Radiotherapy uses electromagnetic radiation to produce cell damage, which leads to arrest of proliferation and, ultimately, destruction of tumors. The damaging effect of radiation occurs via a cascade of ionization of events. Genomic DNA is currently considered the most important cellular target for radiation damage. Ionization at this site causes a spectrum of damage, including interstrand and intrastrand crosslinks, strand breaks, and damage to nucleotide bases.
The majority of DNA lesions are repaired by normal cellular DNA processes. The repair of some lesions, such as double strand breaks, is either incorrect (leading to mutation) or not possible, and the lesions may become lethal, with cells dying when attempting mitosis. Apoptotic death may also be induced by radiation in some tissues.
Although the processes of radiation-induced damage and repair are common to tumor and normal tissues, there are differences that can be exploited to maximize damage to the tumor with the least damage to normal tissue. This is achieved through fractionation (giving radiation dose in small divided doses) usually on a daily basis. Fractionation and the physical ability to localize radiation to tumors with less dose to surrounding normal tissue are the underlying principles of the effectiveness of radiotherapy for the treatment of tumors, including pituitary adenomas. Despite the limited proliferative potential of most pituitary adenomas, it is likely that the arrest of tumor growth after radiotherapy is attributable to the antiproliferative effect of ionizing radiation. The mechanism underlying the lowering of excess hormone production is poorly understood but is also most likely caused by the depletion of secreting tumor cells.
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