Evidence map›Paper›PMID 22615958›Full record

ArticlePloS one2012

Insufficient radiofrequency ablation promotes angiogenesis of residual hepatocellular carcinoma via HIF-1α/VEGFA.

Jian Kong, Jinge Kong, Bing Pan, Shan Ke, Shuying Dong, Xiuli Li, Aimin Zhou, Lemin Zheng, Wen-bing Sun

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
88citing papers in PubMed, 1 pooled it
3.7field-weighted citation impact, top 7% 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

88 citing papers in PubMed, 1 synthesis or guideline pooled it, 129 citations in OpenAlex.

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28 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

9 authors at 5 institutions in 2 countries.

Jian KongDepartment of Hepatobiliary Surgery, West Campus, Capital Medical University, Beijing Chao-yang Hospital, Beijing, People's Republic of China.
Jinge Kong
Bing Pan
Shan Ke
Shuying Dong
Xiuli Li
Aimin Zhou
Lemin Zheng
Wen-bing Sun
Beijing Chao-Yang Hospital · CNPeking University · CNCapital Medical University · CNChinese PLA General Hospital · CNCleveland State University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe mechanism of rapid growth of the residual tumor after radiofrequency (RF) ablation is poorly understood. In this study, we investigated the effect of hyperthermia on HepG2 cells and generated a subline with enhanced viability and dys-regulated angiogenesis in vivo, which was used as a model to further determine the molecular mechanism of the rapid growth of residual HCC after RF ablation. METHODOLOGY/PRINCIPAL

findingsHeat treatment was used to establish sublines of HepG2 cells. A subline (HepG2 k) with a relatively higher viability and significant heat tolerance was selected. The cellular protein levels of VEGFA, HIF-1α and p-Akt, VEGFA mRNA and secreted VEGFA were measured, and all of these were up-regulated in this subline compared to parental HepG2 cells. HIF-1α inhibitor YC-1 and VEGFA siRNA inhibited the high viability of the subline. The conditioned media from the subline exerted stronger pro-angiogenic effects. Bevacizumab, VEGFA siRNA and YC-1 inhibited proangiogenic effects of the conditioned media of HepG2 k cells and abolished the difference between parental HepG2 cells and HepG2 k cells. For in vivo studies, a nude mouse model was used, and the efficacy of bavacizumab was determined. HepG2 k tumor had stronger pro-angiogenic effects than parental HepG2 tumor. Bevacizumab could inhibit the tumor growth and angiogenesis, and also eliminate the difference in tumor growth and angiogenesis between parental HepG2 tumor and HepG2 k tumor in vivo. CONCLUSIONS/SIGNIFICANCE: The angiogenesis induced by HIF1α/VEGFA produced by altered cells after hyperthermia treatment may play an important role in the rapid growth of residual HCC after RF ablation. Bevacizumab may be a good candidate drug for preventing and treating the process.

Indexed as

AnimalsAntibodies, Monoclonal, HumanizedBevacizumabCarcinoma, HepatocellularCatheter AblationCell SurvivalCulture Media, ConditionedHep G2 CellsHot TemperatureHumansHyperthermia, InducedHypoxia-Inducible Factor 1, alpha SubunitIndazolesLiver NeoplasmsMiceNeovascularization, Pathologic3-(5'-hydroxymethyl-2'-furyl)-1-benzylindazoleAntibodies, Monoclonal, HumanizedBevacizumabCulture Media, ConditionedHypoxia-Inducible Factor 1, alpha SubunitIndazolesRNA, Small InterferingVascular Endothelial Growth Factor A

Identifiers

PMID22615958
PMCPMC3352883
OpenAlexW2049028002

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.