Evidence map›Paper›PMID 23770988›Full record

ReviewActa pharmacologica Sinica2013

The roles of PIKE in tumorigenesis.

Qi Qi, Keqiang Ye

Open access · bronzeAbstract readReview
In one paragraph

Review in Acta pharmacologica Sinica, 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
0.8field-weighted citation impact, top 25% 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, 13 citations in OpenAlex.

  1. Article
  2. The Hypoxia-Long Noncoding RNA Interaction in Solid Cancers.International journal of molecular sciences · 2021
    Review
  3. AGAP2: Modulating TGFβ1-Signaling in the Regulation of Liver Fibrosis.International journal of molecular sciences · 2020
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. 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

2 authors at 1 institution in 1 country.

Qi QiDepartment of Pathology and Laboratory Medicine, Emory University School of Medicine, Atlanta, GA 30322, USA.
Keqiang Ye
Emory University · US

Funding

Molecular Regulation and Biological Functions of PIKE-AR01CA127119 · NCI · EMORY UNIVERSITY · PI YE, KEQIANG · 2008 to 2012
$1.6M
NCI NIH HHS R01 CA127119
6 · The paper itself

Abstract

Tumorigenesis is the process by which normal cells evolve the capacity to evade and overcome the constraints usually placed upon their growth and survival. To ensure the integrity of organs and tissues, the balance of cell proliferation and cell death is tightly maintained. The proteins controlling this balance are either considered oncogenes, which promote tumorigenesis, or tumor suppressors, which prevent tumorigenesis. Phosphoinositide 3-kinase enhancer (PIKE) is a family of GTP-binding proteins that possess anti-apoptotic functions and play an important role in the central nervous system. Notably, accumulating evidence suggests that PIKE is a proto-oncogene involved in tumor progression. The PIKE gene (CENTG1) is amplified in a variety of human cancers, leading to the resistance against apoptosis and the enhancement of invasion. In this review, we will summarize the functions of PIKE proteins in tumorigenesis and discuss their potential implications in cancer therapy.

Indexed as

AnimalsCarcinogenesisCell Transformation, NeoplasticGTPase-Activating ProteinsGTP-Binding ProteinsHumansNeoplasm InvasivenessPhosphatidylinositol 3-KinasesProto-Oncogene MasAGAP2 protein, humanGTPase-Activating ProteinsGTP-Binding ProteinsMAS1 protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Mas

Identifiers

PMID23770988
PMCPMC3733165
OpenAlexW2059442454

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.