ArticleLeukemia2004
MEIS 1 expression is downregulated through promoter hypermethylation in AML1-ETO acute myeloid leukemias.
Article in Leukemia, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 40 citations in OpenAlex.
- Reconstructing DNA methylation maps of ancient populations.Nucleic acids research · 2024Article
- HOXA9 has the hallmarks of a biological switch with implications in blood cancers.Nature communications · 2022Article
- MEIS1 and its potential as a cancer therapeutic target (Review).International journal of molecular medicine · 2021Review
- TET2 as a tumor suppressor and therapeutic target in T-cell acute lymphoblastic leukemia.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Oncogenic and tumor suppressor function of MEIS and associated factors.Turkish journal of biology = Turk biyoloji dergisi · 2020Article
- Epigenetic silencing of downstream genes mediated by tandem orientation in lung cancer.Scientific reports · 2017Article
- HOXB13 mutations and binding partners in prostate development and cancer: Function, clinical significance, and future directions.Genes & diseases · 2017Article
- Predicting the molecular role of MEIS1 in esophageal squamous cell carcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- PML-RARA requires DNA methyltransferase 3A to initiate acute promyelocytic leukemia.The Journal of clinical investigation · 2016Article
- Promoter methylation and expression levels of selected hematopoietic genes in pediatric B-cell acute lymphoblastic leukemia.Blood research · 2015Article
- Review
- Salivary gland cancers: biology and molecular targets for therapy.Current oncology reports · 2012Article
- RUNX1 and RUNX1-ETO: roles in hematopoiesis and leukemogenesis.Frontiers in bioscience (Landmark edition) · 2012Review
- Asthma and COPD - The C/EBP Connection.The open respiratory medicine journal · 2012Article
- Article
- Identification of E74-like factor 1 (ELF1) as a transcriptional regulator of the Hox cofactor MEIS1.Experimental hematology · 2010Article
- Article
- Using cell fate attractors to uncover transcriptional regulation of HL60 neutrophil differentiation.BMC systems biology · 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
Retroviral insertional mutagenesis in BXH2 mice commonly induces myeloid leukemias. One of the most frequently involved genes in experimental studies is Meis 1. In contrast to other genes in murine models, Meis 1 has not been affected by recurrent chromosomal translocations or point mutations in human leukemias. We found a constant downregulation of the Meis 1 gene mRNA in AML1-ETO acute myeloid leukemias and in those cases harboring in frame mutations in the bZIP domain of CEBPalpha. The absence of the Meis 1 mRNA was not caused by inactivating point mutations in the coding sequence. Promoter hypermethylation was present in more than half of the cases (9/14), including samples obtained from the widely employed Kasumi-1 cell line. Double treatment with 5-Aza-2'-deoxycytidine and trichostatin A of the Kasumi-1 cell line partially reverses Meis 1 inhibition. HoxA9 levels were also low. In a cell line model (U937 Tet AML1-ETO), AML1-ETO expression was not associated with Meis 1 suppression at 72 h. Nevertheless, Meis 1 repression is dependent on the AML1-ETO transcript levels in treated leukemic patients. Chimeric products that arise from chromosomal translocations may be associated with locus-specific epigenetic inactivation. It remains to be investigated when this methylation process is acquired and which are the basic mechanisms underlying these molecular events in AML1-ETO and CEBPalpha-mutated AML.
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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.