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Rapid and dramatic responses to dabrafenib and trametinib in BRAF V600E‐mutated lung adenocarcinoma
V‐raf murine sarcoma viral oncogene homologue B1 (BRAF) is a proto‐oncogene that regulates cell proliferation and survival. BRAF V600E‐mutated lung cancer has aggressive characteristics and is resistant to chemotherapies. Combination of BRAF‐specific inhibitor dabrafenib and mitogen‐activated protei...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley & Sons, Ltd
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8403980/ https://www.ncbi.nlm.nih.gov/pubmed/34484797 http://dx.doi.org/10.1002/rcr2.841 |
Sumario: | V‐raf murine sarcoma viral oncogene homologue B1 (BRAF) is a proto‐oncogene that regulates cell proliferation and survival. BRAF V600E‐mutated lung cancer has aggressive characteristics and is resistant to chemotherapies. Combination of BRAF‐specific inhibitor dabrafenib and mitogen‐activated protein kinase kinase (MEK) inhibitor trametinib is the standard treatment for BRAF V600E‐mutated lung cancer. We report a case of BRAF V600E‐mutated lung adenocarcinoma, which presented with respiratory distress due to deterioration of advanced cancer. The tumour responded rapidly and significantly to BRAF/MEK inhibitors, and the patient's symptoms improved within 2 weeks. BRAF/MEK inhibitors are effective treatment in BRAF‐mutated lung cancer even under critical conditions. |
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