Evidence map›Paper›PMID 38245923›Full record

ArticleNeoplasia (New York, N.Y.)2024

DNA methylation landscape reveals GNAS as a decitabine-responsive marker in patients with acute myeloid leukemia.

Shujiao He, Yan Li, Lei Wang, Yisheng Li, Lu Xu, Diya Cai, Jingfeng Zhou, Li Yu

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neoplasia (New York, N.Y.), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
1.2field-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

3 citing papers in PubMed, 5 citations in OpenAlex.

  1. Review
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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 3 institutions in 1 country.

Shujiao HeDepartment of Hematology and Oncology, International Cancer Center, Shenzhen Key Laboratory, Hematology Institution of Shenzhen University, Shenzhen University General Hospital, Shenzhen University Health Science Center, Shenzhen University, Xueyuan Ave 1098, Nanshan District, Shenzhen 518000, China.
Yan LiDepartment of Hematology, Peking Third Hospital, 49 North Garden Road, Beijing 100191, China; Department of Haematology, Chinese People's Liberation Army General Hospital, Beijing 100853, China.
Lei WangDepartment of Hematology and Oncology, International Cancer Center, Shenzhen Key Laboratory, Hematology Institution of Shenzhen University, Shenzhen University General Hospital, Shenzhen University Health Science Center, Shenzhen University, Xueyuan Ave 1098, Nanshan District, Shenzhen 518000, China.
Yisheng LiShenzhen Haoshi Biotechnology Co., Ltd, 155 Hong Tian Rd, Baoan District, Shenzhen 518125, China; Shenzhen University-Haoshi Cell Therapy Institute, 155 Hong Tian Rd, Baoan District, Shenzhen 518125, China.
Lu XuDepartment of Hematology and Oncology, International Cancer Center, Shenzhen Key Laboratory, Hematology Institution of Shenzhen University, Shenzhen University General Hospital, Shenzhen University Health Science Center, Shenzhen University, Xueyuan Ave 1098, Nanshan District, Shenzhen 518000, China.
Diya CaiDepartment of Hematology and Oncology, International Cancer Center, Shenzhen Key Laboratory, Hematology Institution of Shenzhen University, Shenzhen University General Hospital, Shenzhen University Health Science Center, Shenzhen University, Xueyuan Ave 1098, Nanshan District, Shenzhen 518000, China.
Jingfeng ZhouDepartment of Hematology and Oncology, International Cancer Center, Shenzhen Key Laboratory, Hematology Institution of Shenzhen University, Shenzhen University General Hospital, Shenzhen University Health Science Center, Shenzhen University, Xueyuan Ave 1098, Nanshan District, Shenzhen 518000, China. Electronic address: Jingfengzhou@szu.edu.cn.
Li YuDepartment of Hematology and Oncology, International Cancer Center, Shenzhen Key Laboratory, Hematology Institution of Shenzhen University, Shenzhen University General Hospital, Shenzhen University Health Science Center, Shenzhen University, Xueyuan Ave 1098, Nanshan District, Shenzhen 518000, China. Electronic address: yuli@szu.edu.cn.
Shenzhen University Health Science Center · CNChinese People's Liberation Army · CNShenzhen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe demethylation agent decitabine (DAC) is a pivotal non-intensive alternative treatment for acute myeloid leukemia (AML). However, patient responses to DAC are highly variable, and predictive biomarkers are warranted. Herein, the DNA methylation landscape of patients treated with a DAC-based combination regimen was compared with that of patients treated with standard chemotherapy to develop a molecular approach for predicting clinical response to DAC.

methodsTwenty-five non-M3 AML patients were enrolled and subjected to DNA methylation sequencing and profiling to identify differentially methylated regions (DMRs) and genes of interest. Moreover, the effects of a DAC-based regimen on apoptosis and gene expression were explored using Kasumi-1 and K562 cells.

resultsOverall, we identified 541 DMRs that were specifically responsive to DAC, among which 172 DMRs showed hypomethylation patterns upon treatment and were aligned with the promoter regions of 182 genes. In particular, GNAS was identified as a critical DAC-responsive gene, with in vitro GNAS downregulation leading to reduced cell apoptosis induced by DAC and cytarabine combo treatment.

conclusionsWe found that GNAS is a DAC-sensitive gene in AML and may serve as a prognostic biomarker to assess the responsiveness of patients with AML to DAC-based therapy.

Indexed as

AzacitidineLeukemia, Myeloid, AcuteAntineoplastic Combined Chemotherapy ProtocolsChromograninsDecitabineDNA MethylationGTP-Binding Protein alpha Subunits, GsHumansAzacitidineChromograninsDecitabineGNAS protein, humanGTP-Binding Protein alpha Subunits, GsAcute myeloid leukemiaDecitabineDifferentially methylated regionDNA methylation sequencingGNASPrognostic biomarker

Identifiers

PMID38245923
PMCPMC10830847
OpenAlexW4391074680

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.