ArticleOncotarget2015
Molecular spectrum of BRAF, NRAS and KRAS gene mutations in plasma cell dyscrasias: implication for MEK-ERK pathway activation.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 73 citations in OpenAlex.
- Phenotypic plasticity in plasma cell myeloma: a CD138-negative case with a rare BRAF G469R mutation.Journal of pathology and translational medicine · 2026Article
- PARP1 trapping activates cGAS-STING pathway to induce immunogenic cell death in multiple myeloma.Cancer cell international · 2026Article
- Precision Medicine in Colorectal Cancer: Targeted Therapies and Biomarker Insights.Current cancer drug targets · 2026Review
- Resistance to immunomodulatory drugs in multiple myeloma: the cereblon pathway and beyond.Haematologica · 2025Review
- Functional Investigation ofCancers · 2024Article
- pyComBat, a Python tool for batch effects correction in high-throughput molecular data using empirical Bayes methods.BMC bioinformatics · 2023Article
- Molecular genetic aberrations in the pathogenesis of multiple myeloma.Asian biomedicine : research, reviews and news · 2023Review
- Article
- Liquid Biopsy-Derived DNA Sources as Tools for Comprehensive Mutation Profiling in Multiple Myeloma: A Comparative Study.Cancers · 2022Article
- Correlation of plasma cell assessment by phenotypic methods and molecular profiles by NGS in patients with plasma cell dyscrasias.BMC medical genomics · 2022Article
- Genomics of Plasma Cell Leukemia.Cancers · 2022Review
- Article
- miR-22 Modulates Lenalidomide Activity by Counteracting MYC Addiction in Multiple Myeloma.Cancers · 2021Article
- Where We Stand With Precision Therapeutics in Myeloma: Prosperity, Promises, and Pipedreams.Frontiers in oncology · 2021Review
- Article
- Amino acid depletion triggered by ʟ-asparaginase sensitizes MM cells to carfilzomib by inducing mitochondria ROS-mediated cell death.Blood advances · 2020Article
- Article
- Genetic Basis of Extramedullary Plasmablastic Transformation of Multiple Myeloma.The American journal of surgical pathology · 2020Article
- Application of Next-Generation Sequencing for the Genomic Characterization of Patients with Smoldering Myeloma.Cancers · 2020Article
- Expression Pattern and Biological Significance of the lncRNA ST3GAL6-AS1 in Multiple Myeloma.Cancers · 2020Article
Corrections and comments
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Authors and funding
16 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multiple myeloma (MM) is a clinically and genetically heterogeneous plasma cell (PC) malignancy. Whole-exome sequencing has identified therapeutically targetable mutations such as those in the mitogen-activated protein kinase (MAPK) pathway, which are the most prevalent MM mutations. We used deep sequencing to screen 167 representative patients with PC dyscrasias [132 with MM, 24 with primary PC leukemia (pPCL) and 11 with secondary PC leukemia (sPCL)] for mutations in BRAF, NRAS and KRAS, which were respectively found in 12%, 23.9% and 29.3% of cases. Overall, the MAPK pathway was affected in 57.5% of the patients (63.6% of those with sPCL, 59.8% of those with MM, and 41.7% of those with pPCL). The majority of BRAF variants were comparably expressed at transcript level. Additionally, gene expression profiling indicated the MAPK pathway is activated in mutated patients. Finally, we found that vemurafenib inhibition of BRAF activation in mutated U266 cells affected the expression of genes known to be associated with MM. Our data confirm and extend previous published evidence that MAPK pathway activation is recurrent in myeloma; the finding that it is mediated by BRAF mutations in a significant fraction of patients has potentially immediate clinical implications.
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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.