Evidence map›Paper›PMID 25530875›Full record

ArticleTranslational neuroscience2013

ASYMMETRIC CELL DIVISION: IMPLICATIONS FOR GLIOMA DEVELOPMENT AND TREATMENT.

Kate Marie Lewis, Claudia Petritsch

Open access · hybridAbstract read
In one paragraph

Article in Translational neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.6field-weighted citation impact, top 32% 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

9 citing papers in PubMed, 17 citations in OpenAlex.

  1. Review
  2. Role of Diet in Stem and Cancer Stem Cells.International journal of molecular sciences · 2022
    Review
  3. Article
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  5. Review
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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

2 authors at 1 institution in 1 country.

Kate Marie LewisDepartment of Neurological Surgery, University of California San Francisco, San Francisco 94158, CA, USA.
Claudia PetritschDepartment of Neurological Surgery, University of California San Francisco, San Francisco 94158, CA, USA ; Brain Tumor Research Center, UCSF Helen Diller Comprehensive Cancer Center, UCSF Ely and Edythe Broad Institute of Regeneration Medicine.
Neurological Surgery · US

Funding

BRAF Mutation in Malignant Astrocytoma Origin, Evolution, and Response to TherapyR01NS080619 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI JAMES, CHARLES DAVID, PETRITSCH, CLAUDIA KATHARINA · 2012 to 2016
$1.8M
A causal role for asymmetric cell division defects in glioma initiationR01CA164746 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI PETRITSCH, CLAUDIA KATHARINA · 2012 to 2016
$1.6M
NCI NIH HHS R01 CA164746NINDS NIH HHS R01 NS080619
6 · The paper itself

Abstract

Glioma is a heterogeneous disease process with differential histology and treatment response. It was previously thought that the histological features of glial tumors indicated their cell of origin. However, the discovery of continuous neuro-gliogenesis in the normal adult brain and the identification of brain tumor stem cells within glioma have led to the hypothesis that these brain tumors originate from multipotent neural stem or progenitor cells, which primarily divide asymmetrically during the postnatal period. Asymmetric cell division allows these cell types to concurrently self-renew whilst also producing cells for the differentiation pathway. It has recently been shown that increased symmetrical cell division, favoring the self-renewal pathway, leads to oligodendroglioma formation from oligodendrocyte progenitor cells. In contrast, there is some evidence that asymmetric cell division maintenance in tumor stem-like cells within astrocytoma may lead to acquisition of treatment resistance. Therefore cell division mode in normal brain stem and progenitor cells may play a role in setting tumorigenic potential and the type of tumor formed. Moreover, heterogeneous tumor cell populations and their respective cell division mode may confer differential sensitivity to therapy. This review aims to shed light on the controllers of cell division mode which may be therapeutically targeted to prevent glioma formation and improve treatment response.

Indexed as

AstrocytomaAsymmetric cell divisionBrain tumorCancer stem cellCell of originChemotherapyOligodendrogliomaProgenitor cellStem cellSymmetrical cell division

Identifiers

PMID25530875
PMCPMC4269374
OpenAlexW1977615104

What OpenQuestion holds

Textmetadata
LicenceTDM
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.