ArticleBlood2016
MAF protein mediates innate resistance to proteasome inhibition therapy in multiple myeloma.
Article in Blood, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
39 citing papers in PubMed, 1 synthesis or guideline pooled it, 78 citations in OpenAlex.
- DNA methylation in monozygotic twins discordant for acute lymphoblastic leukemia: a case report and systematic review.Clinical epigenetics · 2025Pooled it
- Ixazomib or Lenalidomide combined with cyclophosphamide and dexamethasone in the treatment of elderly transplant-ineligible newly diagnosed multiple myeloma.Scientific reports · 2025Trial
- Multiple myeloma: A tale of deregulated transcription factors.HemaSphere · 2026Review
- Hi-C for genome-wide detection of enhancer-hijacking rearrangements in routine lymphoid cancer biopsies.Cell genomics · 2026Article
- Targeting of SKP2 to combat drug resistance in multiple myeloma.Scientific reports · 2025Article
- Review
- Review
- Pathways to therapy resistance: The sheltering effect of the bone marrow microenvironment to multiple myeloma cells.Heliyon · 2024Review
- A novel 2-iminobenzimidazole compound, XYA1353, displays in vitro and in vivo anti-myeloma activity via targeting NF-κB signaling.Molecular and cellular biochemistry · 2024Article
- Bruceine B Displays Potent Antimyeloma Activity by Inducing the Degradation of the Transcription Factor c-Maf.ACS pharmacology & translational science · 2024Article
- Prognostic impact of translocation t(14;16) in multiple myeloma according to the presence of additional genetic lesions.Blood cancer journal · 2023Article
- Lactate Decreases Bortezomib Sensitivity and Predicts Poor Clinical Outcomes of Multiple Myeloma.Current medical science · 2023Article
- Transformation of arginine into zero-dimensional nanomaterial endows the material with antibacterial and osteoinductive activity.Science advances · 2023Article
- The ubiquitin ligase HERC4 suppresses MafA transcriptional activity triggered by GSK3β in myeloma by atypical K63-linked polyubiquitination.The Journal of biological chemistry · 2023Article
- The role and regulation of Maf proteins in cancer.Biomarker research · 2023Review
- Expression of integrin β-7 is epigenetically enhanced in multiple myeloma subgroups with high-risk cytogenetics.Clinical epigenetics · 2023Article
- Linked-read whole-genome sequencing resolves common and private structural variants in multiple myeloma.Blood advances · 2022Article
- β adrenergic signaling regulates hematopoietic stem and progenitor cell commitment and therapy sensitivity in multiple myeloma.Haematologica · 2022Article
- Review
- Metabolic Vulnerabilities in Multiple Myeloma.Cancers · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Multiple myeloma (MM) patients with the t(14;16) translocation have a poor prognosis, and unlike other molecular subgroups, their outcome has not improved with the introduction of bortezomib (Bzb). The mechanism underlying innate resistance of MM to Bzb is unknown. In the present study, we have investigated how MAF overexpression impacts resistance to proteasome inhibitor (PI) therapy (Bzb and carfilzomib). High levels of MAF protein were found in t(14;16) cell lines; cell lines from the t(4;14) subgroup had intermediate levels, whereas cell lines from the other subgroups had low levels. High expression of MAF protein in t(14;16) was associated with significantly higher PI half-maximum inhibitory concentration values compared with other molecular subgroups. PI exposure abrogated glycogen synthase kinase 3β (GSK3β)-mediated degradation of MAF protein, resulting in increased MAF protein stability and PI resistance. Subsequent studies using loss-of-function and gain-of-function models showed that silencing MAF led to increased sensitivity to PIs, enhanced apoptosis, and activation of caspase-3, -7, -8, -9, poly (ADP-ribose) polymerase, and lamin A/C. In contrast, overexpression of MAF resulted in increased resistance to PIs and reduced apoptosis. These results define the role of MAF and GSK3 in the resistance of t(14;16) MM to PIs and identifies a novel mechanism by which MAF protein levels are regulated by PIs, which in turn confers resistance to PIs.
Indexed as
Identifiers
What OpenQuestion holds
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.