Variation in response to mutagens amongst normal and repair-defective human cells.

Abstract

Over the past five years we have been examining the mutability of a variety of human fibroblast strains established from both normal individuals and patients suffering from cancer-prone genetic diseases. The objective of these experiments was to determine if cancer proneness at the level of the individual is correlated with either hypersensitivity to the lethal effects or hypermutability to the mutagenic effects of DNA damaging agents. The existence of hypersensitivity and particularly hypermutability implies the presence of defects in repair of DNA damage and underlines the importance of effective repair processes for human health (1).