ArticleOncogene2009
Pbx1 is a downstream target of Evi-1 in hematopoietic stem/progenitors and leukemic cells.
Article in Oncogene, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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
34 citing papers in PubMed, 64 citations in OpenAlex.
- MECOM promotes leukemia progression and inhibits mast cell differentiation through functional competition with GATA2.Leukemia · 2026Article
- Clinical significance of dynamic monitoring of EVI1 gene expression in pediatric acute myeloid leukemia.BMC pediatrics · 2024Article
- CRISPR-Cas9-mediated deletion enhancer of MECOM play a tumor suppressor role in ovarian cancer.Functional & integrative genomics · 2024Article
- Regulation and signaling pathways in cancer stem cells: implications for targeted therapy for cancer.Molecular cancer · 2023Review
- EVI1-mediated Programming of Normal and Malignant Hematopoiesis.HemaSphere · 2023Review
- Mosaic Chromosomal Alterations Are Associated With Increased Lung Cancer Risk: Insight From the INTEGRAL-ILCCO Cohort Analysis.Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · 2023Article
- Comprehensive overview of the role of PBX1 in mammalian kidneys.Frontiers in molecular biosciences · 2023Review
- CRISPR-mediated MECOM depletion retards tumor growth by reducing cancer stem cell properties in lung squamous cell carcinoma.Molecular therapy : the journal of the American Society of Gene Therapy · 2022Article
- Targeting histone methylation to reprogram the transcriptional state that drives survival of drug-tolerant myeloid leukemia persisters.iScience · 2022Article
- Hematopoietic Stem Cell Factors: Their Functional Role in Self-Renewal and Clinical Aspects.Frontiers in cell and developmental biology · 2022Review
- PBX1: a key character of the hallmarks of cancer.Journal of molecular medicine (Berlin, Germany) · 2021Review
- EVI1 dysregulation: impact on biology and therapy of myeloid malignancies.Blood cancer journal · 2021Review
- Myeloid neoplasms associated with t(3;12)(q26.2;p13) are clinically aggressive, show myelodysplasia, and frequently harbor chromosome 7 abnormalities.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2021Article
- Article
- EVI1 overexpression reprograms hematopoiesis via upregulation of Spi1 transcription.Nature communications · 2018Article
- Loss of p53 induces leukemic transformation in a murine model of Jak2 V617F-driven polycythemia vera.Oncogene · 2017Article
- The central nervous system microenvironment influences the leukemia transcriptome and enhances leukemia chemo-resistance.Haematologica · 2017Article
- Expression of MECOM is associated with unfavorable prognosis in glioblastoma multiforme.OncoTargets and therapy · 2016Article
- Article
- EVI1 promotes tumor growth via transcriptional repression of MS4A3.Journal of hematology & oncology · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ecotropic viral integration site-1 (Evi-1) is a nuclear transcription factor, which is essential for the proliferation/maintenance of hematopoietic stem cells (HSCs). Aberrant expression of Evi-1 has been frequently found in myeloid leukemia, and is associated with a poor patient survival. Recently, we reported candidate target genes of Evi-1 shared in HSCs and leukemic cells using gene expression profiling analysis. In this study, we identified Pbx1, a proto-oncogene in hematopoietic malignancy, as a target gene of Evi-1. Overexpression of Evi-1 increased Pbx1 expression in hematopoietic stem/progenitor cells. An analysis of the Pbx1 promoter region revealed that Evi-1 upregulates Pbx1 transcription. Furthermore, reduction of Pbx1 levels through RNAi-mediated knockdown significantly inhibited Evi-1-induced transformation. In contrast, knockdown of Pbx1 did not impair bone marrow transformation by E2A/HLF or AML1/ETO, suggesting that Pbx1 is specifically required for the maintenance of bone marrow transformation mediated by Evi-1. These results indicate that Pbx1 is a target gene of Evi-1 involved in Evi-1-mediated leukemogenesis.
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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.