Evidence map›Paper›PMID 29518912›Full record

ReviewBiomedicines2018

Role of Akt Isoforms Controlling Cancer Stem Cell Survival, Phenotype and Self-Renewal.

Sergio Rivas, Carla Gómez-Oro, Inés M Antón, Francisco Wandosell

Open access · goldAbstract readReview
In one paragraph

Review in Biomedicines, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

29 citing papers in PubMed, 50 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
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  6. Review
  7. Article
  8. Article
  9. Article
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  11. Article
  12. Article
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  14. Article
  15. Article
  16. Targeting Phosphatases and Kinases: How to Checkmate Cancer.Frontiers in cell and developmental biology · 2021
    Review
  17. Regulation of cancer stem cells in triple negative breast cancer.Cancer drug resistance (Alhambra, Calif.) · 2021
    Review
  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

4 authors at 2 institutions in 1 country.

Sergio RivasCentro de Biología Molecular Severo Ochoa (CSIC-UAM), 28049 Madrid, Spain. srivas@cnb.csic.es.ORCID 0000-0002-6543-3603
Carla Gómez-OroCentro Nacional de Biotecnología (CNB-CSIC), 28049 Madrid, Spain. cgomez@cnb.csic.es.
Inés M AntónCentro Nacional de Biotecnología (CNB-CSIC), 28049 Madrid, Spain. ianton@cnb.csic.es.
Francisco WandosellCentro de Biología Molecular Severo Ochoa (CSIC-UAM), 28049 Madrid, Spain. fwandosell@cbm.csic.es.
Biomedical Research Networking Center on Neurodegenerative Diseases · ESCentro Nacional de Biotecnología · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The cancer stem cell (CSC) hypothesis suggests that tumours are maintained by a subpopulation of cells with stem cell properties. Although the existence of CSCs was initially described in human leukaemia, less evidence exists for CSCs in solid tumours. Recently, a CD133+ cell subpopulation was isolated from human brain tumoursexhibiting stem cell properties in vitro as well as the capacity to initiate tumours in vivo. In the present work, we try to summarize the data showing that some elements of the Phosphoinositide 3-kinase Class I (PI3K)/ Thymoma viral oncogene protein kinase (Akt) pathway, such the activity of PI3K Class I or Akt2, are necessary to maintain the CSC-like phenotype as well as survival of CSCs (also denoted as tumour-initiating cells (TICs)). Our data and other laboratory data permit a working hypothesis in which each Akt isoform plays an important and specific role in CSC/TIC growth, self-renewal, maintaining survival, and epithelial-mesenchymal transition (EMT) phenotype, not only in breast cancer, but also in glioma. We suggest that a more complete understanding is needed of the possible roles of isoforms in human tumours (iso-signalling determination). Thus, a comprehensive analysis of how hierarchical signalling is assembled during oncogenesis, how cancer landmarks are interconnected to favour CSC and tumour growth, and how some protein isoforms play a specific role in CSCs to ensure that survival and proliferation must be done in order to propose/generate new therapeutic approaches (alone or in combination with existing ones) to use against cancer.

Indexed as

AktCSCsgliomaPI3Kproliferationsignaling in cancersurvivalTICs

Identifiers

PMID29518912
PMCPMC5874686
OpenAlexW2794372787

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.