Evidence map›Paper›PMID 28452111›Full record

ArticleJournal of cellular and molecular medicine2017

Epigenetic dysregulation of ID4 predicts disease progression and treatment outcome in myeloid malignancies.

Jing-Dong Zhou, Ting-Juan Zhang, Xi-Xi Li, Ji-Chun Ma, Hong Guo, Xiang-Mei Wen, Wei Zhang, Lei Yang, Yang Yan, Jiang Lin and 1 more

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
5.4field-weighted citation impact, top 4% 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

31 citing papers in PubMed, 49 citations in OpenAlex.

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  17. Methylation-independentAmerican journal of translational research · 2020
    Review
  18. Article
  19. Article
  20. Aging · 2019
    Article
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

11 authors at 2 institutions in 1 country.

Jing-Dong ZhouDepartment of Hematology, Affiliated People's Hospital of Jiangsu University, Zhenjiang, Jiangsu, China.
Ting-Juan ZhangDepartment of Hematology, Affiliated People's Hospital of Jiangsu University, Zhenjiang, Jiangsu, China.
Xi-Xi LiDepartment of Hematology, Affiliated People's Hospital of Jiangsu University, Zhenjiang, Jiangsu, China.
Ji-Chun MaLaboratory Center, Affiliated People's Hospital of Jiangsu University, Zhenjiang, Jiangsu, China.
Hong GuoLaboratory Center, Affiliated People's Hospital of Jiangsu University, Zhenjiang, Jiangsu, China.
Xiang-Mei WenLaboratory Center, Affiliated People's Hospital of Jiangsu University, Zhenjiang, Jiangsu, China.
Wei ZhangDepartment of Hematology, Affiliated People's Hospital of Jiangsu University, Zhenjiang, Jiangsu, China.
Lei YangDepartment of Hematology, Affiliated People's Hospital of Jiangsu University, Zhenjiang, Jiangsu, China.
Yang YanSchool of Medicine, Jiangsu University, Zhenjiang, Jiangsu, China.
Jiang LinLaboratory Center, Affiliated People's Hospital of Jiangsu University, Zhenjiang, Jiangsu, China.
Jun QianDepartment of Hematology, Affiliated People's Hospital of Jiangsu University, Zhenjiang, Jiangsu, China.
Affiliated Hospital of Jiangsu University · CNJiangsu University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Promoter hypermethylation-mediated inactivation of ID4 plays a crucial role in the development of solid tumours. This study aimed to investigate ID4 methylation and its clinical relevance in myeloid malignancies. ID4 hypermethylation was associated with higher IPSS scores, but was not an independent prognostic biomarker affecting overall survival (OS) in myelodysplastic syndrome (MDS). However, ID4 hypermethylation correlated with shorter OS and leukaemia-free survival (LFS) time and acted as an independent risk factor affecting OS in acute myeloid leukaemia (AML). Moreover, ID4 methylation was significantly decreased in the follow-up paired AML patients who achieved complete remission (CR) after induction therapy. Importantly, ID4 methylation was increased during MDS progression to AML and chronic phase (CP) progression to blast crisis (BC) in chronic myeloid leukaemia (CML). Epigenetic studies showed that ID4 methylation might be one of the mechanisms silencing ID4 expression in myeloid leukaemia. Functional studies in vitro showed that restoration of ID4 expression could inhibit cell proliferation and promote apoptosis in both K562 and HL60 cells. These findings indicate that ID4 acts as a tumour suppressor in myeloid malignancies, and ID4 methylation is a potential biomarker in predicting disease progression and treatment outcome.

Indexed as

Epigenesis, GeneticAdolescentAdultAgedAged, 80 and overAntineoplastic AgentsAzacitidineCase-Control StudiesCell ProliferationDecitabineDisease ProgressionDNA MethylationFemaleHL-60 CellsHumansInhibitor of Differentiation ProteinsAntineoplastic AgentsAzacitidineDecitabineID4 protein, humanInhibitor of Differentiation ProteinsID4methylationmyeloid malignanciesprognosisprogression

Identifiers

PMID28452111
PMCPMC5542913
OpenAlexW2608406409

What OpenQuestion holds

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Registered trials

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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.