Journal
LANCET ONCOLOGY
Volume 6, Issue 7, Pages 520-528Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/S1470-2045(05)70246-1
Keywords
-
Categories
Funding
- NCI NIH HHS [P01 CA 095227] Funding Source: Medline
Ask authors/readers for more resources
Ionising radiation has been an important part of cancer treatment for almost a century, being used in external-beam radiotherapy, brachytherapy, and targeted radionuclide therapy. At the molecular and cellular level, cell killing has been attributed to deposition of energy from the radiation in the DNA within the nucleus, with production of DNA double-strand breaks playing a central part. However, this DNA-centric model has been questioned because cell-death pathways, in which direct relations between cell killing and DNA damage diverge, have been reported. These pathways include membrane-dependent signalling pathways and bystander responses (when cells respond not to direct radiation exposure but to the irradiation of their neighbouring cells). New insights into mechanisms of these responses coupled with technological advances in targeting of cells in experimental systems with microbeams have led to a reassessment of the model of how cells are killed by ionising radiation. This review provides an update on these mechanisms.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available