ArticleNature communications2020
Combating acquired resistance to MAPK inhibitors in melanoma by targeting Abl1/2-mediated reactivation of MEK/ERK/MYC signaling.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
What it found
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Who cites it
36 citing papers in PubMed, 46 citations in OpenAlex.
- Therapeutic Resistance in Melanoma: Molecular Mechanisms and Emerging Pharmaceutical Strategies.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Targeting ABL kinases overcomes melanoma immune evasion following resistance to MAPK inhibition.Nature communications · 2026Article
- Nilotinib induces immunogenic cuproptosis to potentiate cancer immunotherapy.Cell reports. Medicine · 2026Article
- Global landscape of protein-coding and long non-coding RNA alternative splicing and regulation in the human esophageal squamous cell carcinoma.Cancer cell international · 2026Article
- ABL kinases regulate FGF signaling independent of CRK phosphorylation to prevent Peters anomaly type II.Nature communications · 2026Article
- An RNA-sequencing analysis to determine potential upstream transcriptional regulators of essential amino acid deficiency responses in bovine mammary epithelial cells.BMC genomics · 2026Article
- Comprehensive transcriptomic characterization of two melanoma cell lines with acquired dual resistance to BRAF and MEK inhibitors.Scientific reports · 2026Article
- BRAF inhibitor resistance in melanoma: from resistance mechanisms to therapeutic innovations.Molecular biomedicine · 2026Review
- 14-3-3ε-dependent deubiquitination and translocation of NLRP3 activates the inflammasome during sepsis.JCI insight · 2026Article
- MYC as a key target for melanoma therapy.Frontiers in cell and developmental biology · 2026Review
- Interpretable Differential Abundance Signature (iDAS).Small methods · 2026Article
- Targeting KRAS mutations: orchestrating cancer evolution and therapeutic challenges.Signal transduction and targeted therapy · 2025Review
- Conserved Gαq-PLCβ-PKC signaling mediates trametinib resistance in BRAFbioRxiv : the preprint server for biology · 2025Article
- Integrated multi-omics characterization across clinically relevant subgroups of long COVID.National science review · 2025Article
- Signaling and transcriptional dynamics underlying early adaptation to oncogenic BRAF inhibition.Cell systems · 2025Article
- The dual HDAC/PI3K inhibitor CUDC-907 inhibits the growth and proliferation of MYC-driven Group 3 medulloblastoma.Cell death discovery · 2025Article
- A New Paradigm for Generative Adversarial Networks based on Randomized Decision Rules.Statistica Sinica · 2025Article
- CDKN2A, a key gene in copper-induced cell death model, influencing melanoma invasion and apoptosis.Discover oncology · 2025Article
- Second-generation BRAF inhibitor Encorafenib resistance is regulated by NCOA4-mediated iron trafficking in the drug-resistant malignant melanoma cells.Scientific reports · 2025Article
- PARP inhibitors in melanoma treatment: potential, challenges, and future directions.Frontiers in oncology · 2025Review
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 1 country.
Funding
Abstract
Metastatic melanoma remains an incurable disease for many patients due to the limited success of targeted and immunotherapies. BRAF and MEK inhibitors reduce metastatic burden for patients with melanomas harboring BRAF mutations; however, most eventually relapse due to acquired resistance. Here, we demonstrate that ABL1/2 kinase activities and/or expression are potentiated in cell lines and patient samples following resistance, and ABL1/2 drive BRAF and BRAF/MEK inhibitor resistance by inducing reactivation of MEK/ERK/MYC signaling. Silencing/inhibiting ABL1/2 blocks pathway reactivation, and resensitizes resistant cells to BRAF/MEK inhibitors, whereas expression of constitutively active ABL1/2 is sufficient to promote resistance. Significantly, nilotinib (2
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.