ReviewPigment cell & melanoma research2014
Adaptive resistance to RAF inhibitors in melanoma.
Review in Pigment cell & melanoma research, 2014. 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
36 citing papers in PubMed.
- BRAF mutations and targeted therapy in unclassified pericytic tumors: insights from genetic analysis and clinical response.BMC cancer · 2025Article
- Preclinical Therapeutic Efficacy of RAF/MEK/ERK and IGF1R/AKT/mTOR Inhibition in Neuroblastoma.Cancers · 2024Article
- Protein phosphatase 6 activates NF-κB to confer sensitivity to MAPK pathway inhibitors inScience signaling · 2024Article
- Mcl-1 mediates intrinsic resistance to RAF inhibitors in mutant BRAF papillary thyroid carcinoma.Cell death discovery · 2024Article
- Extracellular Vesicles-Based Cell-Cell Communication in Melanoma: New Perspectives in Diagnostics and Therapy.International journal of molecular sciences · 2023Review
- BRAF Inhibitor Resistance in Melanoma: Mechanisms and Alternative Therapeutic Strategies.Current treatment options in oncology · 2022Review
- Mechanisms underlying melanoma invasion as a consequence of MLK3 loss.Experimental cell research · 2022Article
- Co-Treatment of Chloroquine and Trametinib Inhibits Melanoma Cell Proliferation and Decreases Immune Cell Infiltration.Frontiers in oncology · 2022Article
- Article
- HER3-Receptor-Mediated STAT3 Activation Plays a Central Role in Adaptive Resistance toward Vemurafenib in Melanoma.Cancers · 2020Article
- Prognostic value of key genes of the JAK-STAT signaling pathway in patients with cutaneous melanoma.Oncology letters · 2020Article
- Topical 2'-Hydroxyflavanone for Cutaneous Melanoma.Cancers · 2019Article
- Enhancing the Efficacy of Melanocortin 1 Receptor-Targeted Radiotherapy by Pharmacologically Upregulating the Receptor in Metastatic Melanoma.Molecular pharmaceutics · 2019Article
- Stem Cell-Derived Models of Neural Crest Are Essential to Understand Melanoma Progression and Therapy Resistance.Frontiers in molecular neuroscience · 2019Review
- Targeted Therapy-Resistant Melanoma Cells Acquire Transcriptomic Similarities with Human Melanoblasts.Cancers · 2018Article
- ErbB3 Targeting Enhances the Effects of MEK Inhibitor in Wild-Type BRAF/NRAS Melanoma.Cancer research · 2018Article
- ERK-mediated phosphorylation regulates SOX10 sumoylation and targets expression in mutant BRAF melanoma.Nature communications · 2018Article
- Comparing the genomes of cutaneous melanoma tumors to commercially available cell lines.Oncotarget · 2017Article
- New role of ID3 in melanoma adaptive drug-resistance.Oncotarget · 2017Article
- Future perspectives in melanoma research "Melanoma Bridge", Napoli, November 30th-3rd December 2016.Journal of translational medicine · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
The discovery of activating mutations in BRAF at high frequency in cutaneous melanoma opened the door to new treatment options, which have resulted in significantly better patient outcomes. Treatments such as the FDA-approved RAF inhibitor vemurafenib and the more recently approved dabrafenib and trametinib combination therapy are designed to target the ERK1/2 pathway. Initial success in targeting this pathway is evidenced by the high percentage of melanoma patients who undergo tumor remission. However, the beneficial effects of these targeted therapies are usually short-lived due to the development of resistance, which leads to disease progression. As a result, studies have focused on the acquired forms of resistance that develop following continued exposure to therapy. Conversely, far fewer studies have investigated the adaptive forms of resistance, which activate rapidly, promote cell survival, and may underlie the development of acquired resistance by providing melanoma cells the time to develop additional mutations. We provide a detailed review of the known mechanisms of adaptive resistance in melanoma and relate them to similar responses to targeted therapies in other tumor types.
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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.