Evidence map›Paper›PMID 25142864›Full record

ArticleJournal of cellular biochemistry2015

Reduction of myeloid-derived suppressor cells and lymphoma growth by a natural triterpenoid.

Faisal F Y Radwan, Azim Hossain, Jason M God, Nathan Leaphart, Michelle Elvington, Mitzi Nagarkatti, Stephen Tomlinson, Azizul Haque

Open access · greenAbstract read
In one paragraph

Article in Journal of cellular biochemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.2field-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.

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

21 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
  2. Review
  3. CanPharmaceuticals (Basel, Switzerland) · 2025
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
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  12. Screening Immunoactive Compounds ofFrontiers in pharmacology · 2020
    Article
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  14. Article
  15. Article
  16. Article
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  18. Article
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  20. Observational
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

8 authors at 3 institutions in 1 country.

Faisal F Y RadwanDepartment of Microbiology and Immunology, Medical University of South Carolina, 173 Ashley Avenue, Charleston, 29425, South Carolina; Hollings Cancer Center, Medical University of South Carolina, 173 Ashley Avenue, Charleston, 29425, South Carolina; Children's Research Institute, Medical University of South Carolina, 173 Ashley Avenue, Charleston, 29425, South Carolina.
Azim Hossain
Jason M God
Nathan Leaphart
Michelle Elvington
Mitzi Nagarkatti
Stephen Tomlinson
Azizul Haque
Medical University of South Carolina · USMUSC Hollings Cancer Center · USUniversity of South Carolina · US

Funding

Translational Science Laboratory Shared ResourceP30CA138313 · NCI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI RAYMOND N. DUBOIS · 2009 to 2026
$42.7M
Complement, anti-tumor immunity and apoptosis-based therapyR01CA158179 · NCI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI TOMLINSON, STEPHEN · 2012 to 2016
$1.5M
Disruption of HLA Class II-Mediated Immune Recognition of B-Cell LymphomasR01CA129560 · NCI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI HAQUE, AZIZUL · 2009 to 2013
$1.5M
NCI NIH HHS P30 CA138313NCI NIH HHS R01 CA129560NCI NIH HHS R01 CA129560-S1NCI NIH HHS R01 CA158179
6 · The paper itself

Abstract

Lymphoma is a potentially life threatening disease. The goal of this study was to investigate the therapeutic potential of a natural triterpenoid, Ganoderic acid A (GA-A) in controlling lymphoma growth both in vitro and in vivo. Here, we show that GA-A treatment induces caspase-dependent apoptotic cell death characterized by a dose-dependent increase in active caspases 9 and 3, up-regulation of pro-apoptotic BIM and BAX proteins, and a subsequent loss of mitochondrial membrane potential with release of cytochrome c. In addition to GA-A's anti-growth activity, we show that lower doses of GA-A enhance HLA class II-mediated antigen (Ag) presentation and CD4+ T cell recognition of lymphoma cells in vitro. The therapeutic relevance of GA-A treatment was also tested in vivo using the EL4 syngeneic mouse model of metastatic lymphoma. GA-A-treatment significantly prolonged survival of EL4 challenged mice and decreased tumor metastasis to the liver, an outcome accompanied by a marked down-regulation of STAT3 phosphorylation, reduction myeloid-derived suppressor cells (MDSCs), and enhancement of cytotoxic CD8+ T cells in the host. Thus, GA-A not only selectively induces apoptosis in lymphoma cells, but also enhances cell-mediated immune responses by attenuating MDSCs, and elevating Ag presentation and T cell recognition. The demonstrated therapeutic benefit indicates that GA-A is a candidate for future drug design for the treatment of lymphoma.

Indexed as

AnimalsCell Line, TumorCell SurvivalHumansLymphomaMaleMiceMice, Inbred C57BLTriterpenesXenograft Model Antitumor Assaysganoderic acidTriterpenesAPOPTOSISCASPASESHLA CLASS II PROTEINSLYMPHOMAMITOCHONDRIAMYELOID-DERIVED SUPPRESSOR CELLSSTAT3T CELLSTRITERPENOID

Identifiers

PMID25142864
PMCPMC5012903
OpenAlexW2142926447

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.