ReviewBioMed research international2015
Constitutive NF- κ B Activation Underlines Major Mechanism of Drug Resistance in Relapsed Refractory Diffuse Large B Cell Lymphoma.
Review in BioMed research international, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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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
23 citing papers in PubMed.
- Zanubrutinib plus R-CHOP for the treatment of newly diagnosed double-expressor lymphoma: A phase 2 clinical study.Cancer · 2025Trial
- Mechanisms of chemoresistance in diffuse large B‑cell lymphoma and novel therapeutic strategies (Review).International journal of oncology · 2026Review
- Redox destabilization by ibrutinib promotes ferroptosis in diffuse large B-cell lymphoma (DLBCL).Cell death discovery · 2025Article
- Treatment outcomes of zanubrutinib-based regimen in newly diagnosed patients with MYC/BCL2 double-expressor diffuse large B-cell lymphoma: a retrospective multicenter real-world study.Annals of hematology · 2025Article
- Enhanced glycolysis induced by activation of AKT/NF-κB signaling pathway contributes to doxorubicin resistance in DLBCL.American journal of cancer research · 2025Article
- Identification and overcoming rituximab resistance in diffuse large B-cell lymphoma using next-generation sequencing.The Korean journal of internal medicine · 2023Article
- Efficacy of coxsackievirus A21 against drug-resistant neoplastic B cells.Molecular therapy oncolytics · 2023Article
- The Metabolism and Immune Environment in Diffuse Large B-Cell Lymphoma.Metabolites · 2023Review
- Drug-Resistance Mechanism and New Targeted Drugs and Treatments of Relapse and Refractory DLBCL.Cancer management and research · 2023Review
- TBL1X: At the crossroads of transcriptional and posttranscriptional regulation.Experimental hematology · 2022Review
- miRNAs in Lymphocytic Leukaemias-The miRror of Drug Resistance.International journal of molecular sciences · 2022Review
- An Autophagy-Related Gene Signature can Better Predict Prognosis and Resistance in Diffuse Large B-Cell Lymphoma.Frontiers in genetics · 2022Article
- Melatonin increases the chemosensitivity of diffuse large B-cell lymphoma cells to epirubicin by inhibiting P-glycoprotein expression via the NF-κB pathway.Translational oncology · 2021Article
- Expression of IL-34 correlates with macrophage infiltration and prognosis of diffuse large B-cell lymphoma.Clinical & translational immunology · 2019Article
- Z-VRPR-FMK can inhibit the growth and invasiveness of diffuse large B-cell lymphoma by depressing NF-κB activation and MMP expression induced by MALT1.International journal of clinical and experimental pathology · 2019Article
- Analysis of Genomic Alteration in Primary Central Nervous System Lymphoma and the Expression of Some Related Genes.Neoplasia (New York, N.Y.) · 2018Article
- Novel BAFF-Receptor Antibody to Natively Folded Recombinant Protein Eliminates Drug-Resistant Human B-cell MalignanciesClinical cancer research : an official journal of the American Association for Cancer Research · 2018Article
- Expression of exportin-1 in diffuse large B-cell lymphoma: immunohistochemistry and TCGA analyses.International journal of clinical and experimental pathology · 2018Article
- DCZ3301, a novel cytotoxic agent, inhibits proliferation in diffuse large B-cell lymphoma via the STAT3 pathway.Cell death & disease · 2017Article
- Microenvironmental agonists generateBlood advances · 2017Article
Corrections and comments
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Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diffuse large B cell lymphoma (DLBCL) is the most common subtype of B cell non-Hodgkin's lymphoma (NHL), encompassing 30-40% of the estimated 70,000 cases of NHL in 2014 in the USA. Despite major improvements with immune-chemotherapy, the fraction of patients who still succumb to a refractory or relapsed disease remains high. This review addresses whether the better understanding of the biology of DLBCL defines new therapeutic avenues that may overcome the emerging resistance of this disease to traditional immune-chemotherapy, such as rituximab in combination with traditional chemotherapy agents. Emerging targeted therapy for relapsed refractory DLBCL encompasses more complex molecular abnormalities involving signaling pathways other than NF-κB as mechanism of resistance to immune-chemotherapy. Our review suggests that NF-κB pathway is an important crossroad where other pathways converge as phenotype of resistance that emerges in patients who fail frontline and salvage immune-chemotherapy. Future efforts should aim at targeting the role of NF-κB resistance in clinical trials, where novel agents like lenalidomide and proteasome inhibitors with established activity in this perspective will be an important component in combination therapy, along with new monoclonal antibody, BTK-inhibitors, and other novel therapy agents.
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