Evidence map›Paper›PMID 22232214›Full record

ArticleThe Journal of clinical investigation2012

CD27 signaling on chronic myelogenous leukemia stem cells activates Wnt target genes and promotes disease progression.

Christian Schürch, Carsten Riether, Matthias S Matter, Alexandar Tzankov, Adrian F Ochsenbein

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed
5.4field-weighted citation impact, top 3% 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

66 citing papers in PubMed, 109 citations in OpenAlex.

  1. TheHematology reports · 2026
    Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. TNIK in disease: from molecular insights to therapeutic prospects.Apoptosis : an international journal on programmed cell death · 2024
    Review
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article

6 more citing papers are in PubMed but not listed here.

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

5 authors at 2 institutions in 1 country.

Christian SchürchTumor Immunology, Department of Clinical Research, University of Bern, Bern, Switzerland.
Carsten Riether
Matthias S Matter
Alexandar Tzankov
Adrian F Ochsenbein
University of Bern · CHUniversity Hospital of Basel · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic myelogenous leukemia (CML) results from a chromosomal translocation in hematopoietic stem or early progenitor cells that gives rise to the oncogenic BCR/ABL fusion protein. Clinically, CML has a chronic phase that eventually evolves into an accelerated stage and blast crisis. A CML-specific immune response is thought to contribute to the control of disease. Whether the immune system can also promote disease progression is not known. In the present study, we investigated the possibility that the TNF receptor family member CD27 is present on leukemia stem cells (LSCs) and mediates effects of the immune system on CML. In a mouse model of CML, BCR/ABL+ LSCs and leukemia progenitor cells were found to express CD27. Binding of CD27 by its ligand, CD70, increased expression of Wnt target genes in LSCs by enhancing nuclear localization of active β-catenin and TRAF2- and NCK-interacting kinase (TNIK). This resulted in increased proliferation and differentiation of LSCs. Blocking CD27 signaling in LSCs delayed disease progression and prolonged survival. Furthermore, CD27 was expressed on CML stem/progenitor cells in the bone marrow of CML patients, and CD27 signaling promoted growth of BCR/ABL+ human leukemia cells by activating the Wnt pathway. Since expression of CD70 is limited to activated lymphocytes and dendritic cells, our results reveal a mechanism by which adaptive immunity contributes to leukemia progression. In addition, targeting CD27 on LSCs may represent an attractive therapeutic approach to blocking the Wnt/β-catenin pathway in CML.

Indexed as

Disease ProgressionAdaptive ImmunityAdultAgedAnimalsCell CycleCell ProliferationCells, CulturedFemaleHumansKaplan-Meier EstimateLeukemia, Myelogenous, Chronic, BCR-ABL PositiveMaleMiceMice, Inbred C57BLMice, KnockoutProtein Serine-Threonine KinasesRecombinant Fusion ProteinsTNF Receptor-Associated Factor 2TNIK protein, mouseTumor Necrosis Factor Receptor Superfamily, Member 7Wnt Proteins

Identifiers

PMID22232214
PMCPMC3266773
OpenAlexW2110774869

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.