ArticleCancer cell2014
Widespread genetic heterogeneity in multiple myeloma: implications for targeted therapy.
Article in Cancer cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 636 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.
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Who cites it
636 citing papers in PubMed.
- The genomic profiling of high-risk smoldering myeloma patients treated with an intensive strategy unveils potential markers of resistance and progression.Blood cancer journal · 2024Trial
- Cell-free DNA for the detection of emerging treatment failure in relapsed/ refractory multiple myeloma.Leukemia · 2022Trial
- Phase 2 study of venetoclax plus carfilzomib and dexamethasone in patients with relapsed/refractory multiple myeloma.Blood advances · 2021Trial
- Integrated Genomic and Epigenomic Analysis Reveals Epigenetic Plasticity in Disease Progression and Multidrug Resistance in Multiple Myeloma.Cancer research · 2026Article
- A single-cell atlas of multiple myeloma defines malignant archetypes and proliferative states.Nature genetics · 2026Article
- Comprehensive Analyses of SOX7 Provide Novel Insights on Its Tumor Suppressor Role and Its Target Genes with Therapeutic Implications in Multiple Myeloma.International journal of molecular sciences · 2026Article
- Prognostic Significance of Cell-Free DNA Derived 5-Hydroxymethylcytosine Signatures in Newly Diagnosed Multiple Myeloma.JCO precision oncology · 2026Article
- Genetic and clinical insights into the coexistence of multiple myeloma and diffuse large B cell lymphoma from a case report and systematic review with bioinformatics analysis.Discover oncology · 2026Article
- Pharmacological targeting of IRF4 as a therapeutic strategy for multiple myeloma.Nature chemical biology · 2026Article
- Ribonuclease DIS3 delays aging and senescence by generating tRNA halves.Nature communications · 2026Article
- Electrorotation as a tool for the dielectric characterization of tumor plasma cells in multiple myeloma.Scientific reports · 2026Article
- The Evolving Role of Genomic Technologies in Multiple Myeloma: Implications for Diagnosis, Risk Stratification and Resistance.Molecular diagnosis & therapy · 2026Review
- Clinical and genomic features of macrofocal multiple myeloma: a distinct profile.Haematologica · 2026Article
- Circulating Plasma Cells as a Minimally Invasive Adjunct to Bone Marrow Aspirates for Genetic Analysis of ER Stress and Autophagy in Multiple Myeloma: A Feasibility Study.Biomedicines · 2026Article
- DIS3 mutations enhance AID-driven translocations during B-cell activation, promoting transformation to multiple myeloma.Nature communications · 2026Article
- The intersection of disorders of sex development and cardiovascular diseases.Biology of sex differences · 2026Review
- Plasma cell leukemia: genomic features and their potential relevance for exploring clinical actionability.Blood advances · 2026Article
- Genome-wide copy number profiling enhances risk stratification in multiple myeloma by shallow whole-genome sequencing.Blood advances · 2026Article
- Inferring and summarizing tumor phylogenies from bulk DNA data.Algorithms for molecular biology : AMB · 2026Article
- Epigenetic reprogramming in multiple myeloma-Challenges and opportunities.International journal of cancer · 2026Review
576 more citing papers are in PubMed but not listed here.
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.
Funding
Abstract
We performed massively parallel sequencing of paired tumor/normal samples from 203 multiple myeloma (MM) patients and identified significantly mutated genes and copy number alterations and discovered putative tumor suppressor genes by determining homozygous deletions and loss of heterozygosity. We observed frequent mutations in KRAS (particularly in previously treated patients), NRAS, BRAF, FAM46C, TP53, and DIS3 (particularly in nonhyperdiploid MM). Mutations were often present in subclonal populations, and multiple mutations within the same pathway (e.g., KRAS, NRAS, and BRAF) were observed in the same patient. In vitro modeling predicts only partial treatment efficacy of targeting subclonal mutations, and even growth promotion of nonmutated subclones in some cases. These results emphasize the importance of heterogeneity analysis for treatment decisions.
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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.