Evidence map›Paper›PMID 24818748›Full record

ReviewTrends in biochemical sciences2014

Emerging roles of the p38 MAPK and PI3K/AKT/mTOR pathways in oncogene-induced senescence.

Yingxi Xu, Na Li, Rong Xiang, Peiqing Sun

Open access · greenAbstract readReview
In one paragraph

Review in Trends in biochemical sciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 166 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
166citing papers in PubMed, 1 pooled it
11.5field-weighted citation impact, top 1% 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

166 citing papers in PubMed, 1 synthesis or guideline pooled it, 274 citations in OpenAlex.

  1. A systematic review of p53 regulation of oxidative stress in skeletal muscle.Redox report : communications in free radical research · 2018
    Pooled it
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106 more citing papers are in PubMed but not listed here.

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

4 authors at 2 institutions in 2 countries.

Yingxi XuCollege of Medicine, Nankai University, 94 Weijin Road, Tianjin, China, 300071; Department of Cell and Molecular Biology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.
Na LiCollege of Medicine, Nankai University, 94 Weijin Road, Tianjin, China, 300071.
Rong XiangCollege of Medicine, Nankai University, 94 Weijin Road, Tianjin, China, 300071.
Peiqing SunDepartment of Cell and Molecular Biology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA. Electronic address: pqsun@scripps.edu.
Nankai University · CNScripps Research Institute · US

Funding

Tip60 in p38 and PRAK Mediated Oncogene-Induced Senescence and Tumor SuppressionR01CA131231 · NCI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI SUN, PEIQING · 2009 to 2018
$3.5M
P38 MAPK in Ras-induced Senescence and TransformationR01CA106768 · NCI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI SUN, PEIQING · 2005 to 2014
$3.3M
The role of microRNA in oncogene-induced senescence and cancer developmentR01CA172115 · NCI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI SUN, PEIQING · 2014 to 2018
$1.8M
NCI NIH HHS CA106768NCI NIH HHS CA131231NCI NIH HHS CA172115NCI NIH HHS R01 CA106768NCI NIH HHS R01 CA131231NCI NIH HHS R01 CA172115
6 · The paper itself

Abstract

Oncogene-induced senescence (OIS) is a tumor-suppressing response that must be disrupted for cancer to develop. Mechanistic insights into OIS have begun to emerge. Activation of the p53/p21(WAF1) and/or p16(INK4A) tumor-suppressor pathways is essential for OIS. Moreover, the DNA damage response, chromatin remodeling, and senescence-associated secretory phenotype (SASP) are important for the initiation and maintenance of OIS. This review discusses recent advances in elucidating the mechanisms of OIS, focusing on the roles of the p38 mitogen-activated protein kinase (MAPK) and phosphoinositide 3-kinase (PI3K)/cellular homolog of murine thymoma virus AKT/mammalian target of rapamycin (mTOR) pathways. These studies indicate that OIS is mediated by an intricate signaling network. Further delineation of this network may lead to development of new cancer therapies targeting OIS.

Indexed as

OncogenesAnimalsCellular SenescenceHumansp38 Mitogen-Activated Protein KinasesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionTOR Serine-Threonine Kinasesp38 Mitogen-Activated Protein KinasesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesAKToncogene-induced senescencep38phosphoinositide 3-kinase

Identifiers

PMID24818748
PMCPMC4358807
OpenAlexW1976973627

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.