ArticleLeukemia2008
Leukemia suppressor function of Egr-1 is dependent on transforming oncogene.
Article in Leukemia, 2008. 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed, 22 citations in OpenAlex.
- miR-let-7c-3p targeting on Egr-1 contributes to the committed differentiation of leukemia cells into monocyte/macrophages.Oncology letters · 2022Article
- CIGB-300-Regulated Proteome Reveals Common and Tailored Response Patterns of AML Cells to CK2 Inhibition.Frontiers in molecular biosciences · 2022Article
- CDK6 Inhibition: A Novel Approach in AML Management.International journal of molecular sciences · 2020Review
- Loss of Egr1, a human del5q gene, accelerates BCR-ABL driven chronic myelogenous leukemia.Oncotarget · 2017Article
- Prognostic cancer gene signatures share common regulatory motifs.Scientific reports · 2017Article
- The progress of early growth response factor 1 and leukemia.Intractable & rare diseases research · 2016Review
- Induced myelomonocytic differentiation in leukemia cells is accompanied by noncanonical transcription factor expression.FEBS open bio · 2015Article
- Antiangiogenic Effects and Therapeutic Targets of Azadirachta indica Leaf Extract in Endothelial Cells.Evidence-based complementary and alternative medicine : eCAM · 2012Article
- WT1/EGR1-mediated control of STIM1 expression and function in cancer cells.Frontiers in bioscience (Landmark edition) · 2011Review
- Batf promotes growth arrest and terminal differentiation of mouse myeloid leukemia cells.Molecular cancer research : MCR · 2011Article
- Article
- Src family kinase gene targets during myeloid differentiation: identification of the EGR-1 gene as a direct target.Leukemia · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
We have shown that deregulated expression of either c-Myb or E2F-1 blocks terminal differentiation of M1 myeloid leukemia cells at the blast stage, whereas deregulated c-Myc blocks differentiation at the intermediate stage. Each of these oncogenes potentiates M1 leukemia in vivo. The zinc-finger transcription factor Egr-1 abrogates the block in M1 terminal differentiation imparted by oncogenic c-Myc or E2F-1, suppressing their leukemia-promoting function in nude mice. In this study, we asked whether Egr-1 also abrogates the block in terminal differentiation and suppresses leukemia imparted by deregulated c-Myb. Interestingly, the ectopic expression of Egr-1 in M1 cells expressing deregulated c-Myb only partially abrogated the block in terminal differentiation and did not suppress the leukemic phenotype. Two important implications from these data are that the leukemia suppressor function of Egr-1 is not directly related to how early the transforming oncogene blocks the differentiation program and that the tumor suppressor function of Egr-1 is dependent on the specific oncogene. Egr-1 is dominant to c-Myc- and E2F-1-, but not to c-Myb-, driven leukemia. These findings extend the notion that the molecular nature of genetic lesions responsible for leukemia determines the effectiveness of any given tumor suppressor.
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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.