Evidence map›Paper›PMID 37891580›Full record

ArticleJournal of translational medicine2023

Spatiotemporal evolution of AML immune microenvironment remodeling and RNF149-driven drug resistance through single-cell multidimensional analysis.

Xin Wu, Zhongguang Wu, Woding Deng, Rong Xu, Chunmei Ban, Xiaoying Sun, Qiangqiang Zhao

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

4 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Senescent T Cells: The Silent Culprit in Acute Myeloid Leukemia Progression?International journal of molecular sciences · 2024
    Review
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

7 authors at 4 institutions in 1 country.

Xin WuDepartment of spine surgery, Third Xiangya Hospital, Central South University, Changsha, 410013, Hunan, China.
Zhongguang WuDepartment of Clinical Laboratory Medicine, The Eighth Affiliated Hospital, Sun Yat-sen University, Shenzhen, 518033, Guangdong, P.R. China.
Woding DengXiangya School of Medicine, Central South University, Changsha, 410013, Hunan, China.
Rong XuDepartment of Pathology, The First People's Hospital of Changde City, Changde, 415003, Hunan, China.
Chunmei BanDepartment of Hematology, The People's Hospital of Liuzhou City, Guangxi, 545026, People's Republic of China.
Xiaoying SunThe First Hospital of Sun Yat-sen University, Guangzhou, 510080, Guangdong, China. 1069776629@qq.com.
Qiangqiang ZhaoDepartment of Hematology, The People's Hospital of Liuzhou City, Guangxi, 545026, People's Republic of China. zgxyws@163.com.ORCID 0000-0002-1622-7547
Central South University · CNSun Yat-sen University · CNThe First People's Hospital of Changde · CNThe People's Hospital of Guangxi Zhuang Autonomous Region · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe composition of the bone marrow immune microenvironment in patients with acute myeloid leukaemia (AML) was analysed by single-cell sequencing and the evolutionary role of different subpopulations of T cells in the development of AML and in driving drug resistance was explored in conjunction with E3 ubiquitin ligase-related genes.

methodsTo elucidate the mechanisms underlying AML-NR and Ara-C resistance, we analyzed the bone marrow immune microenvironment of AML patients by integrating multiple single-cell RNA sequencing datasets. When compared to the AML disease remission (AML-CR) cohort, AML-NR displayed distinct cellular interactions and alterations in the ratios of CD4

resultsOur findings indicate that the E3 ubiquitin ligase RNF149 accelerates AML progression, modifies the AML immune milieu, triggers CD8

conclusionIn essence, the immune microenvironments of AML-CR and AML-NR diverge considerably, spotlighting RNF149's tumorigenic function in AML and cementing its status as a potential prognostic indicator and innovative therapeutic avenue for countering AML resistance.

Indexed as

Leukemia, Myeloid, AcuteBone MarrowCytarabineDrug ResistanceHumansTumor MicroenvironmentUbiquitin-Protein LigasesCytarabineUbiquitin-Protein LigasesAcute myeloid leukaemiaBone marrow microenvironmentImmune cellsRNF149Single-cell sequencing

Identifiers

PMID37891580
PMCPMC10612211
OpenAlexW4387971664

What OpenQuestion holds

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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.