ReviewCancer letters2007
Oncogenic pathways of AML1-ETO in acute myeloid leukemia: multifaceted manipulation of marrow maturation.
Review in Cancer letters, 2007. 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
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
19 citing papers in PubMed, 53 citations in OpenAlex.
- t(8;21)AML patients with RUNX1e6::RUNX1T19a splice variant have poor prognosis.Annals of hematology · 2025Article
- Research and Development Progression of Oridonin for Hematological Malignancies Therapy.Current medicinal chemistry · 2025Review
- Combination of eriocalyxin B and homoharringtonine exerts synergistic anti-tumor effects against t(8;21) AML.Acta pharmacologica Sinica · 2024Article
- Ventx Family and Its Functional Similarities with Nanog: Involvement in Embryonic Development and Cancer Progression.International journal of molecular sciences · 2022Review
- Roles of Histone Deacetylases in Acute Myeloid Leukemia With Fusion Proteins.Frontiers in oncology · 2021Review
- Article
- Acute myeloid leukemia in an 86-year-old man with AML1/ETO treated with Homoharringtonine and Arsenic Trioxide: A case report.Medicine · 2019Article
- Different roles of E proteins in t(8;21) leukemia: E2-2 compromises the function of AETFC and negatively regulates leukemogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Celastrol Induces Cell Apoptosis and Inhibits the Expression of the AML1-ETO/C-KIT Oncoprotein in t(8;21) Leukemia.Molecules (Basel, Switzerland) · 2016Article
- Esculetin Downregulates the Expression of AML1-ETO and C-Kit in Kasumi-1 Cell Line by Decreasing Half-Life of mRNA.Journal of oncology · 2015Article
- Perspectives of differentiation therapies of acute myeloid leukemia: the search for the molecular basis of patients' variable responses to 1,25-dihydroxyvitamin d and vitamin d analogs.Frontiers in oncology · 2014Review
- A histone acetyltransferase p300 inhibitor C646 induces cell cycle arrest and apoptosis selectively in AML1-ETO-positive AML cells.PloS one · 2013Article
- Molecular mechanisms of leukemia-associated protein degradation.Frontiers of medicine in China · 2010Review
- Article
- Article
- Aberrant expression of CD19 in AML with t(8;21) involves a poised chromatin structure and PAX5.Oncogene · 2010Article
- A Drosophila model identifies calpains as modulators of the human leukemogenic fusion protein AML1-ETO.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
- Twist-2 controls myeloid lineage development and function.PLoS biology · 2008Article
- 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
2 authors at 1 institution in 1 country.
Funding
Abstract
The leukemic fusion protein AML1-ETO occurs frequently in human acute myeloid leukemia (AML) and has received much attention over the past decade. An initial model for its pathogenetic effects emphasized the conversion of a hematopoietic transcriptional activator, RUNX1 (or AML1), into a leukemogenic repressor which blocked myeloid differentiation at the level of target gene regulation. This view has been absorbed into a larger picture of AML1-ETO pathogenesis, encompassing dysregulation of hematopoietic stem cell homeostasis at several mechanistic levels. Recent reports have highlighted a multifaceted capacity of AML1-ETO directly to inhibit key hematopoietic transcription factors that function as tumor suppressors at several nodal points during hematopoietic differentiation. A new model is presented in which AML1-ETO coordinates expansion of the stem cell compartment with diminished lineage commitment and with genome instability.
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.