NORMAL REACTIVATION OF PLASMID DNA INACTIVATED BY UV IRRADIATION BY LYMPHOCYTES FROM INDIVIDUALS WITH HEREDITARY DYSPLASTIC NEVUS SYNDROME

被引:6
作者
HANSSON, J
LOOW, H
机构
[1] Division of Experimental Oncology, Department of General Oncology, Radiumhemmet, Karolinska Hospital, Stockholm, S-171 76
关键词
DNA REPAIR; DYSPLASTIC NEVUS SYNDROME; UV IRRADIATION;
D O I
10.1097/00008390-199406000-00004
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Hereditary dysplastic naevus syndrome (DNS) is a familial disorder characterized by dysplastic naevi and an approximately 85-fold increased risk of developing malignant cutaneous melanoma. Cell lines from individuals with DNS have shown hypermutability following exposure to UV irradiation. The cause of this hypermutability is unknown, and no DNA repair defect has been identified. We have studied the capacity of lymphocytes from individuals with DNS to reactivate the chloramphenicol acetyltransferase gene in transfected plasmids that had been inactivated by UV irradiation. We found no difference in plasmid reactivation between lymphocytes from individuals with DNS and those obtained from healthy control persons matched for sex, age and smoking habits. This finding indicates that DNS is not associated with a significant quantitative defect in nucleotide excision repair of DNA.
引用
收藏
页码:163 / 167
页数:5
相关论文
共 28 条
[1]  
Lynch H.T., Fusaro RM, (1991)
[2]  
Greene M.H., Clark W.H., Tucker M.A., Et al., Acquired precursors of cutaneous malignant melanoma: The familial dysplastic nevus syndrome, Nengl J Med, 312, pp. 91-97, (1985)
[3]  
Tucker M.A., Fraser M.C., Goldstein A.M., Et al., Risk of melanoma and other cancers in melanoma-prone families, J Invest Dermatol, 100, pp. 350S-355S, (1993)
[4]  
Bale S.J., Dracopoli N.C., Tucker M.A., Et al., Mapping the gene for hereditary cutaneous malignant melanoma-dysplastic nevus to chromosome lp, N Engl J Med, 320, pp. 1367-1372, (1989)
[5]  
Van Haeringen A., Bergman W., Nelen M.R., Et al., Exclusion of the dysplastic nevus syndrome (DNS) locus from the short arm of chromosome 1 by linkage studies in Dutch families, Genomics, 5, (1989)
[6]  
Cannon-Albright L.A., Goldgar D.E., Wright E.C., Et al., Evidence against the reported linkage of the cutaneous melanoma-dysplastic nevus syndrome locus to chromosome lp36, Am J Hum Genet, 46, pp. 912-918, (1990)
[7]  
Kefford R.F., Salmon J., Shaw H.M., Et al., Hereditary melanoma in Australia. Variable association with dysplastic naevi and absence of genetic linkage to chromosome lp, Cancer Genet Cytogenet, 51, pp. 45-55, (1991)
[8]  
Goldstein A.M., Dracopoli N.C., Ho E.C., Etal. Further evidence for a locus for cutaneous malignant melanoma-dysplastic nevus (CMM/DN) on chromosome lp, and evidence for genetic heterogeneity, Am J Hum Genet, 52, pp. 537-550, (1993)
[9]  
Cannon-Albright L.A., Goldgar D.E., Meyer L.J., Et al., Assignment of a locus for familial melanoma, MLM, to chromosome 9p13-p22, Science, 258, pp. 1148-1152, (1992)
[10]  
Howell J.N., Greene M.H., Corner R.C., Et al., Fibroblasts from patients with hereditary cutaneous malignant melanoma are abnormally sensitive to the mutagenic effect of simulated sunlight and 4-nitroquinoline 1-oxide, Proc Natl Acad Sci USA, 81, pp. 1179-1183, (1984)