Dabrafenib–trametinib combination therapy re-challenge in advanced BRAFV600E-mutant non–small-cell lung cancer

We read with great interest the article by Facchinetti et al. [ [1] Facchinetti F. Lacroix L. Mezquita L. Scoazec J.Y. Loriot Y. Tselikas L. et al. Molecular mechanisms of resistance to BRAF and MEK inhibitors in BRAFV600E non-small cell lung cancer. Eur J Canc. 2020; 132: 211-223https://doi.org/10.1016/j.ejca.2020.03.025 Abstract Full Text Full Text PDF PubMed Scopus (19) Google Scholar ] about the molecular mechanisms of resistance to BRAF and MEK inhibitors in BRAFV600E-mutant non–small-cell lung cancer (NSCLC). The article indicates that understanding the mechanisms of acquired resistance to BRAF and MEK inhibitors in NSCLC is important to discover novel treatment strategies. Currently, it is difficult for clinicians to perform molecular re-analysis in the real world. Here, we report the case of achieving a long-term partial response (PR) to dabrafenib-trametinib combination therapy (D/T) re-challenge in advanced BRAFV600E-mutant NSCLC. Molecular mechanisms of resistance to BRAF and MEK inhibitors in BRAFV600E non–small cell lung cancerEuropean Journal of CancerVol. 132PreviewBRAF is a confirmed therapeutic target in non–small cell lung cancer (NSCLC), as the BRAF inhibitor dabrafenib, in combination with the MEK inhibitor trametinib, is approved for the treatment of NSCLC harbouring BRAF V600E mutation. Scant evidence is available concerning the mechanisms of resistance to BRAF/MEK inhibitors in BRAFV600E NSCLC. Full-Text PDF