ArticleScientific reports2016
Enhanced release of primary signals may render intercellular signalling ineffective due to spatial aspects.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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.
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Who cites it
4 citing papers in PubMed.
- Variations among glioblastoma cell lines in boron-mediated enhancement of cell killing by proton beams.Scientific reports · 2025Article
- Influence of ionizing radiation and cell density on the kinetics of autocrine destruction and intercellular induction of apoptosis in precancerous cells.Scientific reports · 2022Article
- Physiological homeostasis alteration and cellular structure damage of Chlorella vulgaris exposed to silver nanoparticles with various microstructural morphologies.Environmental science and pollution research international · 2022Article
- Analytical formulas representing track-structure simulations on DNA damage induced by protons and light ions at radiotherapy-relevant energies.Scientific reports · 2020Article
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Authors and funding
2 authors.
Funding
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Abstract
Detailed mechanistic modelling has been performed of the intercellular signalling cascade between precancerous cells and their normal neighbours that leads to a selective removal of the precancerous cells by apoptosis. Two interconnected signalling pathways that were identified experimentally have been modelled, explicitly accounting for temporal and spatial effects. The model predicts highly non-linear behaviour of the signalling. Importantly, under certain conditions, enhanced release of primary signals by precancerous cells renders the signalling ineffective. This counter-intuitive behaviour arises due to spatial aspects of the underlying signalling scheme: Increased primary signalling by precancerous cells does, upon reaction with factors derived from normal cells, produce higher yields of apoptosis-triggering molecules. However, the apoptosis-triggering signals are formed farther from the precancerous cells, so that these are attacked less efficiently. Spatial effects thus may represent a novel analogue of negative feedback mechanisms.
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