ArticleOncotarget2018
Characterization of TRKA signaling in acute myeloid leukemia.
Article in Oncotarget, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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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.
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- Review
- Recent Advances in FLT3-Based Dual Inhibitors: A Promising Strategy for the Treatment of Acute Myeloid Leukemia.Current medicinal chemistry · 2026Review
- Kinome expression profiling improves risk stratification and therapeutic targeting in myelodysplastic syndromes.Blood advances · 2024Article
- Nerve Growth Factor and the Role of Inflammation in Tumor Development.Current issues in molecular biology · 2024Review
- Systemic Optimization of Gene Electrotransfer Protocol Using Hard-to-Transfect UT-7 Cell Line as a Model.Biomedicines · 2022Article
- Discovery and characterization of targetable NTRK point mutations in hematologic neoplasms.Blood · 2020Article
- Review
- Antileukemia Effects of Notch-Mediated Inhibition of Oncogenic PLK1 in B-Cell Acute Lymphoblastic Leukemia.Molecular cancer therapeutics · 2019Article
- Two Receptors, Two Isoforms, Two Cancers: Comprehensive Analysis of KIT and TrkA Expression in Neuroblastoma and Acute Myeloid Leukemia.Frontiers in oncology · 2019Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Tropomyosin-related kinase A (TRKA) translocations have oncogenic potential and have been found in rare cases of solid tumors. Accumulating evidence indicates that TRKA and its ligand, nerve growth factor (NGF), may play a role in normal hematopoiesis and may be deregulated in leukemogenesis. Here, we report a comprehensive evaluation of TRKA signaling in normal and leukemic cells. TRKA expression is highest in common myeloid progenitors and is overexpressed in core binding factor and megakaryocytic leukemias, especially Down syndrome-related AML. Importantly, NGF can rescue GM-CSF dependent TF-1 AML cells, but does not drive proliferation in other TRKA-expressing lines. Although TRKA expression is heterogeneous between and within AML samples, NGF stimulation broadly induces ERK signaling, demonstrating the functional ability of AML cells to respond to NGF/TRKA signaling. However, neither shRNA knockdown nor pharmacologic inhibition have significant anti-proliferative effects on human AML cells
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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.