Although, more than six million people are endemically exposed to inorganic
arsenic in West Bengal, India by drinking heavily contaminated groundwater, only about 300,000 people show
arsenic induced skin lesions. This suggests that genetic variability plays an important role in
arsenic induced skin lesions and
skin cancers.
Arsenic induced
keratosis is considered as a possible precancerous state of in situ
carcinoma. Several reports have suggested the role of p53 polymorphisms as potential marker for risk assessment of different types of
cancers. This prompted us to study the association of three p53 polymorphisms with
arsenic induced
keratosis in a population exposed to
arsenic through
drinking water. A total of 366 unrelated individuals (177 individuals with
arsenic induced
keratosis and 189 individuals with no
arsenic induced skin lesions) were recruited from North 24 Parganas, Nadia and Murshidabad districts between January 2003 and February 2005 for the study of the genotypic distribution of three p53 polymorphisms (16bp duplication at intron 3,
codon 72
Arg/Pro and G>A at intron 6 [nt 13,494]) by PCR-RFLP. The
arginine homozygous genotype at
codon 72, and homozygous genotype of no duplication polymorphism at intron 3 were over represented in the individuals with
keratosis compared with individuals with no skin lesions (OR=2.086; 95% CI=1.318-3.299 and OR=2.086; 95% CI=1.257-3.457, respectively). This study indicates that individuals carrying the
arginine homozygous genotype at
codon 72, and/or no duplication homozygous genotype at intron 3 are at risk for the development of
arsenic induced
keratosis.