Evidence map›Paper›PMID 30592157›Full record

ArticleCancer medicine2019

Oxaliplatin regulates myeloid-derived suppressor cell-mediated immunosuppression via downregulation of nuclear factor-κB signaling.

Na-Rae Kim, Yeon-Jeong Kim

Open access · goldAbstract read
In one paragraph

Article in Cancer medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

23 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Review
  11. Review
  12. Review
  13. Review
  14. Review
  15. Immunity, immunotherapy, and rectal cancer: A clinical and translational science review.Translational research : the journal of laboratory and clinical medicine · 2021
    Review
  16. Article
  17. Frontiers in immunology · 2021
    Review
  18. Review
  19. Review
  20. Article
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

2 authors at 1 institution in 1 country.

Na-Rae KimLaboratory of Microbiology and Immunology, College of Pharmacy, Inje University, Gimhae, Korea.
Yeon-Jeong KimLaboratory of Microbiology and Immunology, College of Pharmacy, Inje University, Gimhae, Korea.ORCID 0000-0002-5159-828X
Inje University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myeloid-derived suppressor cells (MDSCs) represent one of the major types of immunoregulatory cells present under abnormal conditions, including cancer. These cells are characterized by their immature phenotype and suppressive effect on various immune effectors. In both human and mouse, there are two main subsets of MDSCs: polymorphonuclear (PMN)-MDSCs and mononuclear (Mo)-MDSCs. Thus, strategies to regulate MDSC-mediated immunosuppression could result in the enhancement of anticancer immune responses. Oxaliplatin, a platinum-based anticancer agent, is widely used in clinical settings. It is known to induce cell death by interfering with double-stranded DNA and interrupting its replication and transcription. In this study, we found that oxaliplatin has the potential to regulate MDSC-mediated immunosuppression in cancer. First, oxaliplatin selectively depleted MDSCs, especially Mo-MDSCs, but only minimally affected T cells. In addition, sublethal doses of oxaliplatin eliminated the immunosuppressive capacity of MDSCs and induced the differentiation of MDSCs into mature cells. Oxaliplatin treatment diminished the expression of the immunosuppressive functional mediators arginase 1 (ARG1) and NADPH oxidase 2 (NOX2) in MDSCs, while an MDSC-depleting agent, gemcitabine, did not downregulate these factors significantly. Oxaliplatin-conditioned MDSCs had no tumor-promoting activity in vivo. In addition, oxaliplatin modulated the intracellular NF-κB signaling in MDSCs. Thus, oxaliplatin has the potential to be used as an immunoregulatory agent as well as a cytotoxic drug in cancer treatment.

Indexed as

AnimalsAntineoplastic AgentsCell Line, TumorCell SurvivalDeoxycytidineGemcitabineImmune ToleranceMice, Inbred BALB CMyeloid-Derived Suppressor CellsNeoplasmsNF-kappa BOxaliplatinT-LymphocytesAntineoplastic AgentsDeoxycytidineGemcitabineNF-kappa BOxaliplatinanticancer agentimmunosuppressionmyeloid-derived suppressor cellNF-κBoxaliplatin

Identifiers

PMID30592157
PMCPMC6346236
OpenAlexW2908006163

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.