PMID: 9637247Jun 24, 1998Paper

Impaired DNA repair capacity in skin fibroblasts from various hereditary cancer-prone syndromes

Mutation Research
P J AbrahamsA J van der Eb

Abstract

Host-cell reactivation (HCR) of UV-C-irradiated herpes simplex virus type 1 (HSV-1) has been determined in skin fibroblasts from the following hereditary cancer-prone syndromes: aniridia (AN), dysplastic nevus syndrome (DNS), Von Hippel-Lindau syndrome (VHL), Li-Fraumeni syndrome (LFS) and a family with high incidence of breast and ovarian cancer. Cells from AN, DNS or VHL patients were found to exhibit heterogeneity in HCR. Cells from individuals belonging to an LFS family show reduced HCR in all cases where the cells were derived from persons carrying one mutated p53 allele, whereas cells derived from members with two wild-type alleles show normal HCR. LFS cells with reduced HCR also reveal reduced genome overall repair, and a slower gene-specific repair of the active adenosine deaminase (ADA) gene, but little if any repair of the inactive 754 gene. In the breast/ovarian cancer family, reduced HCR is observed in skin fibroblasts derived from both afflicted and unaffected individuals. In addition, these cells display lower survival after exposure to UV-C and exhibit higher levels of SCEs than those in normal cells. These observations indicate that various hereditary cancer-prone syndromes, carrying mutations in different tumor...Continue Reading

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Citations

Sep 18, 2002·Lung Cancer : Journal of the International Association for the Study of Lung Cancer·Chikako KiyoharaJulian M Hopkin
Apr 24, 1999·Biochimie·C Petit, A Sancar
Aug 12, 2010·The Journal of Biological Chemistry·Tadi Satish KumarSathees C Raghavan
Dec 20, 2008·Clinics in Dermatology·Robert J FriedmanEdward R Heilman
Oct 17, 2002·Dermatologic Clinics·Thomas G Salopek

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