Transient Splicing-Associated Isoform Remodeling Defines Early MAPKi Resistance Adaptation in Melanoma
A long-standing question in targeted therapy resistance is how tumor cells rapidly enter drug-tolerant states before stable resistance emerges. In BRAF-mutant melanoma, early adaptation to MAPK inhibitor (MAPKi) therapy is accompanied by profound phenotypic plasticity, yet the molecular mechanisms that enable this transition remain poorly understood. Here, we show that MAPKi adaptation is…
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