Evidence map›Paper›PMID 25678856›Full record

ArticleCancer cell international2015

Evaluating the evidence for targeting FOXO3a in breast cancer: a systematic review.

Simon Taylor, Matthew Lam, Chathyan Pararasa, James Ep Brown, Amtul R Carmichael, Helen R Griffiths

Open access · goldAbstract read
In one paragraph

Article in Cancer cell international, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
8.6field-weighted citation impact, top 2% 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

25 citing papers in PubMed, 146 citations in OpenAlex.

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  12. Airborne Particulate Matter (PMInternational journal of molecular sciences · 2020
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  14. New insights into the roles of theUpsala journal of medical sciences · 2019
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  18. 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

6 authors at 2 institutions in 1 country.

Simon TaylorLife and Health Sciences, Aston University, Aston Triangle, Birmingham, B4 7ET UK.
Matthew LamLife and Health Sciences, Aston University, Aston Triangle, Birmingham, B4 7ET UK.
Chathyan PararasaLife and Health Sciences, Aston University, Aston Triangle, Birmingham, B4 7ET UK.
James Ep BrownLife and Health Sciences, Aston University, Aston Triangle, Birmingham, B4 7ET UK.
Amtul R CarmichaelRussells Hall Hospital, Dudley, DY1 2HQ UK.
Helen R GriffithsLife and Health Sciences, Aston University, Aston Triangle, Birmingham, B4 7ET UK.
Aston University · GBRussells Hall Hospital · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTumour cells show greater dependency on glycolysis so providing a sufficient and rapid energy supply for fast growth. In many breast cancers, estrogen, progesterone and epidermal growth factor receptor-positive cells proliferate in response to growth factors and growth factor antagonists are a mainstay of treatment. However, triple negative breast cancer (TNBC) cells lack receptor expression, are frequently more aggressive and are resistant to growth factor inhibition. Downstream of growth factor receptors, signal transduction proceeds via phosphatidylinositol 3-kinase (PI3k), Akt and FOXO3a inhibition, the latter being partly responsible for coordinated increases in glycolysis and apoptosis resistance. FOXO3a may be an attractive therapeutic target for TNBC. Therefore we have undertaken a systematic review of FOXO3a as a target for breast cancer therapeutics.

methodsArticles from NCBI were retrieved systematically when reporting primary data about FOXO3a expression in breast cancer cells after cytotoxic drug treatment.

resultsIncreased FOXO3a expression is common following cytotoxic drug treatment and is associated with apoptosis and cell cycle arrest. There is some evidence that metabolic enzyme expression is also altered and that this effect is also elicited in TNBC cells. FOXO3a expression serves as a positive prognostic marker, especially in estrogen (ER) receptor positive cells. DISCUSSION: FOXO3a is upregulated by a number of receptor-dependent and -independent anti-cancer drugs and associates with apoptosis. The identification of microRNA that regulate FOXO3a directly suggest that it offers a tangible therapeutic target that merits wider evaluation.

Indexed as

ApoptosisGlycolysisMetabolismOxidative stressPhosphatidylinositol 3-kinaseTriple negative breast cancer

Identifiers

PMID25678856
PMCPMC4325954
OpenAlexW2147756339

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.