Evidence map›Paper›PMID 24618834›Full record

ArticleCancer biology & therapy2014

New methods to control neuroblastoma growth.

Paul Dent

Open access · hybridAbstract readComment
In one paragraph

Article in Cancer biology & therapy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.6field-weighted citation impact, top 29% 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

4 citing papers in PubMed, 6 citations in OpenAlex.

  1. Taxifolin, Extracted from WasteDrug design, development and therapy · 2021
    Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Paul DentDepartment of Biochemistry and Molecular Biology; Massey Cancer Center; Virginia Commonwealth University; Richmond, VA USA.
VCU Massey Comprehensive Cancer Center

Funding

SIGNALING PATHWAYS REGULATING EPITHELIAL CELL SURVIVALR01DK052825 · NIDDK · VIRGINIA COMMONWEALTH UNIVERSITY · PI DENT, PAUL · 1999 to 2013
$3.3M
NIDDK NIH HHS R01 DK052825NIDDK NIH HHS R01 DK52825
6 · The paper itself

Abstract

Downstream of growth factor receptors, signaling by the phosphoinositide 3 kinase (PI3K) pathway is known to play an important role in the growth and survival of many tumor types. The PI3K pathway simplistically comprises PI3K itself, followed by PDK-1, then AKT and finally glycogen synthase kinase 3 (GSK3). PI3K/AKT signaling promotes increased GSK3 phosphorylation, that is associated with reduced GSK3 activity. There are two isoforms of GSK3, GSK3α and GSK3β, which have a high degree of sequence homology. GSK3 plays a role not only in the regulation of glycogen synthase activity but in the expression of multiple other proteins that play a role in cancer biology, including cyclins and anti-apoptotic proteins.

Indexed as

Antineoplastic AgentsBiomarkers, TumorBone Marrow NeoplasmsCell ProliferationGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHumansNeuroblastomaThiazolesUreaAntineoplastic AgentsBiomarkers, TumorGlycogen Synthase Kinase 3glycogen synthase kinase 3 alphaGlycogen Synthase Kinase 3 betaGSK3B protein, humanN-(4-methoxybenzyl)-N'-(5-nitro-1,3-thiazol-2-yl)ureaThiazolesUreaapoptosisAR-A014418GSK3neuroblastoma

Identifiers

PMID24618834
PMCPMC4026067
OpenAlexW2069611074

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.