Elucidation of molecular-targeted drug resistance mechanism by lung cancer cells

(Kanazawa University) We revealed that ALK-positive lung cancer cells, treated with crizonitib, a molecular target drug, acquired resistance to the drug not only by genetic mutation but also by concomitant epithelial-to-mesenchymal transition (EMT). Further, in animal experiments, mesenchymal cancer cells due to EMT were shown to revert to epithelial ones by quisinostat, a histone deacetylase (HDAC) inhibitor; they regained sensitivity to the molecular-targeted drug. These results indicate a significant potential of overcoming resistance to molecular-targeted drugs.
Source: EurekAlert! - Cancer - Category: Cancer & Oncology Source Type: news