ReviewNaunyn-Schmiedeberg's archives of pharmacology2015
The case for extracellular Nm23-H1 as a driver of acute myeloid leukaemia (AML) progression.
Review in Naunyn-Schmiedeberg's archives of pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed, 10 citations in OpenAlex.
- Pathogen and human NDPK-proteins promote AML cell survival via monocyte NLRP3-inflammasome activation.PloS one · 2023Article
- 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
- "Inverse Drug Discovery" Strategy To Identify Proteins That Are Targeted by Latent Electrophiles As Exemplified by Aryl Fluorosulfates.Journal of the American Chemical Society · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Studies in the 1990s identified a link between extracellular Nm23 proteins and acute myeloid leukaemia (AML). Confidence in the importance of these observations was undermined by a lack of appreciation that extracellular Nm23 proteins were relevant to either normal or pathophysiology coupled with the lack of demonstrable activity of Nm23 proteins against human AML cell lines. However, independent studies have highlighted the importance of Nm23-H1 in AML and have identified an elaborate Nm23-H1-mediated cross talk between cells within the AML clone. In other studies, roles for Nm23-H1 have now also been implicated in the maintenance of the stem cell state of embryonic stem (ES) cells and induced pluripotent stem (IPS) cells. In this review, we have generated a unifying model of the action of Nm23-H1 in AML, including previously unpublished data from our laboratory, and provide arguments as to why we consider this role to be distinct from that in ES and IPS cells.
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.