ArticleAdvances in hematology2012
Extracellular NM23 Protein as a Therapeutic Target for Hematologic Malignancies.
Article in Advances in hematology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed.
- Evaluation of serum nucleoside diphosphate kinase A for the detection of colorectal cancer.Scientific reports · 2016Trial
- Structure and analysis of nucleoside diphosphate kinase from Borrelia burgdorferi prepared in a transition-state complex with ADP and vanadate moieties.Acta crystallographica. Section F, Structural biology communications · 2018Article
- The 'known-knowns', and 'known-unknowns' of extracellular Nm23-H1/NDPK proteins.Laboratory investigation; a journal of technical methods and pathology · 2018Review
- Extracellular NME proteins: a player or a bystander?Laboratory investigation; a journal of technical methods and pathology · 2018Review
- Dynamin controls extracellular level of Awd/Nme1 metastasis suppressor protein.Naunyn-Schmiedeberg's archives of pharmacology · 2016Article
- The case for extracellular Nm23-H1 as a driver of acute myeloid leukaemia (AML) progression.Naunyn-Schmiedeberg's archives of pharmacology · 2015Review
- Erythropoietin increases neuronal NDPKA expression, and NDPKA up-regulation as well as exogenous application protects cortical neurons from in vitro ischemia-related insults.Cellular and molecular neurobiology · 2014Article
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
An elevated serum level of NM23-H1 protein is a poor prognostic factor in patients with various hematologic malignancies. The extracellular NM23-H1 protein promotes the in vitro growth and survival of acute myelogenous leukemia (AML) cells and inversely inhibits the in vitro survival of normal peripheral blood monocytes in primary culture at concentrations equivalent to the levels found in the serum of AML patients. The growth and survival promoting activity to AML cells is associated with cytokine production and activation of mitogen-activated protein kinases (MAPKs) and signal transducers and activators of transcription (STAT) signaling pathways. Inhibitors specific for MAPK signaling pathways inhibit the growth/survival-promoting activity of NM23-H1. These findings indicate a novel biological action of extracellular NM23-H1 and its association with poor prognosis. These results suggest an important role of extracellular NM23-H1 in the malignant progression of leukemia and a potential therapeutic target for these malignancies.
Identifiers
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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.