ArticleCell cycle (Georgetown, Tex.)2021
WT1 inhibits AML cell proliferation in a p53-dependent manner.
Article in Cell cycle (Georgetown, Tex.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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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.
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.
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Who cites it
12 citing papers in PubMed, 16 citations in OpenAlex.
- Myelodysplastic Syndromes-Transformed Acute Myeloid Leukemia With Concurrent DEK::CAN Fusion Gene Positivity and WT1 Overexpression: A Case Report and Literature Review.Cancer reports (Hoboken, N.J.) · 2026Review
- WT1 gene: a potential therapeutic target for multiple cancer treatment strategies.Clinical and experimental medicine · 2025Review
- Article
- A Study ofGenes · 2024Article
- Glutamine metabolism-related genes predict the prognostic risk of acute myeloid leukemia and stratify patients by subtype analysis.Hereditas · 2024Article
- Transforming growth factor-β1 and vascular endothelial growth factor levels in senile acute myeloid leukemia and correlation with prognosis.World journal of clinical cases · 2024Article
- Upregulation of HOXA3 by isoform-specific Wilms tumour 1 drives chemotherapy resistance in acute myeloid leukaemia.British journal of haematology · 2024Article
- WT1 and TP53 as valuable diagnostic biomarkers for relapse after hematopoietic stem cell transplantation in acute myeloid leukemia.Molecular biology reports · 2024Article
- Detection of genetic variation in bovineAnimal biotechnology · 2023Article
- Review
- Shikonin as a WT1 Inhibitor Promotes Promyeloid Leukemia Cell Differentiation.Molecules (Basel, Switzerland) · 2022Article
- The dual role of autophagy in acute myeloid leukemia.Journal of hematology & oncology · 2022Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
WT1 has been reported to function as an oncogene and a tumor suppressor in acute myeloid leukemia (AML). The molecular mechanisms have not yet been fully elucidated. Here, we report that p53, served as a tumor suppressor, plays a critical role in regulating the function of WT1 in AML. For details, we performed a meta-analysis on 1131 AML cases, showing that WT1 gene mutation and TP53 gene exhibited a mutually exclusive predisposition in AML. p53 can be recruited to the promoter region of WT1's target genes to modulate their expression by physically interacting with WT1. The AML-derived p53 mutation (p53
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Registered trials
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.