ArticleBlood2010
An evolutionarily conserved PTEN-C/EBPalpha-CTNNA1 axis controls myeloid development and transformation.
Article in Blood, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 36 citations in OpenAlex.
- Detection and functional assessment of structural variants using whole-genome re-sequencing data in Nellore cattle.Scientific reports · 2025Article
- Article
- The Role of CTNNA1 in Malignancies: An Updated Review.Journal of Cancer · 2023Review
- Zebrafish as a Model for Anticancer Nanomedicine Studies.Pharmaceuticals (Basel, Switzerland) · 2021Review
- PTEN in Regulating Hematopoiesis and Leukemogenesis.Cold Spring Harbor perspectives in medicine · 2020Review
- JMJD3 facilitates C/EBPβ-centered transcriptional program to exert oncorepressor activity in AML.Nature communications · 2018Article
- CTNNA1 hypermethylation, a frequent event in acute myeloid leukemia, is independently associated with an adverse outcome.Oncotarget · 2016Article
- The Role of PTEN in Myeloid Malignancies.Hematology reports · 2015Review
- New functions for alpha-catenins in health and disease: from cancer to heart regeneration.Cell and tissue research · 2015Review
- Zebrafish as a model for leukemia and other hematopoietic disorders.Journal of hematology & oncology · 2015Review
- Article
- Pten regulates homeostasis and inflammation-induced migration of myelocytes in zebrafish.Journal of hematology & oncology · 2014Article
- Regulation of monocyte differentiation by specific signaling modules and associated transcription factor networks.Cellular and molecular life sciences : CMLS · 2014Review
- A novel insertion ins(18;5)(q21.1;q31.2q35.1) in acute myeloid leukemia associated with microdeletions at 5q31.2, 5q35.1q35.2 and 18q12.3q21.1 detected by oligobased array comparative genomic hybridization.Molecular cytogenetics · 2014Article
- Emergence of zebrafish models in oncology for validating novel anticancer drug targets and nanomaterials.Drug discovery today · 2013Review
- Article
- Article
- Regulation and deregulation of mRNA translation during myeloid maturation.Experimental hematology · 2011Review
- Differential effects of sumoylation on the activities of CCAAT enhancer binding protein alpha (C/EBPα) p42 versus p30 may contribute in part, to aberrant C/EBPα activity in acute leukemias.Hematology reports · 2011Article
Corrections and comments
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Authors and funding
22 authors at 6 institutions in 2 countries.
Funding
Abstract
Loss of function of tumor suppressor genes, such as PTEN, CEBPAlpha, and CTNNA1 (encoding the alpha-catenin protein), has been found to play an essential role in leukemogenesis. However, whether these genes genetically interact remains largely unknown. Here, we show that PTEN-mammalian target of rapamycin signaling acts upstream to dictate the ratio of wild-type p42 C/EBPalpha to its dominant-negative p30 isoform, which critically determines whether p30 C/EBPalpha (lower p42/p30 ratio) or p42 C/EBPalpha (higher p42/p30 ratio) binds to the proximal promoter of the retained CTNNA1 allele. Binding of p30 C/EBPalpha recruits the polycomb repressive complex 2 to suppress CTNNA1 transcription through repressive H3K27me3 modification, whereas binding of p42 C/EBPalpha relieves this repression and promotes CTNNA1 expression through activating H3K4me3 modification. Loss of Pten function in mice and zebrafish induces myelodysplasia with abnormal invasiveness of myeloid progenitors accompanied by significant reductions in both wild-type C/EBPalpha and alpha-catenin protein. Importantly, frame-shift mutations in either PTEN or CEBPA were detected exclusively in the primary LICs with low CTNNA1 expression. This study uncovers a novel molecular pathway, PTEN-C/EBPalpha-CTNNA1, which is evolutionarily conserved and might be therapeutically targeted to eradicate LICs with low CTNNA1 expression.
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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.