ArticleLeukemia2018
Kinase domain activation through gene rearrangement in multiple myeloma.
Article in Leukemia, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 33 citations in OpenAlex.
- The Gut Microbiome Role in Multiple Myeloma: Emerging Insights and Therapeutic Opportunities.Hematology reports · 2025Review
- Multiomic Mapping of Acquired Chromosome 1 Copy-Number and Structural Variants to Identify Therapeutic Vulnerabilities in Multiple Myeloma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023Article
- Myeloma Genome Project Panel is a Comprehensive Targeted Genomics Panel for Molecular Profiling of Patients with Multiple Myeloma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022Article
- The genetic heterogeneity and drug resistance mechanisms of relapsed refractory multiple myeloma.Nature communications · 2022Article
- Pathogenesis and treatment of multiple myeloma.MedComm · 2022Review
- Chromothripsis as a pathogenic driver of multiple myeloma.Seminars in cell & developmental biology · 2022Review
- Pathogenic signaling in multiple myeloma.Seminars in oncology · 2022Article
- KRAS and RAS-MAPK Pathway Deregulation in Mature B Cell Lymphoproliferative Disorders.Cancers · 2022Review
- Exonic variants in multiple myeloma patients associated with relapsed/ refractory and response to bortezomib regimens.Saudi journal of biological sciences · 2022Article
- Plasma cell myeloma: role of histopathology, immunophenotyping, and genetic testing.Skeletal radiology · 2022Review
- Integrative multi-omics identifies high risk multiple myeloma subgroup associated with significant DNA loss and dysregulated DNA repair and cell cycle pathways.BMC medical genomics · 2021Article
- Non-secretory multiple myeloma with unusual TFG-ALK fusion showed dramatic response to ALK inhibition.NPJ genomic medicine · 2021Article
- Evolution and structure of clinically relevant gene fusions in multiple myeloma.Nature communications · 2020Article
- Review
- Poor overall survival in hyperhaploid multiple myeloma is defined by double-hit bi-allelic inactivation ofOncotarget · 2019Article
- Germline Risk Contribution to Genomic Instability in Multiple Myeloma.Frontiers in genetics · 2019Review
- Protein Kinase D 1 Predicts Poor Treatment Response and Unfavorable Survival of Bortezomib-Based Treatment, and Its Knockdown Enhances Drug Sensitivity to Bortezomib in Multiple Myeloma.Technology in cancer research & treatmentArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
22 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chromosomal rearrangements that result in oncogenic kinase activation are present in many solid and hematological malignancies, but none have been reported in multiple myeloma (MM). Here we analyzed 1421 samples from 958 myeloma patients using a targeted assay and detected fusion genes in 1.5% of patients. These fusion genes were in-frame and the majority of them contained kinase domains from either receptor tyrosine kinases (ALK, ROS1, NTRK3, and FGFR1) or cytoplasmic kinases (BRAF, MAP3K14, and MAPK14), which would result in the activation of MEK/ERK, NF-κB, or inflammatory signaling pathways. Fusion genes were present in smoldering MM, newly diagnosed MM, and relapse patient samples indicating they are not solely late events. Most fusion genes were subclonal in nature, but one EML4-ALK fusion was clonal indicating it is a driver of disease pathogenesis. Samples with fusions of receptor tyrosine kinases were not found in conjunction with clonal Ras/Raf mutations indicating a parallel mechanism of MEK/ERK pathway activation. Fusion genes involving MAP3K14 (NIK), which regulates the NF-κB pathway, were detected as were t(14;17) rearrangements involving NIK in 2% of MM samples. Activation of kinases in myeloma through rearrangements presents an opportunity to use treatments existing in other cancers.
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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.