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X‐ray‐induced chromatid damage in relation to dna repair and cancer incidence in family members
Author(s) -
Knight Robert D.,
Parshad Ram,
Price Floyd M.,
Tarone Robert E.,
Sanford Katherine K.
Publication year - 1993
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.2910540412
Subject(s) - chromatid , colcemid , cancer , dna repair , biology , dna damage , genetics , radiosensitivity , cancer research , dna , radiation therapy , immunology , microbiology and biotechnology , oncology , medicine , chromosome , cell culture , gene
The cytogenetic response to G 2 ‐phase X‐irradiation was examined in phytohemagglutinin‐stimulated peripheral‐blood lymphocytes from 69 individuals, a few of whom were cancer patients. The cancer patients had not received radiation or chemotherapy. The responses of cells arrested by Colcemid 30 to 90 min after X‐irradiation (58R) could be divided into 2 distinct categories: 51 individuals had aberration frequencies typical of normal individuals in previous studies, while 18 others had a 2‐ to 3‐fold higher frequency of chromatid breaks and gaps. Because chromatid breaks and gaps result from unre paired DNA strand breaks, the first category may represent an efficient DNA repair phenotype, while the second may repre sent a deficient repair phenotype. The individuals with the deficient G 2 response reported having first‐ and second‐degree relatives with a 3.6‐ and 2.2‐fold higher mean frequency of cancer, respectively. The present results, together with those from earlier studies of families with a genetic disorder predispos ing to cancer, suggest that this deficient cytogenetic response to G 2 phase X‐irradiation is associated with a high risk of cancer.