X-RAY-INDUCED CHROMATID DAMAGE IN RELATION TO DNA-REPAIR AND CANCER INCIDENCE IN FAMILY MEMBERS

被引:64
|
作者
KNIGHT, RD
PARSHAD, R
PRICE, FM
TARONE, RE
SANFORD, KK
机构
[1] NCI,CELLULAR & MOLEC BIOL LAB,BLDG 37,RM 2015,BETHESDA,MD 20892
[2] NCI,BIOSTAT BRANCH,BETHESDA,MD 20892
[3] WALTER REED ARMY INST RES,DIV HEMATOL,WASHINGTON,DC 20307
[4] HOWARD UNIV,COLL MED,DEPT PATHOL,WASHINGTON,DC 20059
关键词
D O I
10.1002/ijc.2910540412
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The cytogenetic response to G2-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 unrepaired DNA strand breaks, the first category may represent an efficient DNA repair phenotype, while the second may represent a deficient repair phenotype. The individuals with the deficient G2 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 predisposing to cancer, suggest that this deficient cytogenetic response to G2 phase X-irradiation is associated with a high risk of cancer. (C) 1993 Wiley-Liss, Inc.
引用
收藏
页码:589 / 593
页数:5
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