Evidence map›Paper›PMID 20880107›Full record

ArticleBritish journal of haematology2010

The class-I HDAC inhibitor MGCD0103 induces apoptosis in Hodgkin lymphoma cell lines and synergizes with proteasome inhibitors by an HDAC6-independent mechanism.

Daniela Buglio, Vidya Mamidipudi, Noor M Khaskhely, Helen Brady, Carla Heise, Jeffrey Besterman, Robert E Martell, Kyle MacBeth, Anas Younes

Open access · bronzeAbstract read
In one paragraph

Article in British journal of haematology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.7field-weighted citation impact, top 7% 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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

26 citing papers in PubMed, 57 citations in OpenAlex.

  1. Trial
  2. Review
  3. Review
  4. Advances in the treatment of Hodgkin's lymphoma (Review).International journal of oncology · 2023
    Review
  5. Review
  6. Article
  7. Review
  8. Article
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  16. Phase I study of panobinostat plus everolimus in patients with relapsed or refractory lymphoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2013
    Article
  17. Review
  18. Article
  19. Article
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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

9 authors at 2 institutions in 2 countries.

Daniela BuglioM. D. Anderson Cancer Center, Department of Lymphoma/Myeloma, Houston, University of Texas, TX, USA.
Vidya Mamidipudi
Noor M Khaskhely
Helen Brady
Carla Heise
Jeffrey Besterman
Robert E Martell
Kyle MacBeth
Anas Younes
The University of Texas MD Anderson Cancer Center · USPyrogenesis (Canada) · CA

Funding

UT M.D. Anderson Cancer Center Lymphoma SPOREP50CA136411 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI KWAK, LARRY W · 2009 to 2011
$1.5M
Clinical Activity of MGCD-0103 in Hodgkin LymphomaR21CA133876 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI YOUNES, ANAS · 2008 to 2009
$500k
Clinical Activity of 17-AAG in LymphomaR21CA117070 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI YOUNES, ANAS · 2006 to 2007
$431k
NCI NIH HHS 1P50CA136411-01A1NCI NIH HHS 1 R21 CA117070-01NCI NIH HHS P50 CA136411NCI NIH HHS R21 CA117070NCI NIH HHS R21 CA133876
6 · The paper itself

Abstract

Inhibition of histone deacetylase 6 (HDAC6)-dependent aggresome function by pan HDAC inhibitors was recently reported to be a key mechanism underlying the synergistic activity between proteasome inhibitors and HDAC inhibitors in a variety of tumour types. Because these combinations induce significant thrombocytopenia in vivo, we examined whether less toxic, isotype-selective HDAC inhibitors may still synergize with proteasome inhibitors, and if so, by what mechanisms. Here, we showed that the class I HDAC inhibitor, MGCD0103, has a potent antiproliferative activity in Hodgkin lymphoma (HL) cell lines. Furthermore, MGCD0103 induced tumour necrosis factor α (TNF-α) expression and secretion, which was associated with nuclear factor (NF)-κB activation. Selective inhibition of TNF-α expression by short interfering mRNA, or inhibition of MGCD0103-induced NF-kB activation by proteasome inhibitors enhanced MGCD0103-induced cell death. Thus, our results demonstrate that MGCD0103 may synergize with proteasome inhibitors by HDAC6-independent mechanisms, providing mechanistic rationale for exploring this potentially less toxic combination for the treatment of lymphoma.

Indexed as

Antineoplastic AgentsApoptosisBenzamidesBoronic AcidsBortezomibCytokinesDrug Screening Assays, AntitumorDrug SynergismGene Expression ProfilingGene Expression Regulation, NeoplasticHistone Deacetylase 6Histone Deacetylase InhibitorsHistone DeacetylasesHodgkin DiseaseHumansNF-kappa BAntineoplastic AgentsBenzamidesBoronic AcidsBortezomibCytokinesHDAC6 protein, humanHistone Deacetylase 6Histone Deacetylase InhibitorsHistone DeacetylasesmocetinostatNF-kappa BProtease InhibitorsPyrazinesPyrimidinesTumor Necrosis Factor-alpha

Identifiers

PMID20880107
PMCPMC3189488
OpenAlexW1929921628

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.