ArticleBlood2012
Intraclonal heterogeneity and distinct molecular mechanisms characterize the development of t(4;14) and t(11;14) myeloma.
Article in Blood, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 144 papers, 2 of them syntheses that pooled it.
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.
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Who cites it
144 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Co-Occurrence of Cytogenetic Abnormalities and High-Risk Disease in Newly Diagnosed and Relapsed/Refractory Multiple Myeloma.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2025Pooled it
- European Myeloma Network recommendations on the evaluation and treatment of newly diagnosed patients with multiple myeloma.Haematologica · 2014Guideline
- An enhanced genetic model of relapsed IGH-translocated multiple myeloma evolutionary dynamics.Blood cancer journal · 2020Trial
- Whole-exome sequencing of primary plasma cell leukemia discloses heterogeneous mutational patterns.Oncotarget · 2015Trial
- Trial
- Mutation of NRAS but not KRAS significantly reduces myeloma sensitivity to single-agent bortezomib therapy.Blood · 2014Trial
- Nucleotide Metabolism in Health and Disease.MedComm · 2026Review
- Plasma cell leukemia: genomic features and their potential relevance for exploring clinical actionability.Blood advances · 2026Article
- Unique molecular assay (UMA): a next-generation sequencing targeted panel for efficient and comprehensive genomic profiling and risk stratification of multiple myeloma.Haematologica · 2025Article
- Review
- RUNX1 expression dynamics in plasma cell differentiation and pathogenesis of multiple myeloma.Frontiers in immunology · 2025Article
- Dissecting the Puzzling Roles of FAM46C: A Multifaceted Pan-Cancer Tumour Suppressor with Increasing Clinical Relevance.Cancers · 2024Review
- Single-cell technologies in multiple myeloma: new insights into disease pathogenesis and translational implications.Biomarker research · 2023Review
- Mass Cytometry reveals unique phenotypic patterns associated with subclonal diversity and outcomes in multiple myeloma.Blood cancer journal · 2023Article
- Concerted Antibody and Antigen Discovery by Differential Whole-cell Phage Display Selections and Multi-omic Target Deconvolution.Journal of molecular biology · 2023Article
- Loss of ribonuclease DIS3 hampers genome integrity in myeloma by disrupting DNA:RNA hybrid metabolism.The EMBO journal · 2022Article
- Uncovering novel mutational signatures byCell genomics · 2022Article
- 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
- SAMHD1 in cancer: curse or cure?Journal of molecular medicine (Berlin, Germany) · 2022Review
84 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
We have used whole exome sequencing to compare a group of presentation t(4;14) with t(11;14) cases of myeloma to define the mutational landscape. Each case was characterized by a median of 24.5 exonic nonsynonymous single-nucleotide variations, and there was a consistently higher number of mutations in the t(4;14) group, but this number did not reach statistical significance. We show that the transition and transversion rates in the 2 subgroups are similar, suggesting that there was no specific mechanism leading to mutation differentiating the 2 groups. Only 3% of mutations were seen in both groups, and recurrently mutated genes include NRAS, KRAS, BRAF, and DIS3 as well as DNAH5, a member of the axonemal dynein family. The pattern of mutation in each group was distinct, with the t(4;14) group being characterized by deregulation of chromatin organization, actin filament, and microfilament movement. Recurrent RAS pathway mutations identified subclonal heterogeneity at a mutational level in both groups, with mutations being present as either dominant or minor subclones. The presence of subclonal diversity was confirmed at a single-cell level using other tumor-acquired mutations. These results are consistent with a distinct molecular pathogenesis underlying each subgroup and have important impacts on targeted treatment strategies. The Medical Research Council Myeloma IX trial is registered under ISRCTN68454111.
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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.