Evidence map›Paper›PMID 26352599›Full record

ArticleOncology reports2015

HDAC1 and HDAC2 independently predict mortality in hepatocellular carcinoma by a competing risk regression model in a Southeast Asian population.

Ser Yeng Ler, Carol Ho Wing Leung, Lay Wai Khin, Guo-Dong Lu, Manuel Salto-Tellez, Mikael Hartman, Philip Tsau Choong Iau, Celestial T Yap, Shing Chuan Hooi

Open access · greenAbstract read
In one paragraph

Article in Oncology reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed, 1 pooled it
3.3field-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

57 citing papers in PubMed, 1 synthesis or guideline pooled it, 93 citations in OpenAlex.

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  9. Genetic screening of liver cancer: State of the art.World 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

9 authors at 5 institutions in 2 countries.

Ser Yeng LerDepartment of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Republic of Singapore.
Carol Ho Wing LeungSchool of Chemical and Life Sciences, Singapore Polytechnic, Singapore, Republic of Singapore.
Lay Wai KhinInvestigational Medicine Unit, Dean's Office, Yong Loo Lin School of Medicine, National University of Singapore and National University Health System, Singapore, Republic of Singapore.
Guo-Dong LuSchool of Public Health, Guangxi Medical University, Nanning, Guangxi, P.R. China.
Manuel Salto-TellezCancer Science Institute of Singapore, National University of Singapore, Singapore, Republic of Singapore.
Mikael HartmanDepartment of Surgery, Yong Loo Lin School of Medicine, National University of Singapore and National University Health System, Singapore, Republic of Singapore.
Philip Tsau Choong IauDepartment of Surgery, Yong Loo Lin School of Medicine, National University of Singapore and National University Health System, Singapore, Republic of Singapore.
Celestial T YapDepartment of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Republic of Singapore.
Shing Chuan HooiDepartment of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Republic of Singapore.
National University of Singapore · SGNational University Health System · SGGuangxi Medical University · CNNational University Cancer Institute, Singapore · SGSingapore Polytechnic · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Histone deacetylases (HDACs) are enzymes involved in transcriptional repression. We aimed to examine the significance of HDAC1 and HDAC2 gene expression in the prediction of recurrence and survival in 156 patients with hepatocellular carcinoma (HCC) among a South East Asian population who underwent curative surgical resection in Singapore. We found that HDAC1 and HDAC2 were upregulated in the majority of HCC tissues. The presence of HDAC1 in tumor tissues was correlated with poor tumor differentiation. Notably, HDAC1 expression in adjacent non-tumor hepatic tissues was correlated with the presence of satellite nodules and multiple lesions, suggesting that HDAC1 upregulation within the field of HCC may contribute to tumor spread. Using competing risk regression analysis, we found that increased cancer-specific mortality was significantly associated with HDAC2 expression. Mortality was also increased with high HDAC1 expression. In the liver cancer cell lines, HEP3B, HEPG2, PLC5, and a colorectal cancer cell line, HCT116, the combined knockdown of HDAC1 and HDAC2 increased cell death and reduced cell proliferation as well as colony formation. In contrast, knockdown of either HDAC1 or HDAC2 alone had minimal effects on cell death and proliferation. Taken together, our study suggests that both HDAC1 and HDAC2 exert pro-survival effects in HCC cells, and the combination of isoform-specific HDAC inhibitors against both HDACs may be effective in targeting HCC to reduce mortality.

Indexed as

AdultAgedApoptosisBiomarkers, TumorCarcinoma, HepatocellularCell Line, TumorCell ProliferationFemaleGene Knockdown TechniquesHistone Deacetylase 1Histone Deacetylase 2HumansLiver NeoplasmsMaleMiddle AgedProportional Hazards ModelsBiomarkers, TumorHDAC1 protein, humanHDAC2 protein, humanHistone Deacetylase 1Histone Deacetylase 2

Identifiers

PMID26352599
PMCPMC4583520
OpenAlexW1863017422

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.