Evidence map›Paper›PMID 36869331›Full record

ArticleCell communication and signaling : CCS2023

Induction of DNMT1-dependent demethylation of SHP-1 by the natural flavonoid compound Baicalein overcame Imatinib-resistance in CML CD34

Xuefen Xu, Shufan Ji, Yuan Chen, Siwei Xia, Yang Li, Li Chen, Yujia Li, Feng Zhang, Zili Zhang, Shizhong Zheng

Open access · goldAbstract readVideo-Audio Media
In one paragraph

Article in Cell communication and signaling : CCS, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

5 citing papers in PubMed, 5 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

10 authors at 1 institution in 1 country.

Xuefen Xu *Department of Pharmacology, School of Medicine and Holistic Integrative Medicine, Nanjing University of Chinese Medicine, No.138, Xianlin Road, Nanjing, Jiangsu, People's Republic of China. 460103@njucm.edu.cn.
Shufan Ji *Jangsu Key Laboratory for Pharmacology and Safety Evaluation of Chinese Materia Medica, School of Pharmacy, Nanjing University of Chinese Medicine, Nanjing, People's Republic of China.
Yuan ChenDepartment of Pharmacology, School of Medicine and Holistic Integrative Medicine, Nanjing University of Chinese Medicine, No.138, Xianlin Road, Nanjing, Jiangsu, People's Republic of China.
Siwei XiaJangsu Key Laboratory for Pharmacology and Safety Evaluation of Chinese Materia Medica, School of Pharmacy, Nanjing University of Chinese Medicine, Nanjing, People's Republic of China.
Yang LiJangsu Key Laboratory for Pharmacology and Safety Evaluation of Chinese Materia Medica, School of Pharmacy, Nanjing University of Chinese Medicine, Nanjing, People's Republic of China.
Li ChenJangsu Key Laboratory for Pharmacology and Safety Evaluation of Chinese Materia Medica, School of Pharmacy, Nanjing University of Chinese Medicine, Nanjing, People's Republic of China.
Yujia LiJangsu Key Laboratory for Pharmacology and Safety Evaluation of Chinese Materia Medica, School of Pharmacy, Nanjing University of Chinese Medicine, Nanjing, People's Republic of China.
Feng ZhangJangsu Key Laboratory for Pharmacology and Safety Evaluation of Chinese Materia Medica, School of Pharmacy, Nanjing University of Chinese Medicine, Nanjing, People's Republic of China.
Zili ZhangJangsu Key Laboratory for Pharmacology and Safety Evaluation of Chinese Materia Medica, School of Pharmacy, Nanjing University of Chinese Medicine, Nanjing, People's Republic of China.
Shizhong ZhengJangsu Key Laboratory for Pharmacology and Safety Evaluation of Chinese Materia Medica, School of Pharmacy, Nanjing University of Chinese Medicine, Nanjing, People's Republic of China. nytws@njucm.edu.cn.
Nanjing University of Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe most significant cause of treatment failure in chronic myeloid leukemia (CML) is a persistent population of minimal residual cells. Emerging evidences showed that methylation of SHP-1 contributed to Imatinib (IM) resistance. Baicalein was reported to have an effect on reversal of chemotherapeutic agents resistance. However, the molecular mechanism of Baicalein on JAK2/STAT5 signaling inhibition against drug resistance in bone marrow (BM) microenvironment that had not been clearly revealed.

methodsWe co-cultured hBMSCs and CML CD34

resultsBCR/ABL-independent activation of JAK2/STAT5 signaling was involved in IM resistance in CML CD34

conclusionsThe mechanism of Baicalein on improving the sensitivity of CD34

Indexed as

Granulocyte-Macrophage Colony-Stimulating FactorLeukemia, Myelogenous, Chronic, BCR-ABL PositiveDemethylationDNA (Cytosine-5-)-Methyltransferase 1FlavanonesFlavonoidsHumansImatinib MesylateMolecular Docking SimulationProtein Tyrosine Phosphatase, Non-Receptor Type 6STAT5 Transcription FactorTumor MicroenvironmentbaicaleinDNA (Cytosine-5-)-Methyltransferase 1DNMT1 protein, humanFlavanonesFlavonoidsGranulocyte-Macrophage Colony-Stimulating FactorImatinib MesylateProtein Tyrosine Phosphatase, Non-Receptor Type 6PTPN6 protein, humanSTAT5 Transcription FactorBaicaleinCML CD34+ cellsDNMT1ResistanceSHP-1

Identifiers

PMID36869331
PMCPMC9985268
OpenAlexW4323041670

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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.