Reversible and adaptive resistance to BRAF(V600E) inhibition in melanoma

By Chong Sun, Liqin Wang, Sidong Huang, Guus Heynen, A. Prahallad, C. Robert, J. Haanen, C. Blank, J. Wesseling, S. Willems and 15 more. Nature, 2014

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Oncogenic Signaling Pathways in The Cancer Genome Atlas (2018, background): “Since oncogenic EGFR can be synthetically lethal with mutated KRAS and can mediate resistance to BRAF inhibition in colon cancer and melanoma (Sun et al., 2014; Unni et al., 2015), these results suggest a similar antagonistic interaction with loss of NF1 or RASA1 .”
Multi-stage differentiation defines melanoma subtypes with differential vulnerability to drug-induced iron-dependent oxidative stress (2018, background): “In some cases, dedifferentiation can be a transient response of adaptive resistance (Fallahi-Sichani et al., 2017; Sun et al., 2014; Titz et al., 2016) and provides a reservoir of cells allowing for expansion or evolution of resistant clones with genetic mechanisms that enable return to the parental”
Rare cell variability and drug-induced reprogramming as a mode of cancer drug resistance (2017, neutral): “com/AstraZeneca-NGS/ VarDict), and Freebayes (15) algorithms.”
Targeting TGF-β signal transduction for fibrosis and cancer therapy (2022, background): “Both of them help increase melanoma metastatic potential and drug resistance [137, 138].”