Evidence map›Paper›PMID 31686003›Full record

ReviewNature reviews. Cancer2020

The PI3K-AKT network at the interface of oncogenic signalling and cancer metabolism.

Gerta Hoxhaj, Brendan D Manning

Open access · greenAbstract readReview
In one paragraph

Review in Nature reviews. Cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1,277 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
1,277citing papers in PubMed, 2 pooled it
62.7field-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

1,277 citing papers in PubMed, 2 syntheses or guidelines pooled it, 2,067 citations in OpenAlex.

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  8. LILRB4 Recruits SHP-1 to Enhance Oxidative Stress and Apoptosis, Aggravating Myocardial Ischemia-Reperfusion Injury.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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1,217 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

2 authors at 1 institution in 1 country.

Gerta HoxhajDepartment of Molecular Metabolism, Harvard T. H. Chan School of Public Health, Boston, MA, USA. [email protected].ORCID http://orcid.org/0000-0001-6179-3583
Brendan D ManningDepartment of Molecular Metabolism, Harvard T. H. Chan School of Public Health, Boston, MA, USA. [email protected].ORCID http://orcid.org/0000-0003-3895-5956
Harvard University · US

Funding

Tuberous Sclerosis-Pathway and PathogenesisP01CA120964 · NCI · BRIGHAM AND WOMEN'S HOSPITAL · PI David J. Kwiatkowski · 2007 to 2026
$35.9M
Decoding and Targeting the PI3K-mTOR Signaling Network in CancerR35CA197459 · NCI · HARVARD UNIVERSITY D/B/A HARVARD SCHOOL OF PUBLIC HEALTH · PI BRENDAN D. MANNING · 2015 to 2026
$10.8M
NCI NIH HHS P01 CA120964NCI NIH HHS R35 CA197459
6 · The paper itself

Abstract

The altered metabolic programme of cancer cells facilitates their cell-autonomous proliferation and survival. In normal cells, signal transduction pathways control core cellular functions, including metabolism, to couple the signals from exogenous growth factors, cytokines or hormones to adaptive changes in cell physiology. The ubiquitous, growth factor-regulated phosphoinositide 3-kinase (PI3K)-AKT signalling network has diverse downstream effects on cellular metabolism, through either direct regulation of nutrient transporters and metabolic enzymes or the control of transcription factors that regulate the expression of key components of metabolic pathways. Aberrant activation of this signalling network is one of the most frequent events in human cancer and serves to disconnect the control of cell growth, survival and metabolism from exogenous growth stimuli. Here we discuss our current understanding of the molecular events controlling cellular metabolism downstream of PI3K and AKT and of how these events couple two major hallmarks of cancer: growth factor independence through oncogenic signalling and metabolic reprogramming to support cell survival and proliferation.

Indexed as

Energy MetabolismSignal TransductionAnimalsDisease SusceptibilityGene Expression Regulation, NeoplasticGlucoseHumansNeoplasmsOncogene ProteinsOxidation-ReductionPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktGlucoseOncogene ProteinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-akt

Identifiers

PMID31686003
PMCPMC7314312
OpenAlexW2984955289

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.