Evidence map›Paper›PMID 38699598›Full record

ArticleSaudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society2024

Pharmacological p38 MAPK inhibitor SB203580 enhances AML stem cell line KG1a chemosensitivity to daunorubicin by promoting late apoptosis, cell growth arrest in S-phase, and miR-328-3p upregulation.

Sara Bahattab, Ali Assiri, Yazeid Alhaidan, Thadeo Trivilegio, Rehab AlRoshody, Sarah Huwaizi, Bader Almuzzaini, Abir Alamro, Manal Abudawood, Zeyad Alehaideb and 1 more

Abstract read
In one paragraph

Article in Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. [Sulforaphane reduces reactive astrocyte-mediated neuron apoptosisNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026
    Article
  2. 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

11 authors.

Sara BahattabBlood and Cancer Research Department, King Abdullah International Medical Research Center (KAIMRC), King Saud bin Abdulaziz University for Health Sciences (KSAU-HS), Ministry of National Guard-Health Affairs (MNG-HA), Riyadh 11481, Saudi Arabia.
Ali AssiriBlood and Cancer Research Department, King Abdullah International Medical Research Center (KAIMRC), King Saud bin Abdulaziz University for Health Sciences (KSAU-HS), Ministry of National Guard-Health Affairs (MNG-HA), Riyadh 11481, Saudi Arabia.
Yazeid AlhaidanMedical Genomics Research Department, KAIMRC, KSAU-HS, MNG-HA, Riyadh 11481, Saudi Arabia.
Thadeo TrivilegioMedical Research Core Facility and Platforms, KAIMRC, KSAU-HS, MNG-HA, Riyadh 11481, Saudi Arabia.
Rehab AlRoshodyBlood and Cancer Research Department, King Abdullah International Medical Research Center (KAIMRC), King Saud bin Abdulaziz University for Health Sciences (KSAU-HS), Ministry of National Guard-Health Affairs (MNG-HA), Riyadh 11481, Saudi Arabia.
Sarah HuwaiziMedical Research Core Facility and Platforms, KAIMRC, KSAU-HS, MNG-HA, Riyadh 11481, Saudi Arabia.
Bader AlmuzzainiMedical Genomics Research Department, KAIMRC, KSAU-HS, MNG-HA, Riyadh 11481, Saudi Arabia.
Abir AlamroBiochemistry Department, College of Science, King Saud University, Riyadh 11451, Saudi Arabia.
Manal AbudawoodDepartment of Clinical Laboratories Sciences, College of Applied Medical Sciences, King Saud University, Riyadh 11362, Saudi Arabia.
Zeyad AlehaidebMedical Genomics Research Department, KAIMRC, KSAU-HS, MNG-HA, Riyadh 11481, Saudi Arabia.
Sabine Matou-NasriBlood and Cancer Research Department, King Abdullah International Medical Research Center (KAIMRC), King Saud bin Abdulaziz University for Health Sciences (KSAU-HS), Ministry of National Guard-Health Affairs (MNG-HA), Riyadh 11481, Saudi Arabia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute myeloid leukaemia (AML) is characterized by uncontrolled proliferation of myeloid progenitor cells and impaired maturation, leading to immature cell accumulation in the bone marrow and bloodstream, resulting in hematopoietic dysfunction. Chemoresistance, hyperactivity of survival pathways, and miRNA alteration are major factors contributing to treatment failure and poor outcomes in AML patients. This study aimed to investigate the impact of the pharmacological p38 mitogen-activated protein kinase (MAPK) inhibitor SB203580 on the chemoresistance potential of AML stem cell line KG1a to the therapeutic drug daunorubicin (DNR). KG1a and chemosensitive leukemic HL60 cells were treated with increasing concentrations of DNR. Cell Titer-Glo®, flow cytometry, phosphokinase and protein arrays, Western blot technology, and reverse transcription-quantitative polymerase chain reaction (RT-qPCR) were employed for assessment of cell viability, half-maximal inhibitory concentration (IC

Indexed as

Acute myeloid leukemiaApoptosisDaunorubicinmiR-328-3pp38 MAPK inhibitorSB203580

Identifiers

PMID38699598
PMCPMC11063648

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.