ArticleLeukemia2007
Lentiviral PU.1 overexpression restores differentiation in myeloid leukemic blasts.
Article in Leukemia, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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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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Who cites it
17 citing papers in PubMed, 29 citations in OpenAlex.
- Review
- Super-enhancer-associated long noncoding RNA lnc-SPI1U mediates SPI1 feedback regulation by interacting with HNRNPH1 and HNRNPF.Oncogene · 2025Article
- LSD1 inhibition modulates transcription factor networks in myeloid malignancies.Frontiers in oncology · 2023Review
- Combined Approach to Leukemic Differentiation Using Transcription Factor PU.1-Enhancing Agents.International journal of molecular sciences · 2022Article
- Expression of the phagocytic receptors αFrontiers in immunology · 2022Article
- Intrinsic disorder controls two functionally distinct dimers of the master transcription factor PU.1.Science advances · 2020Article
- PRDM16s transforms megakaryocyte-erythroid progenitors into myeloid leukemia-initiating cells.Blood · 2019Article
- Pharmacological inhibition of the transcription factor PU.1 in leukemia.The Journal of clinical investigation · 2017Article
- RUNX1 induces DNA replication independent active DNA demethylation at SPI1 regulatory regions.BMC molecular biology · 2017Article
- PML/RARa inhibits PTEN expression in hematopoietic cells by competing with PU.1 transcriptional activity.Oncotarget · 2016Article
- PU.1 downregulation in murine radiation-induced acute myeloid leukaemia (AML): from molecular mechanism to human AML.Carcinogenesis · 2015Review
- Sall4 overexpression blocks murine hematopoiesis in a dose-dependent manner.Experimental hematology · 2015Article
- Induced differentiation of acute myeloid leukemia cells by activation of retinoid X and liver X receptors.Leukemia · 2014Article
- The tumor suppressor gene DAPK2 is induced by the myeloid transcription factors PU.1 and C/EBPα during granulocytic differentiation but repressed by PML-RARα in APL.Journal of leukocyte biology · 2014Article
- Interference with RUNX1/ETO leukemogenic function by cell-penetrating peptides targeting the NHR2 oligomerization domain.BioMed research international · 2013Article
- 5-azacitidine in aggressive myelodysplastic syndromes regulates chromatin structure at PU.1 gene and cell differentiation capacity.Leukemia · 2012Article
- PU.1 activation relieves GATA-1-mediated repression of Cebpa and Cbfb during leukemia differentiation.Molecular cancer research : MCR · 2009Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
PU.1, a transcription factor of the ETS family, plays a pivotal role in normal hematopoiesis, and particularly in myeloid differentiation. Altered PU.1 function is possibly implicated in leukemogenesis, as PU.1 gene mutations were identified in some patients with acute myeloid leukemia (AML) and as several oncogenic products (AML1-ETO, promyelocytic leukemia-retinoic acid receptor alpha, FMS-like receptor tyrosine kinase 3 internal tandem duplication) are associated with PU.1 downregulation. To demonstrate directly a role of PU.1 in the blocked differentiation of leukemic blasts, we transduced cells from myeloid cell lines and primary blasts from AML patients with a lentivector encoding PU.1. In NB4 cells we obtained increases in PU.1 mRNA and protein, comparable to increases obtained with all-trans retinoic acid-stimulation. Transduced cells showed increased myelomonocytic surface antigen expression, decreased proliferation rates and increased apoptosis. Similar results were obtained in primary AML blasts from 12 patients. These phenotypic changes are characteristic of restored blast differentiation. PU.1 should therefore constitute an interesting target for therapeutic intervention in AML.
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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.