Comparison of bleomycin and radiation in the G2 assay of chromatid breaks

AD Adema, J Cloos, RHM Verheijen, BJM Braakhuis, Peter Edward Bryant

Research output: Contribution to journalArticlepeer-review

14 Citations (Scopus)

Abstract

Purpose: To compare bleomycin with radiation in the G2 chromatid break assay. Controversy exists in the literature about whether G2 bleomycin chromatid-break sensitivity links with cancer predisposition in the same way as the G2 chromatid radiosensitivity test (the so-called 'G2 assay'). Although bleomycin is referred to as a 'radiomimetic' agent, it differs from radiation in the way the damage is induced.

Materials and methods: Epstein-Barr virus-immortalized lymphoblastoid cell lines from two head and neck squamous cell carcinoma patients, two breast cancer patients, two ataxia-telangiectasia patients and two normal control persons were used. Chromosomal damage was determined in cells exposed to 0.3-Gy radiation or 5 mU ml(-1) bleomycin. The numbers of chromatid breaks per cell and of aberrations per cell (i.e. breaks and gaps) were determined.

Results: A strong positive correlation was found between the two different damage inducers (r = 0.99; p < 0.001). This correlation was similar for both the breaks per cell and the total aberrations per cell. Inclusion of gaps in the scoring of chromatid breaks was associated with a higher variability of the data, but this did not influence the outcome of this study.

Conclusions: Both bleomycin and radiation give the same sensitivity phenotypes as determined by the G2 assay of chromatid breaks. Thus, when no radiation facility is present, bleomycin seems to be a good alternative to radiation for this type of assay.

Original languageEnglish
Pages (from-to)655-661
Number of pages7
JournalInternational Journal of Radiation Biology
Volume79
Issue number8
DOIs
Publication statusPublished - Aug 2003

Keywords

  • INCREASED MUTAGEN SENSITIVITY
  • SQUAMOUS-CELL CARCINOMA
  • NECK-CANCER PATIENTS
  • CHROMOSOMAL RADIOSENSITIVITY
  • GENETIC PREDISPOSITION
  • PRIMARY TUMORS
  • HEAD
  • MARKER
  • DNA
  • INSTABILITY

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