Evidence map›Paper›PMID 23758044›Full record

ArticleCancer science2013

Sustained upregulation of effector natural killer cells in chronic myeloid leukemia after discontinuation of imatinib.

Izuru Mizoguchi, Takayuki Yoshimoto, Seiichiro Katagiri, Junichiro Mizuguchi, Tetsuzo Tauchi, Yukihiko Kimura, Koiti Inokuchi, Junko H Ohyashiki, Kazuma Ohyashiki

Open access · bronzeAbstract read
In one paragraph

Article in Cancer science, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

24 citing papers in PubMed, 37 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Review
  4. Review
  5. Unleashing the power of NK cells in anticancer immunotherapy.Journal of molecular medicine (Berlin, Germany) · 2022
    Review
  6. Review
  7. Review
  8. Review
  9. CML Chapter.Cancer treatment and research · 2021
    Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. The immune contexture in cancer prognosis and treatment.Nature reviews. Clinical oncology · 2017
    Review
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  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

9 authors at 2 institutions in 1 country.

Izuru MizoguchiDepartment of Immunoregulation, Institute of Medical Science, Tokyo, Japan.
Takayuki Yoshimoto
Seiichiro Katagiri
Junichiro Mizuguchi
Tetsuzo Tauchi
Yukihiko Kimura
Koiti Inokuchi
Junko H Ohyashiki
Kazuma Ohyashiki
Tokyo Medical University · JPNippon Medical School · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A number of CML patients who achieve a sustained complete molecular response (CMR) for at least 2 years during imatinib (IM) therapy can discontinue IM without relapse. With the long-term goal of developing immunological criteria for managing IM therapy in CML patients, we compared the immunophenotypic profiles of three groups of CML patients: those who received IM and had a CMR for more than two consecutive years (CMR group); patients who received IM and did not have a sustained CMR but maintained a major molecular response for more than 2 years (fluctuating CMR group); and patients with a sustained CMR for more than 6 months after IM discontinuation (STOP-IM group), together with healthy controls. The percentages of effector populations of natural killer (NK) cells, such as interferon (IFN)-γ(+) CD3(-) CD56(+) cells, were significantly higher in the STOP-IM and CMR groups than in the fluctuating CMR and control groups. The elevated levels of these effector NK cells were sustained for more than 3 years after IM discontinuation. In contrast, the percentages of effector memory CD8(+) T cells, such as IFN-γ(+) CCR7(-) CD45RO(+) CD8(+) cells, were significantly higher in the STOP-IM and control groups than in the CMR and fluctuating CMR groups, possibly owing to IM intake. These results suggest that the immunological activation status of NK cells contributes to CMR maintenance. Higher activation levels of effector NK cells in CML patients being treated with IM might reflect minimization of BCR-ABL1 transcript levels and therefore could be additive information for determining whether to stop IM.

Indexed as

BenzamidesCD8-Positive T-LymphocytesFemaleFusion Proteins, bcr-ablHumansImatinib MesylateKiller Cells, NaturalLeukemia, Myelogenous, Chronic, BCR-ABL PositiveMaleMiddle AgedNeoplasm Recurrence, LocalPiperazinesPyrimidinesTreatment OutcomeUp-RegulationBenzamidesFusion Proteins, bcr-ablImatinib MesylatePiperazinesPyrimidines

Identifiers

PMID23758044
PMCPMC7656535
OpenAlexW1994501785

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.