Evidence map›Paper›PMID 24966916›Full record

ArticleInternational journal of clinical and experimental pathology2014

Glo1 genetic amplification as a potential therapeutic target in hepatocellular carcinoma.

Shirong Zhang, Xiaodong Liang, Xiaoliang Zheng, Haixiu Huang, Xufeng Chen, Kan Wu, Bing Wang, Shenglin Ma

Open access · greenAbstract read
In one paragraph

Article in International journal of clinical and experimental pathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

28 citing papers in PubMed, 41 citations in OpenAlex.

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  17. Glyoxalases in Urological Malignancies.International journal of molecular sciences · 2018
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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

8 authors at 1 institution in 1 country.

Shirong ZhangDepartment of Oncology, Hangzhou First People's Hospital Hangzhou, Zhejiang, China.
Xiaodong LiangDepartment of Oncology, Hangzhou First People's Hospital Hangzhou, Zhejiang, China.
Xiaoliang ZhengCentre of Molecular Medicine, Zhejiang Academy of Medical Sciences Hangzhou, Zhejiang, China.
Haixiu HuangDepartment of Oncology, Hangzhou First People's Hospital Hangzhou, Zhejiang, China.
Xufeng ChenDepartment of Pathology and Laboratory Medicine, University of California at Los Angeles Los Angeles, CA, USA.
Kan WuCentre of Molecular Medicine, Zhejiang Academy of Medical Sciences Hangzhou, Zhejiang, China.
Bing WangCentre of Molecular Medicine, Zhejiang Academy of Medical Sciences Hangzhou, Zhejiang, China.
Shenglin MaDepartment of Oncology, Hangzhou First People's Hospital Hangzhou, Zhejiang, China.
University of California, Los Angeles · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glyoxalase 1 (Glo1) gene aberrations is associated with tumorigenesis and progression in numerous cancers. In this study, we explored the role of Glo1 genetic amplification and expression in Chinese patients with hepatocellular carcinoma (HCC), and Glo1 genetic amplification as potential therapeutic target for HCC. We used fluorescence in situ hybridization (FISH) analysis and qRT-PCR to examine Glo1 genetic aberrations and Glo1 mRNA expression in paired tumor samples obtained from HCC patients. Glo1 genetic amplification was identified in a subset of HCC patient (6%, 3/50), and up-regulation of Glo1 expression was found in 48% (24/50) of tumor tissues compared with adjacent non-tumorous tissues. Statistic analysis showed that Glo1-upregulation significantly correlated with high serum level of alpha-fetoprotein (AFP). Interfering Glo1 expression with shRNA knocking-down led to significant inhibition of cell growth and induced apoptosis in primarily cultured HCC cells carrying genetic amplified Glo1 gene, while no inhibitory effects on cell proliferation were observed in HCC cells with normal copies of Glo1 gene. Glo1 knockdown also inhibited tumor growth and induced apoptosis in xenograft tumors established from primarily cultured HCC cells with Glo1 gene amplification. In addition, Glo1 knocking-down with shRNA interfering caused cellular accumulation of methylglyoxal, a Glo1 cytotoxic substrate. Our data suggested Glo1 pathway activation is required for cell proliferation and cell survival of HCC cells carrying Glo1 genetic amplification. Intervention of Glo1 activation could be a potential therapeutic option for patients with HCC carrying Glo1 gene amplification.

Indexed as

Gene Amplificationalpha-FetoproteinsAnimalsApoptosisBiomarkers, TumorCarcinoma, HepatocellularCell Line, TumorCell ProliferationChinaFemaleGene Expression Regulation, EnzymologicGene Expression Regulation, NeoplasticHumansLactoylglutathione LyaseLiver NeoplasmsMaleAFP protein, humanalpha-FetoproteinsBiomarkers, TumorLactoylglutathione LyasePyruvaldehydeRNA, Messengerapoptosiscell proliferationgenetic amplificationGlyoxalase 1hepatocellular carcinoma

Identifiers

PMID24966916
PMCPMC4069890
OpenAlexW2294576167

What OpenQuestion holds

Textmetadata
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.