Evidence map›Paper›PMID 26490736›Full record

ArticleBMC cancer2015

Hypermethylation of the GATA binding protein 4 (GATA4) promoter in Chinese pediatric acute myeloid leukemia.

Yan-Fang Tao, Fang Fang, Shao-Yan Hu, Jun Lu, Lan Cao, Wen-Li Zhao, Pei-Fang Xiao, Zhi-Heng Li, Na-Na Wang, Li-Xiao Xu and 9 more

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

10 citing papers in PubMed, 19 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

19 authors at 4 institutions in 1 country.

Yan-Fang TaoDepartment of Hematology and Oncology, Childrens Hospital of Soochow University, Suzhou, China. taoyanfang1982@163.com.
Fang FangDepartment of Hematology and Oncology, Childrens Hospital of Soochow University, Suzhou, China. baseff77@hotmail.com.
Shao-Yan HuDepartment of Hematology and Oncology, Childrens Hospital of Soochow University, Suzhou, China. hsy139@126.com.
Jun LuDepartment of Hematology and Oncology, Childrens Hospital of Soochow University, Suzhou, China. drlujun_sz@163.com.
Lan CaoDepartment of Hematology and Oncology, Childrens Hospital of Soochow University, Suzhou, China. cl2012@sohu.com.
Wen-Li ZhaoDepartment of Hematology and Oncology, Childrens Hospital of Soochow University, Suzhou, China. wenlizhao69@163.com.
Pei-Fang XiaoDepartment of Hematology and Oncology, Childrens Hospital of Soochow University, Suzhou, China. xiaopfdr@gmail.com.
Zhi-Heng LiDepartment of Hematology and Oncology, Childrens Hospital of Soochow University, Suzhou, China. szlizhiheng@hotmail.com.
Na-Na WangDepartment of Hematology and Oncology, Childrens Hospital of Soochow University, Suzhou, China. 570843000@qq.com.
Li-Xiao XuDepartment of Hematology and Oncology, Childrens Hospital of Soochow University, Suzhou, China. xulixiao2013@hotmail.com.
Xiao-Juan DuDepartment of Gastroenterology, the 5th Hospital of Chinese PLA, Yin chuan, China. du_xiaojuan123@163.com.
Li-Chao SunDepartment of Cell and Molecular Biology, Cancer Institute (Hospital), Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, China. sunlichao_1980@hotmail.com.
Yan-Hong LiDepartment of Hematology and Oncology, Childrens Hospital of Soochow University, Suzhou, China. lyh072006@hotmail.com.
Yi-Ping LiDepartment of Hematology and Oncology, Childrens Hospital of Soochow University, Suzhou, China. ray8302880@163.com.
Yun-Yun XuDepartment of Hematology and Oncology, Childrens Hospital of Soochow University, Suzhou, China. rdxyy@163.com.
Jian NiTranslational Research Center, Second Hospital, The Second Clinical School, Nanjing Medical University, Nanjing, China. ni_jian2008@163.com.
Jian WangDepartment of Hematology and Oncology, Childrens Hospital of Soochow University, Suzhou, China. wj196312@vip.163.com.
Xing FengDepartment of Hematology and Oncology, Childrens Hospital of Soochow University, Suzhou, China. xing_feng66@hotmail.com.
Jian PanDepartment of Hematology and Oncology, Childrens Hospital of Soochow University, Suzhou, China. panjian2008@163.com.
Soochow University · CN82th Hospital of Pla · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNSecond Affiliated Hospital of Nanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAcute myeloid leukemia (AML) is the second-most common form of leukemia in children. Aberrant DNA methylation patterns are a characteristic feature of AML. GATA4 has been suggested to be a tumor suppressor gene regulated by promoter hypermethylation in various types of human cancers although the expression and promoter methylation of GATA4 in pediatric AML is still unclear.

methodsTranscriptional expression levels of GATA4 were evaluated by semi-quantitative and real-time PCR. Methylation status was investigated by methylation-specific PCR (MSP) and bisulfate genomic sequencing (BGS). The prognostic significance of GATA4 expression and promoter methylation was assessed in 105 cases of Chinese pediatric acute myeloid leukemia patients with clinical follow-up records.

resultsMSP and BGS analysis showed that the GATA4 gene promoter is hypermethylated in AML cells, such as the HL-60 and MV4-11 human myeloid leukemia cell lines. 5-Aza treatment significantly upregulated GATA4 expression in HL-60 and MV4-11 cells. Aberrant methylation of GATA4 was observed in 15.0 % (3/20) of the normal bone marrow control samples compared to 56.2 % (59/105) of the pediatric AML samples. GATA4 transcript levels were significantly decreased in AML patients (33.06 ± 70.94; P = 0.011) compared to normal bone marrow/idiopathic thrombocytopenic purpura controls (116.76 ± 105.39). GATA4 promoter methylation was correlated with patient leukocyte counts (WBC, white blood cells) (P = 0.035) and minimal residual disease MRD (P = 0.031). Kaplan-Meier survival analysis revealed significantly shorter overall survival time in patients with GATA4 promoter methylation (P = 0.014).

conclusionsEpigenetic inactivation of GATA4 by promoter hypermethylation was observed in both AML cell lines and pediatric AML samples; our study implicates GATA4 as a putative tumor suppressor gene in pediatric AML. In addition, our findings imply that GATA4 promoter methylation is correlated with WBC and MRD. Kaplan-Meier survival analysis revealed significantly shorter overall survival in pediatric AML with GATA4 promoter methylation but multivariate analysis shows that it is not an independent factor. However, further research focusing on the mechanism of GATA4 in pediatric leukemia is required.

Indexed as

PrognosisAdolescentChildChild, PreschoolCpG IslandsDNA MethylationFemaleGATA4 Transcription FactorGene Expression Regulation, LeukemicHL-60 CellsHumansKaplan-Meier EstimateLeukemia, Myeloid, AcuteMalePromoter Regions, GeneticGATA4 protein, humanGATA4 Transcription Factor

Identifiers

PMID26490736
PMCPMC4618362
OpenAlexW1802898611

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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.