ArticleOncogene2018
Wild-type KRAS is a novel therapeutic target for melanoma contributing to primary and acquired resistance to BRAF inhibition.
Article in Oncogene, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 54 citations in OpenAlex.
- Pre-existing cell states predict resistance to multiple treatments.Cell genomics · 2026Article
- Integrative multi-omics defines melanoma drug response networks and ARID1A-dependent resistance mechanisms.Molecular systems biology · 2026Article
- Targeting KRAS mutations: orchestrating cancer evolution and therapeutic challenges.Signal transduction and targeted therapy · 2025Review
- SLAMF8 expression and prognostic significance in melanoma: A multi-omics and Mendelian randomization study.Cancer biomarkers : section A of Disease markers · 2025Observational
- Modeling a mesenchymal cell state by bioprinting for the molecular analysis of dormancy in melanoma.Materials today. Bio · 2025Article
- Cooperative genomic lesions in HRAS-mutant cancers predict resistance to farnesyltransferase inhibitors.Oncogene · 2024Article
- Characterization of two different alginate-based bioinks and the influence of melanoma growth within.Scientific reports · 2024Article
- Alternative Wnt-signaling axis leads to a break of oncogene-induced senescence.Cell death & disease · 2024Article
- Adaptation of a mutual exclusivity framework to identify driver mutations within oncogenic pathways.American journal of human genetics · 2024Article
- Preoperative ctDNA Levels Are Associated With Poor Overall Survival in Patients With Ovarian Cancer.Cancer genomics & proteomics · 2023Article
- TERT Expression Induces Resistance to BRAF and MEK Inhibitors in BRAF-Mutated Melanoma In Vitro.Cancers · 2023Article
- The pleiotropic role of galectin-3 in melanoma progression: Unraveling the enigma.Advances in cancer research · 2023Review
- The future of targeted kinase inhibitors in melanoma.Pharmacology & therapeutics · 2022Review
- Characterization of Vemurafenib-Resistant Melanoma Cell Lines Reveals Novel Hallmarks of Targeted Therapy Resistance.International journal of molecular sciences · 2022Article
- Gene Identification and Potential Drug Therapy for Drug-Resistant Melanoma with Bioinformatics and Deep Learning Technology.Disease markers · 2022Article
- Multiple primary malignant neoplasm: Case report and comprehensive literature review.Frontiers in oncology · 2022Article
- Dimethyl Fumarate Combined With Vemurafenib Enhances Anti-Melanoma EfficacyFrontiers in oncology · 2022Article
- Crosstalk Between Four Types of RNA Modification Writers Characterizes the Tumor Immune Microenvironment Infiltration Patterns in Skin Cutaneous Melanoma.Frontiers in cell and developmental biology · 2022Article
- Nanotechnology Addressing Cutaneous Melanoma: The Italian Landscape.Pharmaceutics · 2021Review
- Proteomics and Phosphoproteomics Profiling of Drug-Addicted BRAFi-Resistant Melanoma Cells.Journal of proteome research · 2021Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Malignant melanoma reveals rapidly increasing incidence and mortality rates worldwide. By now, BRAF inhibition is the standard therapy for advanced melanoma in patients carrying BRAF mutations. However, only approximately 50% of melanoma patients harbor therapeutically attackable BRAF mutations, and overall survival after treatment with BRAF inhibitors is modest. KRAS (Kirsten Rat sarcoma) proteins are acting upstream of BRAF and have a major role in human cancer. Recent approaches awaken the hope to use KRAS inhibition (KRASi) as a clinical tool. In this study, we identified wild-type KRAS as a novel therapeutic target in melanoma. KRASi functions synergistically with BRAF inhibition to reduce melanoma proliferation and to induce apoptosis independently of BRAF mutational status. Moreover, acquired resistance to BRAF inhibitors in melanoma is dependent on dynamic regulation of KRAS expression with subsequent AKT and extracellular-signal regulated kinase activation and can be overcome by KRASi. This suggests KRASi as novel approach in melanoma-alone or in combination with other therapeutic regimes.
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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.