Evidence map›Paper›PMID 24124460›Full record

ArticlePloS one2013

Inhibition of mTOR reduces anal carcinogenesis in transgenic mouse model.

Zhi-Jun Sun, Lu Zhang, Wei Zhang, Bradford Hall, Yansong Bian, Ashok B Kulkarni

Open access · goldAbstract read
In one paragraph

Article in PloS one, 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
1.7field-weighted citation impact, top 16% 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, 15 citations in OpenAlex.

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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

6 authors at 3 institutions in 2 countries.

Zhi-Jun SunThe State Key Laboratory Breeding Base of Basic Science of Stomatology & Key Laboratory of Oral Biomedicine Ministry of Education, School and Hospital of Stomatology, Wuhan University, Wuhan, China ; Functional Genomics Section, Laboratory of Cell and Developmental Biology, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, Maryland, United States of America.
Lu Zhang
Wei Zhang
Bradford Hall
Yansong Bian
Ashok B Kulkarni
National Institutes of Health · USNational Institute of Dental and Craniofacial Research · USWuhan University · CN

Funding

Molecular Roles of Cdk5 in Neuronal Functions and Pain SignalingZIADE000664 · NIDCR · NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH · PI KULKARNI, ASHOK · 2009 to 2025
$20.4M
Molecular Roles of TGF-beta Signaling in Salivary Glands and Oral CancerZIADE000723 · NIDCR · NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH · PI KULKARNI, ASHOK · 2009 to 2012
$2.4M
Molecular Genetics of Tooth Development and DiseaseZ01DE000698 · NIDCR · NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH · PI KULKARNI, ASHOK B. · 1999 to 2008
$1.7M
Molecular Roles of TGF-beta Signaling in Salivary Glands and Oral CancerZ01DE000723 · NIDCR · NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH · PI KULKARNI, ASHOK · 2008 to 2008
$820k
Molecular Genetics of Craniofacial Development and DiseaseZIADE000698 · NIDCR · NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH · PI KULKARNI, ASHOK · 2009 to 2010
$480k
Intramural NIH HHS Z01 DE000698Intramural NIH HHS Z01 DE000723Intramural NIH HHS ZIA DE000698NIDCR NIH HHS ZIA-DE-000698
6 · The paper itself

Abstract

The molecular mechanism of human anal squamous cell carcinoma (ASCC) is unclear, and the accumulating evidence indicate association of ASCC with the activation of the Akt/mTOR pathway. Here we describe a mouse model with spontaneous anal squamous cell cancer, wherein a combined deletion of Tgfbr1 and Pten in stratified squamous epithelia was induced using inducible K14-Cre. Histopathologic analyses confirmed that 33.3% of the mice showed increased susceptibility to ASCC and precancerous lesions. Biomarker analyses demonstrated that the activation of the Akt pathway in ASCC of the Tgfbr1 and Pten double knockout (2cKO) mouse was similar to that observed in human anal cancer. Chemopreventive experiments using mTOR inhibitor-rapamycin treatment significantly delayed the onset of the ASCC tumors and reduced the tumor burden in 2cKO mice by decreasing the phosphorylation of Akt and S6. This is the first conditional knockout mouse model used for investigating the contributions of viral and cellular factors in anal carcinogenesis without carcinogen-mediated induction, and it would provide a platform for assessing new therapeutic modalities for treating and/or preventing this type of cancer.

Indexed as

AnimalsAnti-Bacterial AgentsAnus NeoplasmsBlotting, WesternFemaleImmunohistochemistryIn Situ Nick-End LabelingMaleMiceMice, KnockoutMice, TransgenicPhosphorylationProtein Serine-Threonine KinasesPTEN PhosphohydrolaseReceptors, Transforming Growth Factor betaReceptor, Transforming Growth Factor-beta Type IAnti-Bacterial AgentsProtein Serine-Threonine KinasesPTEN PhosphohydrolaseReceptors, Transforming Growth Factor betaReceptor, Transforming Growth Factor-beta Type ISirolimusTGFBR1 protein, humanTgfbr1 protein, mouseTOR Serine-Threonine Kinases

Identifiers

PMID24124460
PMCPMC3790781
OpenAlexW1973646723

What OpenQuestion holds

Textmetadata
LicenceCC0
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.