Evidence map›Paper›PMID 37341821›Full record

ArticleMedical oncology (Northwood, London, England)2023

RUNX1/ETO regulates reactive oxygen species (ROS) levels in t(8,21) acute myeloid leukaemia via FLT3 and RAC1.

Adam Azlan, Kang Zi Khor, Yaashini Rajasegaran, Aliaa Arina Rosli, Mohamed Saifulaman Mohamed Said, Narazah Mohd Yusoff, Emmanuel Jairaj Moses

Abstract read
PubMed Publisher
In one paragraph

Article in Medical oncology (Northwood, London, England), 2023. 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
0.6field-weighted citation impact, top 30% 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, 4 citations in OpenAlex.

  1. Article
  2. Review
  3. 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

7 authors at 2 institutions in 1 country.

Adam AzlanDepartment of Biomedical Sciences, Advanced Medical and Dental Institute, Universiti Sains Malaysia, Kepala Batas, Malaysia.
Kang Zi KhorDepartment of Biomedical Sciences, Advanced Medical and Dental Institute, Universiti Sains Malaysia, Kepala Batas, Malaysia.
Yaashini RajasegaranDepartment of Biomedical Sciences, Advanced Medical and Dental Institute, Universiti Sains Malaysia, Kepala Batas, Malaysia.
Aliaa Arina RosliDepartment of Biomedical Sciences, Advanced Medical and Dental Institute, Universiti Sains Malaysia, Kepala Batas, Malaysia.
Mohamed Saifulaman Mohamed SaidFaculty of Medicine, Lincoln University College, Petaling Jaya, Malaysia.
Narazah Mohd YusoffDepartment of Biomedical Sciences, Advanced Medical and Dental Institute, Universiti Sains Malaysia, Kepala Batas, Malaysia.
Emmanuel Jairaj MosesDepartment of Biomedical Sciences, Advanced Medical and Dental Institute, Universiti Sains Malaysia, Kepala Batas, Malaysia. emmanuel_jm@usm.my.ORCID http://orcid.org/0000-0003-2939-8473
Universiti Sains Malaysia · MYLincoln University College · MY

Funding

Ministry of Higher Education, Malaysia FRGS/1/2018/SKK08/USM/02/8Universiti Sains Malaysia 1001/CIPPT/8012265Universiti Sains Malaysia 1001/CIPPT/813064
6 · The paper itself

Abstract

Reactive oxygen species (ROS) homeostasis is crucial for leukaemogenesisand deregulation would hamper leukaemic progression. Although the regulatory effects of RUNX1/ETO has been extensively studied, its underlying molecular mechanims in ROS production in t(8,21) AML is yet to be fully elucidated. Here, we report that RUNX1/ETO could directly control FLT3 by occupying several DNA elements on FLT3 locus. The possible hijacking mechanism by RUNX1/ETO over FLT3 mediated ROS modulation in AML t(8;21) was made apparent when suppression of RUNX1/ETO led to decrement in ROS levels and the direct oxidative marker FOXO3 but not in FLT3 and RAC1 suppressed t(8,21) AML cell line Furthermore, nuclear import of RUNX1/ETO was aberrated following RUNX1/ETO and RAC1 suppression suggesting association in ROS control. A different picture was depicted in non t(8;21) cells where suppression of RAC1 and FLT3 led to decreased levels of FOXO3a and ROS. Results alltogether indicate a possible dysregulation of ROS levels by RUNX1/ETO in t(8,21) AML.

Indexed as

Core Binding Factor Alpha 2 SubunitLeukemia, Myeloid, AcuteCell Linefms-Like Tyrosine Kinase 3HumansOncogene Proteins, Fusionrac1 GTP-Binding ProteinReactive Oxygen SpeciesRUNX1 Translocation Partner 1 ProteinTranslocation, GeneticCore Binding Factor Alpha 2 SubunitFLT3 protein, humanfms-Like Tyrosine Kinase 3Oncogene Proteins, Fusionrac1 GTP-Binding ProteinRAC1 protein, humanReactive Oxygen SpeciesRUNX1 protein, humanRUNX1T1 protein, humanRUNX1 Translocation Partner 1 ProteinFLT3RAC1Reactive oxygen speciesRUNX1/ETO

Identifiers

PMID37341821
OpenAlexW4381469860

What OpenQuestion holds

Textmetadata
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.