Pharmacologic Modification of Radiation-Induced Late Normal Tissue Injury View Full Text


Ontology type: schema:Chapter     


Chapter Info

DATE

1998

AUTHORS

J E Moulder , M E Robbins , E P Cohen , J W Hopewell , W F Ward

ABSTRACT

Classically, late radiation-induced normal tissue morbidity has been viewed as due solely to a delayed reduction in the number of surviving clonogens of either parenchymal [1] or vascular [2] target cell populations. These chronic late effects have been held to be inevitable, progressive, and untreatable [2]. In the classical model, the progressive and untreatable nature of late tissue damage follows from the assumption that the decline in clonogen number is due to mitotic cell death that results from genetic injury produced at the time of irradiation and irrevocably fixed in place within hours after irradiation. The long latent period for the expression of injury in tissues such as the kidney, lung, and spinal cord is explained by assuming that the target clonogenic cell population has a very long doubling time. More... »

PAGES

129-151

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/978-1-4615-5769-2_6

DOI

http://dx.doi.org/10.1007/978-1-4615-5769-2_6

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1047311903

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/9513779


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