Evidence map›Paper›PMID 28368413›Full record

ArticleOncogene2017

Co-amplification of phosphoinositide 3-kinase enhancer A and cyclin-dependent kinase 4 triggers glioblastoma progression.

Q Qi, S S Kang, S Zhang, C Pham, H Fu, D J Brat, K Ye

Open access · greenAbstract read
In one paragraph

Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.4field-weighted citation impact, top 17% 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

12 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
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

7 authors at 2 institutions in 2 countries.

Q QiDepartment of Pathology and Laboratory Medicine, Emory University School of Medicine, Atlanta, GA, USA.
S S KangDepartment of Pathology and Laboratory Medicine, Emory University School of Medicine, Atlanta, GA, USA.
S ZhangDepartment of Pathology and Laboratory Medicine, Emory University School of Medicine, Atlanta, GA, USA.
C PhamDepartment of Pharmacology and Emory Chemical Biology Discovery Center, Emory University School of Medicine; Atlanta, GA, USA.
H FuDepartment of Pharmacology and Emory Chemical Biology Discovery Center, Emory University School of Medicine; Atlanta, GA, USA.
D J BratDepartment of Pathology and Laboratory Medicine, Emory University School of Medicine, Atlanta, GA, USA.
K YeDepartment of Pathology and Laboratory Medicine, Emory University School of Medicine, Atlanta, GA, USA.
Emory University · USJinan University · CN

Funding

Winship Cancer Institute Cancer Center Support GrantP30CA138292 · NCI · EMORY UNIVERSITY · PI Suresh S Ramalingam · 2009 to 2026
$47.5M
Systematic discovery of neomorph protein-protein interactions in cancer for oncogenic pathway perturbationU01CA217875 · NCI · EMORY UNIVERSITY · PI FU, HAIAN · 2017 to 2021
$4.5M
HIGH THROUGHPUT PROTEIN-PROTEIN INTERACTION INTERROGATION IN CANCERU01CA168449 · NCI · EMORY UNIVERSITY · PI FU, HAIAN · 2012 to 2016
$4.2M
Molecular Regulation of AEP during AgeingRF1AG051538 · NIA · EMORY UNIVERSITY · PI YE, KEQIANG · 2016 to 2016
$3.4M
Molecular Mechanisms of G5-7 Allosteric Inhibition of Jak2R01CA186918 · NCI · EMORY UNIVERSITY · PI YE, KEQIANG · 2015 to 2019
$1.8M
CCR NIH HHS HHSN261200800001CNCI NIH HHS HHSN261200800001ENCI NIH HHS P30 CA138292NCI NIH HHS R01 CA186918NCI NIH HHS U01 CA168449NCI NIH HHS U01 CA217875NIA NIH HHS RF1 AG051538
6 · The paper itself

Abstract

Glioblastoma (GBM) is the most common primary brain tumor and has a dismal prognosis. Amplification of chromosome 12q13-q15 (Cyclin-dependent kinase 4 (CDK4) amplicon) is frequently observed in numerous human cancers including GBM. Phosphoinositide 3-kinase enhancer (PIKE) is a group of GTP-binding proteins that belong to the subgroup of centaurin GTPase family, encoded by CENTG1 located in CDK4 amplicon. However, the pathological significance of CDK4 amplicon in GBM formation remains incompletely understood. In the current study, we show that co-expression of PIKE-A and CDK4 in TP53/PTEN double knockout GBM mouse model additively shortens the latency of glioma onset and survival compared to overexpression of these genes alone. Consequently, p-mTOR, p-Akt and p-ERK pathways are highly upregulated in the brain tumors, in alignment with their oncogenic activities by CDK4 and PIKE-A stably transfected in GBM cell lines. Hence, our findings support that PIKE amplification or overexpression coordinately acts with CDK4 to drive GBM tumorigenesis.

Indexed as

Chromosome AberrationsGene AmplificationAnimalsBrain NeoplasmsCarcinogenesisCell Line, TransformedCell Line, TumorCell ProliferationChromosomes, Human, Pair 12Cyclin-Dependent Kinase 4GlioblastomaGTPase-Activating ProteinsGTP-Binding ProteinsHumansKaplan-Meier EstimateMiceAGAP2 protein, humanCDK4 protein, humanCyclin-Dependent Kinase 4GTPase-Activating ProteinsGTP-Binding ProteinsPTEN PhosphohydrolasePTEN protein, humanTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID28368413
PMCPMC5552418
OpenAlexW2604194338

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.