ArticleProceedings of the National Academy of Sciences of the United States of America2005
AML1-ETO fusion protein up-regulates TRKA mRNA expression in human CD34+ cells, allowing nerve growth factor-induced expansion.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 67 citations in OpenAlex.
- Kinome expression profiling improves risk stratification and therapeutic targeting in myelodysplastic syndromes.Blood advances · 2024Article
- CSF3R T618I Collaborates With RUNX1-RUNX1T1 to Expand Hematopoietic Progenitors and Sensitizes to GLI Inhibition.HemaSphere · 2023Article
- AML1/ETO and its function as a regulator of gene transcription via epigenetic mechanisms.Oncogene · 2021Review
- Discovery and characterization of targetable NTRK point mutations in hematologic neoplasms.Blood · 2020Article
- Core Binding Factor Leukemia: Chromatin Remodeling Moves Towards Oncogenic Transcription.Cancers · 2019Review
- Review
- Inhibition of Tropomyosin Receptor Kinase A Signaling Negatively Regulates Megakaryopoiesis and induces Thrombopoiesis.Scientific reports · 2019Article
- Two Receptors, Two Isoforms, Two Cancers: Comprehensive Analysis of KIT and TrkA Expression in Neuroblastoma and Acute Myeloid Leukemia.Frontiers in oncology · 2019Article
- Article
- Characterization of TRKA signaling in acute myeloid leukemia.Oncotarget · 2018Article
- Article
- New insights into transcriptional and leukemogenic mechanisms of AML1-ETO and E2A fusion proteins.Frontiers in biology · 2016Article
- Article
- IGF binding protein 2 is a cell-autonomous factor supporting survival and migration of acute leukemia cells.Journal of hematology & oncology · 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 and RUNX1-ETO: roles in hematopoiesis and leukemogenesis.Frontiers in bioscience (Landmark edition) · 2012Review
- Mutations in the transmembrane and juxtamembrane domains enhance IL27R transforming activity.The Biochemical journal · 2011Article
- Molecular pathogenesis of core binding factor leukemia: current knowledge and future prospects.International journal of hematology · 2011Review
- Acute myeloid leukemia with the t(8;21) translocation: clinical consequences and biological implications.Journal of biomedicine & biotechnology · 2011Article
- Article
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
The AML1-ETO fusion protein, generated by the t(8;21) in acute myeloid leukemia (AML), exerts dominant-negative functions and a variety of gains of function, including a positive effect on the growth of primary human CD34+ hematopoietic stem/progenitor cells. We now show that AML1-ETO expression up-regulates the level of TRKA mRNA and protein in these cells and that AML1-ETO-expressing CD34+ hematopoietic cells grown in the presence of five early-acting hematopoietic cytokines further proliferate in response to nerve growth factor (NGF). These cells also show a unique response to NGF and IL-3; namely, they expand in liquid culture. To determine the biological relevance of our findings, we analyzed 262 primary AML patient samples using real-time RT-PCR and found that t(8;21)-positive AML samples express significantly higher levels of TRKA mRNA than other subtypes of AML. NGF, which is normally expressed by bone marrow stromal cells, could provide important proliferative or survival signals to AML1-ETO-expressing leukemic or preleukemic cells, and the NGF/TRKA signaling pathway may be a suitable target for therapeutic approaches to AML.
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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.