In radiotherapy, alongside tumor control, the prevention of severe treatment-related side effects is a major concern. Although the majority of radio-oncological patients tolerate a standard treatment protocol, toxic side effects can be detected in 0.2-10% of the cases.[1,2] The latter can be a result of an increased individual radiosensitivity, caused by a combination of exogenous and endogenous factors including genetic reasons. However, most of the exact underlying mechanisms still remain unknown. Only in few cases increased radiosensitivity is a result of an identified single gene mutation, e.g., in ataxia telangiectasia (AT) or Nijmegen breakage syndrome (NBS) patients, OMIM #208900 and #251260, but in the majority, it is supposed to be modulated by a mixture of different genes.
To have a chance to detect a possible overreaction prior to therapy, the availability of a predictive test system has been the aim for some decades. Although different approaches were tested (e.g., clonogenic cell survival, G2-Assay), there is still no reliable routine assay to identify hypersensitive or less sensitive patients to adjust their therapeutic dose. It is known that chromosomal aberrations are: 1) indicators of a previous exposure to irradiation and 2) can be used to estimate ra-diosensitivity. Previous studies demonstrated that molecular cytogenetic methods are superior to conventional cytogenetic analysis in detection and characterization of aberrations. At this, the frequency of breaks and the occurrence of specific aberration types reflect individual sensitivity to radiation. Especially complex chromosomal aberrations (CCR) were identified as indicators for increased individual radiosensitivity.
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