Genotoxic effects of radiotherapy and chemotherapy on the circulating lymphocytes of breast cancer patients. I. Chromosome aberrations induced in vivo

Rigaud, O.; Guédeney, Geneviève; Duranton, I.; Leroy, Ancy; Doloy, M.T.; Magdelénat, H.

doi:10.1016/0165-1218(90)90095-j

Cited by 25 publications

(11 citation statements)

References 12 publications

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“…One of the possible genes involved is p53, which has been described in almost all human cancers, including breast cancer (27), and plays a role in the repair mechanism of radioinduced damage (9). There is evidence that p53 and rad51 are involved in vivo (28).…”

Section: Discussionmentioning

confidence: 99%

“…Some investigators found a high sensitivity and a reduced repair capacity in peripheral blood lymphocytes from breast cancer patients when exposed to X-rays, gamma and UV light, as evaluated by the determination of chromosome aberrations (9)(10)(11) and by the micronucleus test (12). While Hsu et al (13), using bleomycin in a mutagenic test, did not find a significant difference between blood cells from breast cancer patients and healthy subjects in terms of number of chromatid breaks per cell, Jaloszynski et al (14) reported a high sensitivity and reduced repair capacity in peripheral blood cells from breast cancer patients using the comet assay.…”

Section: Introductionmentioning

confidence: 99%

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Evaluation of radioinduced damage and repair capacity in blood lymphocytes of breast cancer patients

Nascimento

Silva

Oliveira

et al. 2001

Braz J Med Biol Res

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Genetic damage caused by ionizing radiation and repair capacity of blood lymphocytes from 3 breast cancer patients and 3 healthy donors were investigated using the comet assay. The comets were analyzed by two parameters: comet tail length and visual classification. Blood samples from the donors were irradiated in vitro with a 60 Co source at a dose rate of 0.722 Gy/min, with a dose range of 0.2 to 4.0 Gy and analyzed immediately after the procedure and 3 and 24 h later. The basal level of damage and the radioinduced damage were higher in lymphocytes from breast cancer patients than in lymphocytes from healthy donors. The radioinduced damage showed that the two groups had a similar response when analyzed immediately after the irradiations. Therefore, while the healthy donors presented a considerable reduction of damage after 3 h, the patients had a higher residual damage even 24 h after exposure. The repair capacity of blood lymphocytes from the patients was slower than that of lymphocytes from healthy donors. The possible influence of age, disease stage and mutations in the BRCA1 and BRCA2 genes are discussed. Both parameters adopted proved to be sensitive and reproducible: the doseresponse curves for DNA migration can be used not only for the analysis of cellular response but also for monitoring therapeutic interventions. Lymphocytes from the breast cancer patients presented an initial radiosensitivity similar to that of healthy subjects but a deficient repair mechanism made them more vulnerable to the genotoxic action of ionizing radiation. However, since lymphocytes from only 3 patients and 3 normal subjects were analyzed in the present paper, additional donors will be necessary for a more accurate evaluation.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Evaluation of radioinduced damage and repair capacity in blood lymphocytes of breast cancer patients

Nascimento

Silva

Oliveira

et al. 2001

Braz J Med Biol Res

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“…Probably fragilization of lymphocytes by the first-line chemotherapy (VPB) could induce a preferential killing of cells or a reduced ability to respond to phytohaemagglutinin stimulation [ 19], therefore patients studied later than 1 year after the cessation of treatment showed relatively low levels of chromosome aberrations.…”

Section: Discussionmentioning

confidence: 99%

Persistence of Chromosomal Aberrations in Blood Lymphocytes of Testicular Cancer Patients

et al. 1992

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Chromosome aberrations were studied in peripheral blood lymphocytes from untreated testicular cancer patients and others treated with chemo- and/or radiotherapy. A distinct increase in spontaneous aberrations over the level of healthy controls was found in patients treated with surgery alone. Our data suggest the existence of a certain degree of chromosome instability which may be a factor in the development of malignancy for testicular tumours, too. The frequency of aberrant cells was much higher in treated groups than in controls, and the total of aberrations was therapy related. The frequency of aberrant cells was the highest in the first 2 years after the end of treatments similarly to the results of 3 serially examined individuals. The decrease in aberrant cells was time-dependently gradual only in X-ray-treated patients. Real conclusions about the nature of therapy-related persistence of aberrant cells can be drawn from the study of a sufficient number of testicular cancer patients studied more than 1 year after the end of treatments.

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“…Some of these studies have revealed reduced DNA repair capacity in peripheral blood mononuclear cells (PBMCs, exposed in vitro to ionising radiation (IR) or UV) from BC patients, as evaluated by the chromosome aberration assay (Rigaud et al, 1990;Helzlsouer et al, 1995;Parshad et al, 1996) as well as by the MN test (Scott et al, 1998Baeyens et al, 2002). Furthermore, a series of studies have found elevated G2 chromosomal radiosensitivity in the blood cells from BC patients (Baria et al, 2001;Riches et al, 2001;Baeyens et al, 2002).…”

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confidence: 99%

Radiosensitivity in breast cancer assessed by the Comet and micronucleus assays

et al. 2006

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Spontaneous and radiation-induced genetic instability of peripheral blood mononuclear cells derived from unselected breast cancer (BC) patients (n ¼ 50) was examined using the single-cell gel electrophoresis (Comet) assay and a modified G2 micronucleus (MN) test. Cells from apparently healthy donors (n ¼ 16) and from cancer patients (n ¼ 9) with an adverse early skin reaction to radiotherapy (RT) served as references. Nonirradiated cells from the three tested groups exhibited similar baseline levels of DNA fragmentation assessed by the Comet assay. Likewise, the Comet analysis of in vitro irradiated (5 Gy) cells did not reveal any significant differences among the three groups with respect to the initial and residual DNA fragmentation, as well as the DNA repair kinetics. The G2 MN test showed that cells from cancer patients with an adverse skin reaction to RT displayed increased frequencies of both spontaneous and radiation-induced MN compared to healthy control or the group of unselected BC patients. Two patients from the latter group developed an increased early skin reaction to RT, which was associated with an increased initial DNA fragmentation in vitro only in one of them. Cells from the other BC patient exhibited a striking slope in the dose -response curve detected by the G2 MN test. We also found that previous RT strongly increased both spontaneous and in vitro radiation-induced MN levels, and to a lesser extent, the radiation-induced DNA damage assessed by the Comet assay. These data suggest that clinical radiation may provoke genetic instability and/or induce persistent DNA damage in normal cells of cancer patients, thus leading to increased levels of MN induction and DNA fragmentation after irradiation in vitro. Therefore, care has to be taken when blood samples collected postradiotherapeutically are used to assess the radiosensitivity of cancer patients.

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Genotoxic effects of radiotherapy and chemotherapy on the circulating lymphocytes of breast cancer patients. I. Chromosome aberrations induced in vivo

Cited by 25 publications

References 12 publications

Evaluation of radioinduced damage and repair capacity in blood lymphocytes of breast cancer patients

Evaluation of radioinduced damage and repair capacity in blood lymphocytes of breast cancer patients

Persistence of Chromosomal Aberrations in Blood Lymphocytes of Testicular Cancer Patients

Radiosensitivity in breast cancer assessed by the Comet and micronucleus assays

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