Evidence map›Paper›PMID 26022660›Full record

ReviewMolecular cancer2015

The role of the PI3K/Akt/mTOR signalling pathway in human cancers induced by infection with human papillomaviruses.

Lifang Zhang, Jianhong Wu, Ming Tat Ling, Liang Zhao, Kong-Nan Zhao

Open access · goldAbstract readReview
In one paragraph

Review in Molecular cancer, 2015. 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
9.2field-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, 247 citations in OpenAlex.

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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

5 authors at 4 institutions in 2 countries.

Lifang ZhangInstitute of Molecular Virology and Immunology, Wenzhou Medical University, Wenzhou, 325035 , Zhejiang, PR China. wenzhouzlf@126.com.
Jianhong WuAustralian Prostate Cancer Research Centre-Queensland, Institute of Health and Biomedical Innovation, Queensland University of Technology, 37 Kent Street, Woolloongabba, Brisbane, 4102, QLD, Australia. elite53@gmail.com.
Ming Tat LingAustralian Prostate Cancer Research Centre-Queensland, Institute of Health and Biomedical Innovation, Queensland University of Technology, 37 Kent Street, Woolloongabba, Brisbane, 4102, QLD, Australia. mingtat.ling@qut.edu.au.
Liang ZhaoThe University of Queensland, Brisbane, 4072, QLD, Australia. l.zhao@imb.uq.edu.au.
Kong-Nan ZhaoInstitute of Molecular Virology and Immunology, Wenzhou Medical University, Wenzhou, 325035 , Zhejiang, PR China. k.zhao@uq.edu.au.
University of Queensland · AUFudan University · CNQueensland University of Technology · AUWenzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Infection with Human papillomaviruses (HPVs) leads to the development of a wide-range of cancers, accounting for 5% of all human cancers. A prominent example is cervical cancer, one of the leading causes of cancer death in women worldwide. It has been well established that tumor development and progression induced by HPV infection is driven by the sustained expression of two oncogenes E6 and E7. The expression of E6 and E7 not only inhibits the tumor suppressors p53 and Rb, but also alters additional signalling pathways that may be equally important for transformation. Among these pathways, the phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) signalling cascade plays a very important role in HPV-induced carcinogenesis by acting through multiple cellular and molecular events. In this review, we summarize the frequent amplification of PI3K/Akt/mTOR signals in HPV-induced cancers and discuss how HPV oncogenes E6/E7/E5 activate the PI3K/Akt/mTOR signalling pathway to modulate tumor initiation and progression and affect patient outcome. Improvement of our understanding of the mechanism by which the PI3K/Akt/mTOR signalling pathway contributes to the immortalization and carcinogenesis of HPV-transduced cells will assist in devising novel strategies for preventing and treating HPV-induced cancers.

Indexed as

Signal TransductionAnimalsAtaxia Telangiectasia Mutated ProteinsCell Transformation, ViralHumansIntracellular Signaling Peptides and ProteinsLife Cycle StagesMAP-Kinase-Activated Kinase 2Neoplasmsp38 Mitogen-Activated Protein KinasesPapillomaviridaePapillomavirus InfectionsPhosphatidylinositol 3-KinasesProtein Serine-Threonine KinasesProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesAtaxia Telangiectasia Mutated ProteinsIntracellular Signaling Peptides and ProteinsMAP-Kinase-Activated Kinase 2p38 Mitogen-Activated Protein KinasesPhosphatidylinositol 3-KinasesProtein Serine-Threonine KinasesProto-Oncogene Proteins c-aktTOR Serine-Threonine Kinases

Identifiers

PMID26022660
PMCPMC4498560
OpenAlexW2098204011

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.