Evidence map›Paper›PMID 30840887›Full record

ArticleCell reports2019

A Human Papillomavirus-Independent Cervical Cancer Animal Model Reveals Unconventional Mechanisms of Cervical Carcinogenesis.

Chunbo He, Xiangmin Lv, Cong Huang, Peter C Angeletti, Guohua Hua, Jixin Dong, Jin Zhou, Zhengfeng Wang, Bowen Ma, Xingcheng Chen and 4 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
5.5field-weighted citation impact, top 4% 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

45 citing papers in PubMed, 78 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

14 authors at 5 institutions in 2 countries.

Chunbo HeVincent Center for Reproductive Biology, Vincent Department of Obstetrics and Gynecology, Massachusetts General Hospital, Boston, MA 02114, USA; Olson Center for Women's Health, Department of Obstetrics & Gynecology, University of Nebraska Medical Center, Omaha, NE 68198, USA; College of Animal Science and Technology, Huazhong Agricultural University, Wuhan, 430070, China.
Xiangmin LvVincent Center for Reproductive Biology, Vincent Department of Obstetrics and Gynecology, Massachusetts General Hospital, Boston, MA 02114, USA; Olson Center for Women's Health, Department of Obstetrics & Gynecology, University of Nebraska Medical Center, Omaha, NE 68198, USA.
Cong HuangVincent Center for Reproductive Biology, Vincent Department of Obstetrics and Gynecology, Massachusetts General Hospital, Boston, MA 02114, USA.
Peter C AngelettiNebraska Center for Virology, School of Biological Sciences, University of Nebraska-Lincoln, Lincoln, NE 68583, USA.
Guohua HuaOlson Center for Women's Health, Department of Obstetrics & Gynecology, University of Nebraska Medical Center, Omaha, NE 68198, USA; College of Animal Science and Technology, Huazhong Agricultural University, Wuhan, 430070, China.
Jixin DongFred & Pamela Cancer Center, University of Nebraska Medical Center, Omaha NE 68198, USA.
Jin ZhouOlson Center for Women's Health, Department of Obstetrics & Gynecology, University of Nebraska Medical Center, Omaha, NE 68198, USA; Department of Obstetrics and Gynecology, The Eighth Affiliated Hospital of Sun Yat-Sen University, Shenzhen, 518033, China.
Zhengfeng WangOlson Center for Women's Health, Department of Obstetrics & Gynecology, University of Nebraska Medical Center, Omaha, NE 68198, USA; Department of Hepatobiliary Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 45001 China.
Bowen MaOlson Center for Women's Health, Department of Obstetrics & Gynecology, University of Nebraska Medical Center, Omaha, NE 68198, USA.
Xingcheng ChenFred & Pamela Cancer Center, University of Nebraska Medical Center, Omaha NE 68198, USA.
Paul F LambertMcArdle Laboratory for Cancer Research, Department of Oncology, University of Wisconsin-Madison, Madison, WI 53705, USA.
Bo R RuedaVincent Center for Reproductive Biology, Vincent Department of Obstetrics and Gynecology, Massachusetts General Hospital, Boston, MA 02114, USA.
John S DavisOlson Center for Women's Health, Department of Obstetrics & Gynecology, University of Nebraska Medical Center, Omaha, NE 68198, USA; Omaha Veterans Affairs Medical Center, Omaha, NE 68105, USA.
Cheng WangVincent Center for Reproductive Biology, Vincent Department of Obstetrics and Gynecology, Massachusetts General Hospital, Boston, MA 02114, USA; Olson Center for Women's Health, Department of Obstetrics & Gynecology, University of Nebraska Medical Center, Omaha, NE 68198, USA. Electronic address: cwang34@mgh.harvard.edu.
University of Nebraska Medical Center · USEighth Affiliated Hospital of Sun Yat-sen UniversityHuazhong Agricultural University · CNUniversity of Nebraska–Lincoln · USUniversity of Wisconsin–Madison · US

Funding

Visualizing EBV and HCMV DNA Dynamics During InfectionP01CA022443 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI WILLIAM M. SUGDEN · 1985 to 2026
$53.1M
Defining Drivers of HPV-associated CarcinogenesisR35CA210807 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI Paul F. Lambert · 2017 to 2026
$9.2M
The Hippo/YAP Signaling Pathway in Ovarian High Grade Serous CarcinomaR01CA197976 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI WANG, CHENG · 2016 to 2025
$4.0M
Novel Mechanisms of Cervical Cancer Development and ProgressionR01CA201500 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI WANG, CHENG · 2016 to 2020
$1.8M
GPR30 Mediated-Estrogen Action on Ovarian Physiology and Ovarian CancerR00HD059985 · NICHD · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI WANG, CHENG · 2012 to 2014
$716k
NCI NIH HHS P01 CA022443NCI NIH HHS R01 CA197976NCI NIH HHS R01 CA201500NCI NIH HHS R35 CA210807NICHD NIH HHS R00 HD059985
6 · The paper itself

Abstract

HPV infections are common in healthy women and only rarely cause cervical cancer, suggesting that individual genetic susceptibility may play a critical role in the establishment of persistent HPV infection and the development of cervical cancer. Here, we provide convincing in vitro and in vivo evidence showing that differential expression and activation of YAP1 oncogene determine individual susceptibility to HPV infection and cervical carcinogenesis. We found that hyperactivation of YAP1 in mouse cervical epithelium was sufficient to induce invasive cervical cancer. Cervical epithelial cell-specific HPV16 E6/E7 and YAP1 double-knockin mouse model demonstrated that high-risk HPV synergized with hyperactivated YAP1 to promote the initiation and progression of cervical cancer. Our mechanistic studies indicated that hyperactivation of YAP1 in cervical epithelial cells facilitated HPV infection by increasing the putative HPV receptor molecules and disrupting host cell innate immunity. Our finding reveals an unconventional mechanism for cervical carcinogenesis.

Indexed as

AnimalsDisease Models, AnimalFemaleHumansMiceMice, TransgenicPapillomaviridaeUterine Cervical Neoplasmscervical cancer mouse modelcervical carcinogenesisHippo pathwayHPV infectionHPV receptor moleculesinnate immunityinterferon-stimulated genesmolecular mechanismtype I interferonYAP1 oncogene

Identifiers

PMID30840887
PMCPMC6812687
OpenAlexW2918462438

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.