Chromosomal Aberration in Peripheral Lymphocytes and Doses to the Active Bone Marrow in Radiotherapy of Prostate Cancer

Gershkevitsh, E.; Hildebrandt, Guido; Wolf, U.; Kamprad, F; Realo, E.; Trott, Klaus-Rüdiger

doi:10.1007/s00066-002-0886-y

Cited by 12 publications

(10 citation statements)

References 8 publications

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“…The whole organism response could be due to tissue damage either in the tumor or the surrounding healthy tissues, which would induce a defensive physiologic response, e.g., a cytokine-induced inflammatory response. Direct effects could result from a well-known response of cells to radiation where such cells carry within them evidence of the exposure, i.e., radiation-induced heritable damage [10], but also from direct exposure of the bone marrow [16]. Despite a difference of means, the t-test revealed no significant differences in the levels of radiation-induced apoptosis observed before and after the 3 weeks of radiation therapy.…”

Section: Does the Sensitivity Of The T-lymphocytes To Radiation-inducmentioning

confidence: 73%

Apoptotic Response of Irradiated T-Lymphocytes

et al. 2003

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Section: Does the Sensitivity Of The T-lymphocytes To Radiation-inducmentioning

confidence: 73%

Apoptotic Response of Irradiated T-Lymphocytes

et al. 2003

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“…Several studies have examined chromosome aberrations in blood samples from patients undergoing fractionated radiotherapy. These studies, which have used conventional cytogenetics, fluorescence in situ hybridisation (FISH) or both, showed a dosedependent increase in the yields of aberrations, but with substantial interpatient variability [9][10][11]. The same variability in the rate of damage induced in lymphocytes during radiotherapy has been observed in other studies that used different measurements, such as premature chromosome condensation (PCC), micronuclei or c-H2AX foci [12][13][14].…”

mentioning

confidence: 71%

Cytogenetic assessment of heterogeneous radiation doses in cancer patients treated with fractionated radiotherapy

Roch-Lefèvre

Pouzoulet²,

Giraudet³

et al. 2010

BJR

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ABSTRACT. The purpose of this study was to evaluate the in vivo dose-response relation of chromosome aberration formation and distribution in a context of localised and fractionated radiotherapy. Cytogenetic analysis was applied to eight patients, all treated for the same tumour localisation; the same localisation was used to prevent the variability usually observed between patients treated with radiotherapy and to allow the corresponding roles of the size of irradiation field and of the dose rate to be studied. The yield of dicentrics, centric rings and fragments was measured in blood samples taken before treatment, during the course of radiotherapy and up to 6 months after. After the first fraction of radiotherapy, we observed that the whole-body dose estimated from the yield of dicentrics and rings was higher (0.35¡0.2 Gy) than the calculated equivalent whole-body dose (0.07¡0.04 Gy). By contrast, the partial-body dose derived from the Qdr (quotient of dicentrics and rings) model was estimated to be 2.2¡0.3 Gy, which agreed quite well with the dose delivered to the tumour (2.1¡0.1 Gy). We also found a correlation between the yield of induced chromosome aberrations and the target field size (p50.014). U-value analysis showed that the distribution of dicentrics and rings was overdispersed, despite the fractionation of the exposure, and a positive correlation between the U-value and the dose rate was observed (p50.017). Overall, these results suggest that the proportion of undamaged lymphocytes could increase with the dose rate.

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“…While the appearance of the inducible repair for cellular survival has been seen in vitro in a wide range of cell lines using single dose experiments [ a study by Gershkevitsh et al [35] has recently shown data for chromosome aberrations following prostate radiotherapy with fractionated treatments that has an appearance characteristic to the inducible repair effect. This does not appear for all the data sets shown in their study, but given the large variability of biological data it does suggest that inducible repair might appear for chromosome aberrations as well.…”

Section: Resultsmentioning

confidence: 99%

Dose-effect models for risk – relationship to cell survival parameters

Daşu

Toma-Daşu

2005

Acta Oncologica

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There is an increased interest in estimating the induction of cancers following radiotherapy as the patients have nowadays a much longer life expectancy following the treatment. Clinical investigations have shown that the dose response relationship for cancer induction following radiotherapy has either of two main characteristics: an increase of the risk with dose to a maximum effect followed by a decrease or an increase followed by a levelling-off of the risk. While these behaviours have been described qualitatively, there is no mathematical model that can explain both of them on mechanistic terms. This paper investigates the relationship between the shape of the dose-effect curve and the cell survival parameters of a single risk model. Dose response relationships were described with a competition model which takes into account the probability to induce DNA mutations and the probability of cell survival after irradiation. The shape of the curves was analysed in relation to the parameters that have been used to obtain them. It was found that the two main appearances of clinical data for the induction of secondary cancer following radiotherapy could be the manifestations of the particular sets of parameters that describe the induction of mutations and cell kill for fractionated irradiations. Thus, the levelling off appearance of the dose response curve could be either a sign of moderate to high inducible repair effect in cell survival (but weak for DNA mutations) or the effect of heterogeneity, or both. The bell-shaped appearance encompasses all the other cases. The results also stress the importance of taking into account the details of the clinical delivery of dose in radiotherapy, mainly the fractionated character, as the findings of our study did not appear for single dose models. The results thus indicate that the shapes of clinically observed dose response curves for the induction of secondary cancers can be described by using one single competition model. It was also found that data for cancer induction may be linked to in vivo cell survival parameters that may be used for other modelling applications.The increased success of radiotherapy (alone or in combination with other forms of treatment) has led to an increase in the life expectancy for many patients and especially for children who may live for decades after treatment. This success is achieved through advanced treatment techniques such as intensity modulated radiation therapy (IMRT) and conformal radiotherapy techniques (CRT) which result in quite different patterns of irradiation of the healthy tissues. Thus, IMRT causes relatively large volumes of healthy tissues to be irradiated with low doses of radiation, while the conformation of the dose to the target in CRT means that only small volumes of tissue surrounding the clinical target volume are irradiated but not always with very low doses. As the risks for stochastic effects associated with these techniques may not be the same [1,2] it may therefore be necessary to evaluate the various tre...

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Chromosomal Aberration in Peripheral Lymphocytes and Doses to the Active Bone Marrow in Radiotherapy of Prostate Cancer

Cited by 12 publications

References 8 publications

Apoptotic Response of Irradiated T-Lymphocytes

Apoptotic Response of Irradiated T-Lymphocytes

Cytogenetic assessment of heterogeneous radiation doses in cancer patients treated with fractionated radiotherapy

Dose-effect models for risk – relationship to cell survival parameters

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