Evidence map›Paper›PMID 24349636›Full record

ReviewGenes & cancer2013

JNK Signaling in the Control of the Tumor-Initiating Capacity Associated with Cancer Stem Cells.

Chifumi Kitanaka, Atsushi Sato, Masashi Okada

Open access · bronzeAbstract readReview
In one paragraph

Review in Genes & cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

30 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. JNK Pathway in CNS Pathologies.International journal of molecular sciences · 2021
    Review
  8. Article
  9. Article
  10. Selective inhibitors for JNK signalling: a potential targeted therapy in cancer.Journal of enzyme inhibition and medicinal chemistry · 2020
    Review
  11. Article
  12. Article
  13. A tumor-associated splice-isoform ofProceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  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

3 authors at 2 institutions in 1 country.

Chifumi KitanakaDepartment of Molecular Cancer Science, Yamagata University School of Medicine, Yamagata, Japan ; Oncology Research Center, Research Institute for Advanced Molecular Epidemiology, Yamagata University, Yamagata, Japan ; Global Center of Excellence (COE) Program for Medical Sciences, Japan Society for the Promotion of Science, Tokyo, Japan.
Atsushi SatoDepartment of Molecular Cancer Science, Yamagata University School of Medicine, Yamagata, Japan ; Department of Neurosurgery, Yamagata University School of Medicine, Yamagata, Japan.
Masashi OkadaDepartment of Molecular Cancer Science, Yamagata University School of Medicine, Yamagata, Japan.
Yamagata University · JPJapan Society for the Promotion of Science · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Deregulation of c-Jun NH2-terminal kinase (JNK) signaling occurs frequently in a variety of human cancers, yet the exact role(s) of JNK deregulation in cancer cell biology remains to be fully elucidated. Our recent demonstration that the activity of JNK is required not only for self-renewal of glioma stem cells but also for their tumor initiation has, however, identified a new role for JNK in the control of the stemness and tumor-initiating capacity of cancer cells. Significantly, transient JNK inhibition was sufficient to cause sustained loss of the tumor-initiating capacity of glioma stem cells, suggesting that the phenotype of "lost tumor-initiating capacity" may be as stable as the differentiated state and that the tumor-initiating capacity might therefore be under the control of JNK through an epigenetic mechanism that also governs stemness and differentiation. Here, in this article, we review the role and mechanism of JNK in the control of this "stemness-associated tumor-initiating capacity" (STATIC), a new hypothetical concept we introduce in this review article. Since the idea of STATIC is essentially applicable to both cancer types that do and do not follow the cancer stem cell hypothesis, we also give consideration to the possible involvement of JNK-mediated control of STATIC in a wide range of human cancers in which JNK is aberrantly activated. Theoretically, successful targeting of STATIC through JNK could contribute to long-term control of cancer. Issues to be considered before clinical application of therapies targeting this JNK-STATIC axis are also discussed.

Indexed as

cancer stem cellepigenetic controlglioblastomaJNKstemnesstumor-initiating capacity

Identifiers

PMID24349636
PMCPMC3863334
OpenAlexW2112009846

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.