ReviewCancer science2003
Role of AML1/Runx1 in the pathogenesis of hematological malignancies.
Review in Cancer science, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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
14 citing papers in PubMed, 57 citations in OpenAlex.
- RUNX1 expression dynamics in plasma cell differentiation and pathogenesis of multiple myeloma.Frontiers in immunology · 2025Article
- Review
- Characterization of CADD522, a small molecule that inhibits RUNX2-DNA binding and exhibits antitumor activity.Oncotarget · 2017Article
- Article
- Screening of Transcription Factors Involved in Fetal Hemoglobin Regulation Using Phylogenetic Footprinting.Evolutionary bioinformatics online · 2015Article
- Tcf7 is an important regulator of the switch of self-renewal and differentiation in a multipotential hematopoietic cell line.PLoS genetics · 2012Article
- Inducible expression of Runx2 results in multiorgan abnormalities in mice.Journal of cellular biochemistry · 2011Article
- Identification and analysis of the human CD160 promoter: implication of a potential AML-1 binding site in promoter activation.Genes and immunity · 2009Article
- Article
- Article
- Physical and functional interaction of Runt-related protein 1 with hypoxia-inducible factor-1alpha.Oncogene · 2008Article
- Five distinct biological processes and 14 differentially expressed genes characterize TEL/AML1-positive leukemia.BMC genomics · 2007Article
- Article
- Gene expression profiling of acute promyelocytic leukaemia identifies two subtypes mainly associated with flt3 mutational status.Leukemia · 2006Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
AML1/Runx1, originally identified as a gene located at the breakpoint of the t(8;21) translocation, encodes one of the two subunits forming a heterodimeric transcription factor. AML1 contains a highly evolutionally conserved domain called the Runt domain, responsible for both DNA binding and heterodimerization with the partner protein, CBFbeta. AML1 is widely expressed in all hematopoietic lineages, and regulates the expression of a variety of hematopoietic genes. Numerous studies have shown that AML is a critical regulator of hematopoietic development. In addition, AML1 and CBFbeta are frequent targets for chromosomal translocation in human leukemia. Translocations lead to the generation of fusion proteins, which play a causative role for the development of leukemia, primarily by inhibiting AML1 function. Point mutations that impair AML1 function are also associated with familial and sporadic leukemias. Loss of AML1 function is thus implicated in a number of leukemias through multiple pathogenic mechanisms. However, AML1-related translocations or haploinsufficiency of AML1 are not immediately leukemogenic in animal models, suggesting that additional genetic events are required for the development of full-blown leukemia.
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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.