Resistance|
|BRAF||G469L||missense||unknown||BRAF G469L lies within the protein kinase domain of the Braf protein (UniProt.org). G469L has been identified in the scientific literature (PMID: 24035431, PMID: 26301799, PMID: 26200454), but has not been biochemically characterized and therefore, its effect on Braf protein function is unknown (PubMed, May 2022).|
|Molecular Profile||Indication/Tumor Type||Response Type||Therapy Name||Approval Status||Evidence Type||Efficacy Evidence||References|
|BRAF G469L||lung adenocarcinoma||no benefit||Vemurafenib||Case Reports/Case Series||Actionable||In a clinical case study, a lung adenocarcinoma patient harboring BRAF G469L did not respond to Zelboraf (vemurafenib) therapy (PMID: 24035431).||24035431|