Evidence map›Paper›PMID 28584302›Full record

ArticleScientific reports2017

CRISPR/Cas9-mediated p53 and Pten dual mutation accelerates hepatocarcinogenesis in adult hepatitis B virus transgenic mice.

Yongzhen Liu, Xuewei Qi, Zhenzhen Zeng, Lu Wang, Jie Wang, Ting Zhang, Qiang Xu, Congle Shen, Guangde Zhou, Shaomin Yang and 2 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

42 citing papers in PubMed, 63 citations in OpenAlex.

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  8. [Exploring the reasons for liver cancer occurrence still after long-term nucleos(t)ide analogue therapy in patients with chronic hepatitis B].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2024
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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

12 authors at 2 institutions in 1 country.

Yongzhen LiuDepartment of Microbiology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, 100191, P.R. China.
Xuewei QiDepartment of Microbiology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, 100191, P.R. China.
Zhenzhen ZengDepartment of Microbiology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, 100191, P.R. China.
Lu WangDepartment of Microbiology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, 100191, P.R. China.
Jie WangDepartment of Microbiology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, 100191, P.R. China.
Ting ZhangDepartment of Microbiology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, 100191, P.R. China.
Qiang XuDepartment of Microbiology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, 100191, P.R. China.
Congle ShenDepartment of Microbiology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, 100191, P.R. China.
Guangde ZhouDepartment of Pathology and Hepatology, Beijing 302 Hospital, Beijing, 100039, P.R. China.
Shaomin YangDepartment of Pathology, Peking University Health Science Center, Beijing, 100191, P.R. China.
Xiangmei ChenDepartment of Microbiology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, 100191, P.R. China. xm_chen6176@bjmu.edu.cn.
Fengmin LuDepartment of Microbiology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, 100191, P.R. China.
Peking University · CN302 Military Hospital of China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The p53 mutation and altered Pten expression are two most common genetic events in Hepatitis B virus (HBV) infection related hepatocellular carcinoma (HCC). To confirm the causative role of p53 and Pten somatic mutation in HCC development, we established CRISPR/Cas9-mediated somatic gene disruption via hydrodynamic tail vein injection, allowing for in vivo targeting p53 and Pten simultaneously in adult HBV transgenic mice. Here we demonstrated that the utility of this approach resulted in macroscopic liver tumors as early as 4 months' post injection and most tumors harbored both p53 and Pten loss-of-function alterations. Immunohistochemical (IHC) and histopathology analysis demonstrated that the tumors were positive for Glutamine synthetase (GS), a marker of HCC and accompanied with prominent lipid accumulation. The study here indicated that CRISPR/Cas9-mediated p53 and Pten somatic mutation accelerated hepatocarcinogenesis in adult HBV transgenic mice. This method also provides a fast and convenient system for generating mouse model of HCC with HBV infection characteristics.

Indexed as

AnimalsBiopsyCarcinoma, HepatocellularCell Transformation, NeoplasticCRISPR-Cas SystemsDNA Mutational AnalysisGene ExpressionGene OrderGene TargetingGenetic VectorsHepatitis BHepatitis B virusLiver NeoplasmsMiceMice, TransgenicMutationPTEN PhosphohydrolaseRNA, Guide, CRISPR-Cas SystemsTumor Suppressor Protein p53

Identifiers

PMID28584302
PMCPMC5459841
OpenAlexW2619505081

What OpenQuestion holds

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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.