Abstract |
Human tumor cells and cells from cancer-prone individuals, compared with those from normal individuals, show a significantly higher incidence of chromatid breaks and gaps seen in metaphase cells immediately after G2 X irradiation. Previous studies with DNA repair-deficient mutants and DNA repair inhibitors strongly indicate that the enhancement results from a G2 deficiency(ies) in DNA repair. We report here biochemical evidence for a DNA repair deficiency that correlates with the cytogenetic studies. In the alkaline elution technique, after a pulse label with radioactive thymidine in the presence of 3-acetylaminobenzamide (a G2-phase blocker) and X irradiation, DNA from tumor or cancer-prone cells elutes more rapidly during the postirradiation period than that from normal cells. These results indicate that the DNA of tumor and cancer-prone cells either repairs more slowly or acquires more breaks than that of normal cells; breaks can accumulate during incomplete or deficient repair processes. The kinetic difference between normal and tumor or cancer-prone cells in DNA strand-break repair reaches a maximum within 2 h, and this maximum corresponds to the kinetic difference in chromatid aberration incidence following X irradiation reported previously. These findings support the concept that cells showing enhanced G2 chromatid radiosensitivity are deficient in DNA repair. The findings could also lead to a biochemical assay for cancer susceptibility.
|
Authors | R Gantt, R Parshad, F M Price, K K Sanford |
Journal | Radiation research
(Radiat Res)
Vol. 108
Issue 2
Pg. 117-26
(Nov 1986)
ISSN: 0033-7587 [Print] United States |
PMID | 3786672
(Publication Type: Journal Article)
|
Chemical References |
|
Topics |
- Cell Line
- Chromatids
(radiation effects)
- Chromosome Aberrations
- DNA Repair
- DNA, Neoplasm
(radiation effects)
- Disease Susceptibility
- Humans
- In Vitro Techniques
- Interphase
(radiation effects)
- Neoplasms
(genetics)
- Radiation Genetics
- Radiation Tolerance
|