ReviewOncogene2001
Common themes in the pathogenesis of acute myeloid leukemia.
Review in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 87 citations in OpenAlex.
- Automated workflow for the cell cycle analysis of (non-)adherent cells using a machine learning approach.eLife · 2024Article
- Understanding a high-risk acute myeloid leukemia by analyzing the interactome of its major driver mutation.PLoS genetics · 2022Article
- Activation of signaling pathways in models of t(6;9)-acute myeloid leukemia.Annals of hematology · 2022Article
- Artesunate improves venetoclax plus cytarabine AML cell targeting by regulating the Noxa/Bim/Mcl-1/p-Chk1 axis.Cell death & disease · 2022Article
- Chitosan as possible inhibitory agents and delivery systems in leukemia.Cancer cell international · 2021Review
- Identification of predictive genetic signatures of Cytarabine responsiveness using a 3D acute myeloid leukaemia model.Journal of cellular and molecular medicine · 2019Article
- Epidermal growth factor signaling in transformed cells.International review of cell and molecular biology · 2015Review
- AML1/ETO oncoprotein is directed to AML1 binding regions and co-localizes with AML1 and HEB on its targets.PLoS genetics · 2008Article
- Complementing mutations in core binding factor leukemias: from mouse models to clinical applications.Oncogene · 2008Review
- Selective anti-leukaemic activity of low-dose histone deacetylase inhibitor ITF2357 on AML1/ETO-positive cells.Oncogene · 2008Article
- Structural basis for recognition of SMRT/N-CoR by the MYND domain and its contribution to AML1/ETO's activity.Cancer cell · 2007Article
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- Lozenge directly activates argos and klumpfuss to regulate programmed cell death.Genes & development · 2005Article
- Chimaerism and erythroid marker expression after microinjection of human acute myeloid leukaemia cells into murine blastocysts.Oncogene · 2003Article
- Acute myeloid leukemia fusion proteins deregulate genes involved in stem cell maintenance and DNA repair.The Journal of clinical investigation · 2003Article
- Normal and leukemic hematopoiesis: are leukemias a stem cell disorder or a reacquisition of stem cell characteristics?Proceedings of the National Academy of Sciences of the United States of America · 2003Review
- Megakaryoblastic leukemia 1, a potent transcriptional coactivator for serum response factor (SRF), is required for serum induction of SRF target genes.Molecular and cellular biology · 2003Article
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- Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The pathogenesis of acute myeloid leukemia is associated with the appearance of oncogenic fusion proteins generated as a consequence of specific chromosome translocations. Of the two components of each fusion protein, one is generally a transcription factor, whereas the other partner is more variable in function, but often involved in the control of cell survival and apoptosis. As a consequence, AML-associated fusion proteins function as aberrant transcriptional regulators that interfere with the process of myeloid differentiation, determine a stage-specific arrest of maturation and enhance cell survival in a cell-type specific manner. The abnormal regulation of transcriptional networks occurs through common mechanisms that include recruitment of aberrant co-repressor complexes, alterations in chromatin remodeling, and disruption of specific subnuclear compartments. The identification and analysis of common and specific target genes regulated by AML fusion proteins will be of fundamental importance for the full understanding of acute myeloid leukemogenesis and for the implementation of disease-specific drug design.
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.