ArticleBlood2008
t(8;21)(q22;q22) Fusion proteins preferentially bind to duplicated AML1/RUNX1 DNA-binding sequences to differentially regulate gene expression.
Article in Blood, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
26 citing papers in PubMed, 42 citations in OpenAlex.
- Germline Variants and Characteristic Features of Hereditary Hematological Malignancy Syndrome.International journal of molecular sciences · 2024Review
- Article
- KDM4B promotes acute myeloid leukemia associated with AML1-ETO by regulating chromatin accessibility.FASEB bioAdvances · 2021Article
- MicroRNA let-7b downregulates AML1-ETO oncogene expression in t(8;21) AML by targeting its 3'UTR.Experimental hematology & oncology · 2021Article
- Roles of Histone Deacetylases in Acute Myeloid Leukemia With Fusion Proteins.Frontiers in oncology · 2021Review
- Nuclear export of chimeric mRNAs depends on an lncRNA-triggered autoregulatory loop in blood malignancies.Cell death & disease · 2020Article
- The Oncogenic Transcription Factor RUNX1/ETO Corrupts Cell Cycle Regulation to Drive Leukemic Transformation.Cancer cell · 2018Article
- Heterodimerization of AML1/ETO with CBFβ is required for leukemogenesis but not for myeloproliferation.Leukemia · 2017Article
- New insights into transcriptional and leukemogenic mechanisms of AML1-ETO and E2A fusion proteins.Frontiers in biology · 2016Article
- The impact of TEL-AML1 (ETV6-RUNX1) expression in precursor B cells and implications for leukaemia using three different genome-wide screening methods.Blood cancer journal · 2013Article
- A stable transcription factor complex nucleated by oligomeric AML1-ETO controls leukaemogenesis.Nature · 2013Article
- Attenuation of AML1-ETO cellular dysregulation correlates with increased leukemogenic potential.Blood · 2013Article
- AML1-ETO targets and suppresses cathepsin G, a serine protease, which is able to degrade AML1-ETO in t(8;21) acute myeloid leukemia.Oncogene · 2013Article
- RUNX1: A microRNA hub in normal and malignant hematopoiesis.International journal of molecular sciences · 2013Review
- Article
- AML1/ETO and POU4F1 synergy drives B-lymphoid gene expression typical of t(8;21) acute myeloid leukemia.Leukemia · 2012Article
- RUNX1 and RUNX1-ETO: roles in hematopoiesis and leukemogenesis.Frontiers in bioscience (Landmark edition) · 2012Review
- The leukemogenicity of AML1-ETO is dependent on site-specific lysine acetylation.Science (New York, N.Y.) · 2011Article
- MLL fusion proteins preferentially regulate a subset of wild-type MLL target genes in the leukemic genome.Blood · 2011Article
- Acute myeloid leukemia with the t(8;21) translocation: clinical consequences and biological implications.Journal of biomedicine & biotechnology · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Chromosome abnormalities are frequently associated with cancer development. The 8;21(q22;q22) chromosomal translocation is one of the most common chromosome abnormalities identified in leukemia. It generates fusion proteins between AML1 and ETO. Since AML1 is a well-defined DNA-binding protein, AML1-ETO fusion proteins have been recognized as DNA-binding proteins interacting with the same consensus DNA-binding site as AML1. The alteration of AML1 target gene expression due to the presence of AML1-ETO is related to the development of leukemia. Here, using a 25-bp random double-stranded oligonucleotide library and a polymerase chain reaction (PCR)-based DNA-binding site screen, we show that compared with native AML1, AML1-ETO fusion proteins preferentially bind to DNA sequences with duplicated AML1 consensus sites. This finding is further confirmed by both in vitro and in vivo DNA-protein interaction assays. These results suggest that AML1-ETO fusion proteins have a selective preference for certain AML1 target genes that contain multimerized AML1 consensus sites in their regulatory elements. Such selected regulation provides an important molecular mechanism for the dysregulation of gene expression during cancer development.
Indexed as
Identifiers
What OpenQuestion holds
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.