Evidence map›Paper›PMID 42789178›Full record

ArticleMolecular biology reports2026

Dysregulation of circadian clock gene BMAL1 and cell cycle regulator WEE1 in pediatric AML.

Kimia Oraei Sajjadi, Hossein Ayatollahi, Maryam Sheikhi, Mohammad Hossein Ahmadi

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular biology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

4 authors.

Kimia Oraei SajjadiDepartment of Hematology and Blood Banking, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.ORCID http://orcid.org/0009-0009-9423-0053
Hossein AyatollahiDepartment of Hematology and Blood Banking, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.ORCID http://orcid.org/0000-0003-1315-8571
Maryam SheikhiCancer Molecular Pathology Research Center, Mashhad University of Medical Sciences, Mashhad, Iran.ORCID http://orcid.org/0000-0002-2532-7929
Mohammad Hossein AhmadiDepartment of Hematology and Blood Banking, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. ahmadi.hemato@gmail.com.ORCID http://orcid.org/0000-0002-3414-5019

Funding

Mashhad University of Medical Sciences 4031422
6 · The paper itself

Abstract

backgroundGrowing evidence indicates that dysregulation of circadian clock genes and cell cycle regulators plays a role in the pathogenesis of malignancies. BMAL1, a core circadian clock gene, and WEE1, a key regulator of the G2/M cell cycle checkpoint, are involved in controlling cell proliferation and maintaining genomic stability. The present study aimed to evaluate the expression pattern of these two genes in children with acute myeloid leukemia.

methodsIn this study, bone marrow samples from 40 newly diagnosed pediatric AML patients and 20 non-malignant control subjects were analyzed. The expression levels of BMAL1 and WEE1 were measured using real-time quantitative PCR. The association between gene expression and hematological parameters, including white blood cell count, hemoglobin, platelet count, and blast percentage, was also assessed.

resultsThe expression levels of both BMAL1 and WEE1 were significantly lower in AML patients compared with the control group (P < 0.001). The relative expression levels of BMAL1 and WEE1 were 0.18 and 0.31-fold of the control group, respectively. In addition, a significant negative correlation was observed between BMAL1 expression and white blood cell count (r = -0.440, P = 0.004) as well as blast percentage (r = -0.418, P = 0.007). In contrast, WEE1 expression showed no significant correlation with any of the evaluated hematological parameters.

conclusionThe significant downregulation of BMAL1 and WEE1 in pediatric AML suggests a potential role of disrupted circadian clock and cell cycle regulatory pathways in the pathogenesis of this disease.

Indexed as

ARNTL Transcription FactorsCell Cycle ProteinsCircadian ClocksLeukemia, Myeloid, AcuteProtein-Tyrosine KinasesAdolescentCase-Control StudiesChildChild, PreschoolFemaleGene Expression Regulation, LeukemicHumansMaleARNTL Transcription FactorsBMAL1 protein, humanCell Cycle ProteinsProtein-Tyrosine KinasesWEE1 protein, humanAcute myeloid leukemiaBMAL1Cell cycleCircadian clockWEE1

Identifiers

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.