ArticleBlood advances2020
Molecular background delineates outcome of double protein expressor diffuse large B-cell lymphoma.
Article in Blood advances, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.
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Who cites it
26 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.
- A Diagnostic Approach in Large B-Cell Lymphomas According to the Fifth World Health Organization and International Consensus Classifications and a Practical Algorithm in Routine Practice.International journal of molecular sciences · 2024Guideline
- 2026 Update on the Management of Diffuse Large B-Cell Lymphoma.American journal of hematology · 2026Review
- Prognostic impact of TP53 mutations in diffuse large B-cell lymphoma.Annals of hematology · 2026Article
- Primary Diffuse Large B-Cell Lymphoma of the Female Genital Tract: A Rare Case Presentation With Literature Review.Case reports in hematology · 2026Article
- Sequential PD-1 inhibitors as consolidative therapy post-CD19 CART in relapsed/refractory NHL: a propensity score matching cohort study.Journal of translational medicine · 2025Article
- Spatial Analysis of the Tumor Microenvironment in Diffuse Large B-cell Lymphoma Reveals Clinically Relevant Cell Interactions and Recurrent Cellular Neighborhoods.Cancer immunology research · 2025Article
- Multiplexed imaging mass cytometry elicits p-S6 as a therapeutic and prognostic factor in diffuse large B-cell lymphoma.Blood advances · 2025Article
- Recent advancements in double-expressor lymphoma: novel therapeutic approaches and prospects.The oncologist · 2025Review
- Characterization of tumor microenvironment and cell interaction patterns in testicular and diffuse large B-cell lymphomas.Haematologica · 2025Article
- Biomarker-adapted treatment in high-risk large B-cell lymphoma.HemaSphere · 2025Article
- Network Pharmacology, Molecular Docking, and Experimental Validation of the Mechanism of Jeduxiaoliu Formula against Diffuse Large B-Cell Lymphoma.Combinatorial chemistry & high throughput screening · 2025Article
- Disruption of KLHL6 Fuels Oncogenic Antigen Receptor Signaling in B-Cell Lymphoma.Blood cancer discovery · 2024Article
- Patient-specific computational models predict prognosis in B cell lymphoma by quantifying pro-proliferative and anti-apoptotic signatures from genetic sequencing data.Blood cancer journal · 2024Article
- Molecular Subtypes and the Role of TP53 in Diffuse Large B-Cell Lymphoma and Richter Syndrome.Cancers · 2024Review
- Patterns of Oncogene Coexpression at Single-Cell Resolution Influence Survival in Lymphoma.Cancer discovery · 2023Article
- BET inhibitor trotabresib in heavily pretreated patients with solid tumors and diffuse large B-cell lymphomas.Nature communications · 2023Article
- Venetoclax improves CD20 immunotherapy in a mouse model of MYC/BCL2 double-expressor diffuse large B-cell lymphoma.Journal for immunotherapy of cancer · 2023Article
- Article
- Dose-adjusted EPOCH and rituximab for the treatment of double expressor and double-hit diffuse large B-cell lymphoma: impact of TP53 mutations on clinical outcome.Haematologica · 2022Article
- Genetic Subtyping and Phenotypic Characterization of the Immune Microenvironment and MYC/BCL2 Double Expression Reveal Heterogeneity in Diffuse Large B-cell Lymphoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Concomitant deregulation of MYC and BCL2 comprises clinically significant, yet poorly characterized biological high-risk feature in diffuse large B-cell lymphoma (DLBCL). To interrogate these lymphomas, we analyzed translocations and protein expression of BCL2, BCL6, and MYC; correlated the findings with comprehensive mutational, transcriptomic, and clinical data in 181 patients with primary DLBCL; and validated the key findings in independent data sets. Structural variations of BCL2 were subtype-specific and specifically increased BCL2 expression. Molecular dissection of MYC deregulation revealed associations with other lymphoma drivers, including loss of TP53, and distinctive gene expression profiles. Double protein expression (DPE) arose from heterogeneous molecular backgrounds that exhibited subtype-dependent patterns. In the germinal center B-cell (GCB) DLBCL, concurrent alterations of MYC and BCL2 loci gave rise to the majority of DPE DLBCLs, whereas among the activated B-cell (ABC) DLBCLs, concurrent alterations were infrequent. Clinically, DPE DLBCL defined a prognostic entity, which was independent of the International Prognostic Index (IPI) and cell of origin, and together with the loss of TP53 had a synergistic dismal impact on survival. In the DPE DLBCL, the loss of TP53 was associated with a chemorefractory disease, whereas among the other DLBCLs, no correlation with survival was seen. Importantly, BCL6 translocations identified non-GCB lymphomas with favorable BN2/C1-like survival independent of IPI and concurrent DPE status. Taken together, our findings define molecular characteristics of the DPE in DLBCL, and recognize clinically feasible predictors of outcome. Given the emerging taxonomical significance of BCL2, BCL6, MYC, and TP53, our findings provide further depth and validation to the genomic classification of DLBCL.
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