Radiation-induced bystander signalling in cancer therapy
By Kevin M. Prise, J. O’Sullivan. Nature Reviews. Cancer, 2009
797 citations recorded by the source corpus.
Our understanding of how radiation kills normal and tumour cells has been based on an intimate knowledge of the direct induction of DNA damage and its cellular consequences. What has become clear is that, as well as responses to direct DNA damage, cell–cell signalling — known as the bystander effect — mediated through gap junctions and inflammatory responses may have an important role in the response of cells and tissues to radiation exposure and also chemotherapy agents. This Review outlines the key aspects of radiation-induced intercellular signalling and assesses its relevance for existing and future radiation-based therapies.
Subfields: Pulmonary and Respiratory Medicine, Radiation, Radiology, Nuclear Medicine and Imaging
View Paper: https://www.semanticscholar.org/paper/026ad8d8f0b5b91e4ddca4f1e03959a858b7dfe6
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Citations in the corpus
- A senescent cell bystander effect: senescence-induced senescence (2012, background): “We hypothesized that pro-oxidant and pro-inflammatory signals from primary senescent founder cells may trigger DNA damage and premature senescence in surrounding primary cells, similar to the classical bystander effect as induced by ionizing radiation (Prise & O’Sullivan, 2009).”
- Ionizing radiation-induced metabolic oxidative stress and prolonged cell injury (2011, background): “Furthermore, radiationinduced oxidative stress may spread from targeted cells to non-targeted bystander cells through intercellular communication mechanisms [6; 7; 8; 9].”