Plinabulin, a microtubule destabilising agent, in non-small-cell lung cancer: lessons from the DUBLIN-3 trial
Mené sur 559 patients atteints d'un cancer du poumon non à petites cellules de stade avancé ou métastatique, cet essai international de phase III évalue l'efficacité, du point de vue de la survie globale, et la toxicité de l'ajout de la plinabuline au docétaxel en traitement de deuxième et troisième ligne
Résumé en anglais
Non-small-cell lung cancer (NSCLC), especially lung adenocarcinoma, is the leading cause of cancer-related death worldwide and is often metastatic at the time of diagnosis. Biomarkers to identify premalignant lesions (such as atypical adenomatous hyperplasia, adenocarcinoma in situ, and minimally invasive adenocarcinoma) are scarce. Sodium-glucose transport could potentially identify metabolically active lung premalignancy and early-stage lung adenocarcinoma.1 Tobacco use is indicated as a cause in more than 80% of lung cancers in the USA and UK, and 57·5% of lung cancers in men and 13% in women in China. Lung cancer in never smokers is the fifth most common cause of cancer-related deaths worldwide.2 KRAS mutations are present in up to 47% of smoking-related lung adenocarcinomas, with KRASG12C being the most common and accounting for about 41% of these mutations.2 CodeBreak 200 was a randomised trial comparing the efficacy and safety of the KRASG12C inhibitor sotorasib to the standard of care in previously treated patients with advanced KRASG12C mutant NSCLC. A statistically significant increase in progression-free survival was attained for sotorasib compared with docetaxel (5·6 months vs 4·5 months, hazard ratio [HR] 0·66; p=0·0017). Subgroup analyses for progression-free survival reported a noticeable improvement in a small subgroup of Asian patients (8·3 months with sotorasib vs 5·6 months with docetaxel). However, overall survival was not different between the treatment groups (10·6 months in the sotorasib group and 11·3 months in the docetaxel group).
