ArticleOncotarget2016
Whole-exome and transcriptome sequencing of refractory diffuse large B-cell lymphoma.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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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
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Who cites it
31 citing papers in PubMed, 51 citations in OpenAlex.
- The Roles of the PRDM Family in the Neuro-Motor System.Biomolecules · 2026Review
- Characterizing the mutational landscape of sinonasal squamous cell carcinoma using whole-exome sequencing.Oral oncology · 2025Article
- From regulation to deregulation of p53 in hematologic malignancies: implications for diagnosis, prognosis and therapy.Biomarker research · 2024Review
- Genetic and transcriptomic analyses of diffuse large B-cell lymphoma patients with poor outcomes within two years of diagnosis.Leukemia · 2024Article
- Article
- High PDL1/PDL2 gene expression correlates with worse outcome in primary mediastinal large B-cell lymphoma.Blood advances · 2023Article
- Article
- Canine Somatic Mutations from Whole-Exome Sequencing of B-Cell Lymphomas in Six Canine Breeds-A Preliminary Study.Animals : an open access journal from MDPI · 2023Article
- RNA-seq analysis reveals candidate genes associated with proliferation, invasion, and migration in BCL11A knockdown B-NHL cell lines.Annals of hematology · 2023Article
- Transcriptome sequencing reveals novel molecular features of SLE severity.Frontiers in genetics · 2023Article
- Tumor immune contexture is a determinant of anti-CD19 CAR T cell efficacy in large B cell lymphoma.Nature medicine · 2022Article
- Mutated RAS-associating proteins and ERK activation in relapse/refractory diffuse large B cell lymphoma.Scientific reports · 2022Article
- Article
- Biomarkers of response to ibrutinib plus nivolumab in relapsed diffuse large B-cell lymphoma, follicular lymphoma, or Richter's transformation.Translational oncology · 2021Article
- Genetic Landscape of Relapsed and Refractory Diffuse Large B-Cell Lymphoma: A Systemic Review and Association Analysis With Next-Generation Sequencing.Frontiers in genetics · 2021Article
- Molecular Genetics of Relapsed Diffuse Large B-Cell Lymphoma: Insight into Mechanisms of Therapy Resistance.Cancers · 2020Review
- Amerindian Ancestry Influences Genetic Susceptibility to Chronic Obstructive Pulmonary Disease.Journal of personalized medicine · 2020Article
- Transcriptome Profiling Associated with Carcass Quality of Loin Muscles in Crossbred Pigs.Animals : an open access journal from MDPI · 2020Article
- Multifaceted Role of PRDM Proteins in Human Cancer.International journal of molecular sciences · 2020Review
- Identification of dual histone modification-binding protein interaction by combining mass spectrometry and isothermal titration calorimetric analysis.Journal of advanced research · 2020Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diffuse large B-cell lymphoma (DLBCL) is the most common type of non-Hodgkin lymphoma. Although rituximab therapy improves clinical outcome, some patients develop resistant DLBCL; however, the genetic alterations in these patients are not well documented. To identify the genetic background of refractory DLBCL, we conducted whole-exome sequencing and transcriptome sequencing for six patients with refractory and seven with responsive DLBCL. The average numbers of pathogenic somatic single nucleotide variants and indels in coding regions were 71 in refractory patients (range 28-120) and 38 (range 19-66) in responsive patients. Missense mutations of TP53 were exclusive in 50% (3/6) of refractory patients and involved the DNA-binding domain of TP53. All missense mutations of TP53 were accompanied by copy number deletions. RAB11FIP5, PRKCB, PRDM15, FNBP4, AHR, CEP128, BRE, DHX16, MYO6, and NMT1 mutations were recurrent in refractory patients. MYD88, B2M, SORCS3, and WDFY3 mutations were more frequent in refractory patients than in responsive patients. REL-BCL11A fusion was found in two refractory patients; one had both fusion and copy number gain. Recurrent copy gains of POU2AF1, SLC1A4, REL11, FANCL, CACNA1D, TRRAP, and CUX1 with significantly increased average expression were found in refractory patients. The expression profile revealed enriched gene sets associated with treatment resistance, including oxidative phosphorylation and ATP-binding cassette transporters. In conclusion, this study integrated both genomic and transcriptomic alterations associated with refractory DLBCL and found several treatment-resistance alterations that may contribute to refractoriness.
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