428. Int J Radiat Biol Relat Stud Phys Chem Med. 1986 Feb;49(2):357-80.
Cell kinetics and radiation biology.
Denekamp J.
The cell cycle, the growth fraction and cell loss influence the response of cells
to radiation in many ways. The variation in radiosensitivity around the cell
cycle, and the extent of radiation-induced delay in cell cycle progression have
both been clearly demonstrated in vitro. This translates into a variable time of
expression of radiation injury in different normal tissues, ranging from a few
days in intestine to weeks, months or even years in slowly proliferating tissues
like lung, kidney, bladder and spinal cord. The radiosensitivity of tumours, to
single doses, is dominated by hypoxic cells which arise from the imbalance
between tumour cell production and the proliferation and branching of the blood
vessels needed to bring oxygen and other nutrients to each cell. The response to
fractionated radiation schedules is also influenced by the cell kinetic
parameters of the cells comprising each tissue or tumour. This is described in
terms of repair, redistribution, reoxygenation and repopulation. Slowly cycling
cells show much more curved underlying cell survival curves, leading to more
dramatic changes with fractionation, dose rate or l.e.t. Rapidly cycling cells
redistribute around the cell cycle when the cells in sensitive phases have been
killed, and experience less mitotic delay than slowly proliferating cells.
Reoxygenation seems more effective in tumours with rapidly cycling cells and high
natural cell loss rates. Compensatory repopulation within a treatment schedule
may spare skin and mucosa but does not spare slowly proliferating tissues.
Furthermore, tumour cell proliferation during fractionated radiotherapy may be an
important factor limiting the overall success of treatment.
PMID: 3510997 [PubMed - indexed for MEDLINE]