Evidence map›Paper›PMID 23404187›Full record

ArticleJournal of clinical immunology2013

A VEGFR-3 antagonist increases IFN-γ expression on low functioning NK cells in acute myeloid leukemia.

Ji Yoon Lee, Sohye Park, Donghyun Curt Kim, Jae-Ho Yoon, Seung Hwan Shin, Woo-Sung Min, Hee-Je Kim

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of clinical immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

14 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. 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

7 authors at 3 institutions in 2 countries.

Ji Yoon LeeDepartment of Hematology, Catholic Blood and Marrow Transplantation Center, Seoul St. Mary's Hospital, College of Medicine, The Catholic University of Korea, 505 Banpo 4-dong, Seocho-gu, Seoul, 137-701, Korea.
Sohye Park
Donghyun Curt Kim
Jae-Ho Yoon
Seung Hwan Shin
Woo-Sung Min
Hee-Je Kim
Catholic University of Korea · KRSeoul St. Mary's Hospital · KRPRG S&Tech (South Korea)

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeAlthough the importance of vascular endothelial growth factor receptor (VEGFR)-3 has been demonstrated in acute myeloid leukemia (AML), the role of VEGFR-3 in functioning natural killer (NK) cells remains largely unexplored. NK cells can destroy cancer cells by releasing the cytokine interferon (IFN)-γ, but NK cells in AML patients (AML NK cells) have low cytolytic activity. In the present study, we investigated whether lymphatic markers including VEGFR-3 are expressed on low-functioning AML NK cells and VEGFR-3 antagonist can restore expression of IFN-γ in NK cells.

methodsSamples from 67 de novo AML patients and 34 healthy donors were analyzed for lymphatic markers expression using RT-PCR, flow cytometry, and immunostaining. For the cytotoxicity assays, K562 cells and AML NK cells were used as target and effector cells, respectively. To block VEGFR-3, MAZ51 was added to NK cells, which were then subjected to FACS analysis.

resultsCompared with NK cells from healthy donors (healthy NK cells), AML NK cells exhibited higher levels of VEGFR-3 and lower expression of IFN-γ. VEGFR-3-expressing AML NK cells were less potent than healthy NK cells in terms of killing K562 cells. The level of IFN-γ in AML NK cells was increased by VEGFR-3 antagonist treatment, indicating the functional relevance of VEGFR-3 in IFN-γ-secreting NK cells.

conclusionCollectively, our data suggest a relationship between VEGFR-3 and IFN-γ expression in NK cells and raise the possibility of advanced therapeutic approaches involving VEGFR-3 antagonist treatment prior to NK immune cell therapy in AML.

Indexed as

AdolescentAdultAgedCytotoxicity, ImmunologicFemaleGene Expression RegulationHumansIndolesInterferon-gammaK562 CellsKiller Cells, NaturalLeukemia, Myeloid, AcuteMaleMiddle AgedNaphthalenesVascular Endothelial Growth Factor Receptor-33-(4-dimethylamino-naphthalen-1-ylmethylene)-1,3-dihydro-indol-2-oneIndolesInterferon-gammaNaphthalenesVascular Endothelial Growth Factor Receptor-3

Identifiers

PMID23404187
OpenAlexW2035905589

What OpenQuestion holds

Textmetadata
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.