ArticleCancer science2013
Roles of AML1/RUNX1 in T-cell malignancy induced by loss of p53.
Article in Cancer science, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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.
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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
11 citing papers in PubMed, 13 citations in OpenAlex.
- RUNX1 knockdown induced apoptosis and impaired EMT in high-grade serous ovarian cancer cells.Journal of translational medicine · 2023Article
- RUNX1-Regulated Signaling Pathways in Ovarian Cancer.Biomedicines · 2023Review
- Review
- Article
- Runx Transcription Factors in T Cells-What Is Beyond Thymic Development?Frontiers in immunology · 2021Review
- Oncogenic RUNX3: A Link between p53 Deficiency and MYC Dysregulation.Molecules and cells · 2020Review
- The TP53 Apoptotic Network Is a Primary Mediator of Resistance to BCL2 Inhibition in AML Cells.Cancer discovery · 2019Article
- Runx1 Orchestrates Sphingolipid Metabolism and Glucocorticoid Resistance in Lymphomagenesis.Journal of cellular biochemistry · 2017Article
- Addiction to Runx1 is partially attenuated by loss of p53 in the Eµ-Myc lymphoma model.Oncotarget · 2016Article
- [Effects of tumor suppressor gene TCF21 on the proliferation, migration and apoptosis of A549 cells].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2014Article
- Roles of AML1/RUNX1 in T-cell malignancy induced by loss of p53.Cancer science · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
AML1/RUNX1 is a frequent target of chromosome translocations and mutations in myeloid and B-cell leukemias, and upregulation of AML1 is also observed in some cases of T-cell leukemias and lymphomas. This study shows that the incidence of thymic lymphoma in p53-null mice is less frequent in the Aml1(+/-) than in the Aml1(+/+) background. AML1 is upregulated in p53-null mouse bone-marrow cells and embryonic fibroblasts. In the steady state, p53 binds to and inhibits the distal AML1 promoter. When the cells are exposed to stresses, p53 is released from the distal AML1 promoter, resulting in upregulation of AML1. Overexpression of AML1 stimulates T-lymphocyte proliferation. These results suggest that upregulation of AML1 induced by loss of p53 promotes lymphoid-cell proliferation, thereby inducing lymphoma development.
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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.