Evidence map›Paper›PMID 20686505›Full record

ArticleLeukemia2010

HDAC inhibitors augment cytotoxic activity of rituximab by upregulating CD20 expression on lymphoma cells.

R Shimizu, J Kikuchi, T Wada, K Ozawa, Y Kano, Y Furukawa

Registry-linked trialAbstract read
PubMed Publisher
In one paragraph

Article in Leukemia, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02733380 (The Efficacy and Safety of Chidamide Combined With VDDT Regimen(Vinorelbine,Liposomal Doxorubicin,Dexamethasone and Thalidomide) in Relapse and Refractory Patients With Diffuse Large B Cell Lymphoma), which is not on this map. Cited by 63 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed, 1 pooled it
3.0field-weighted citation impact, top 9% of its field
1 · What the graph read from 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.

2 · The registry

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.

NCT02733380 phase2unknown statusnot on this mapstarted 2016, after this paper: background citation

The Efficacy and Safety of Chidamide Combined With VDDT Regimen(Vinorelbine,Liposomal Doxorubicin,Dexamethasone and Thalidomide) in Relapse and Refractory Patients With Diffuse Large B Cell Lymphoma

TypeinterventionalSponsorHenan Cancer HospitalRan2016 to 2021Enrolled20ConditionsDiffuse Large B-cell LymphomaArmsChidamide, Vinorelbine, Liposomal Doxorubicin or mitoxantrone, Dexamethasone, Thalidomide
3 · Its place in the literature

Who cites it

63 citing papers in PubMed, 1 synthesis or guideline pooled it, 100 citations in OpenAlex.

  1. Pooled it
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  8. Modulation of anti-tumour immunity by XPO1 inhibitors.Exploration of targeted anti-tumor therapy · 2025
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3 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

R ShimizuDivision of Stem Cell Regulation, Center for Molecular Medicine, Jichi Medical University, Shimotsuke, Tochigi, Japan.
J Kikuchi
T Wada
K Ozawa
Y Kano
Y Furukawa
Jichi Medical University · JPTochigi Cancer Center · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Anti-CD20 antibody rituximab is now essential for the treatment of CD20-positive B-cell lymphomas. Decreased expression of CD20 is one of the major mechanisms underlying both innate and acquired resistance to rituximab. In this study, we show that histone deacetylase (HDAC) inhibitors augment the cytotoxic activity of rituximab by enhancing the surface expression of CD20 antigen on lymphoma cells. HDAC inhibitors, valproic acid (VPA) and romidepsin, increased CD20 expression at protein and mRNA levels in B-cell lymphoma cell lines with relatively low CD20 expression levels. The VPA-mediated increase in CD20 expression occurred at 1 m, which is clinically achievable and safe, but insufficient for inducing cell death. Chromatin immunoprecipitation assays revealed that HDAC inhibitors transactivated the CD20 gene through promoter hyperacetylation and Sp1 recruitment. HDAC inhibitors potentiated the activity of rituximab in complement-dependent cytotoxic assays. In mouse lymphoma models, HDAC inhibitors enhanced CD20 expression along with histone hyperacetylation in transplanted cells, and acted synergistically with rituximab to retard their growth. The combination with HDAC inhibitors may serve as an effective strategy to overcome rituximab resistance in B-cell lymphomas.

Indexed as

AcetylationAnimalsAntibiotics, AntineoplasticAntibodies, MonoclonalAntibodies, Monoclonal, Murine-DerivedAntigens, CD20Antineoplastic AgentsAntineoplastic Combined Chemotherapy ProtocolsApoptosisBlotting, WesternCell ProliferationChromatin ImmunoprecipitationDepsipeptidesDrug SynergismFlow CytometryHistone Deacetylase InhibitorsAntibiotics, AntineoplasticAntibodies, MonoclonalAntibodies, Monoclonal, Murine-DerivedAntigens, CD20Antineoplastic AgentsDepsipeptidesHistone Deacetylase InhibitorsRituximabRNA, MessengerromidepsinValproic Acid

Identifiers

PMID20686505
OpenAlexW1979840572

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.