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Radiation-induced cell death mechanisms
Umeå University, Faculty of Medicine, Department of Clinical Microbiology, Immunology/Immunchemistry. (Stigbrand)
Umeå University, Faculty of Medicine, Department of Clinical Microbiology, Immunology/Immunchemistry. (Stigbrand)
2010 (English)In: Tumor Biology, ISSN 1010-4283, E-ISSN 1423-0380, Vol. 31, no 4, 363-372 p.Article in journal (Refereed) Published
Abstract [en]

The main goal when treating malignancies with radiation therapy is to deprive tumor cells of their reproductive potential. One approach to achieve this is by inducing tumor cell apoptosis. Accumulating evidences suggest that induction of apoptosis alone is insufficient to account for the therapeutic effect of radiotherapy. It has become obvious in the last few years that inhibition of the proliferative capacity of malignant cells following irradiation, especially with solid tumors, can occur via alternative cell death modalities or permanent cell cycle arrests, i.e., senescence. In this review, apoptosis and mitotic catastrophe, the two major cell deaths induced by radiation, are described and dissected in terms of activating mechanisms. Furthermore, treatment-induced senescence and its relevance for the outcome of radiotherapy of cancer will be discussed. The importance of p53 for the induction and execution of these different types of cell deaths is highlighted. The efficiency of radiotherapy and radioimmunotherapy has much to gain by understanding the cell death mechanisms that are induced in tumor cells following irradiation. Strategies to use specific inhibitors that will manipulate key molecules in these pathways in combination with radiation might potentiate therapy and enhance tumor cell kill.

Place, publisher, year, edition, pages
2010. Vol. 31, no 4, 363-372 p.
Keyword [en]
Radiation, Therapy, Apoptosis, Senescence, Mitotic catastrophe, p53
Identifiers
URN: urn:nbn:se:umu:diva-41987DOI: 10.1007/s13277-010-0042-8ISI: 000283439000016PubMedID: 20490962OAI: oai:DiVA.org:umu-41987DiVA: diva2:408222
Available from: 2011-04-04 Created: 2011-04-04 Last updated: 2017-12-11Bibliographically approved

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