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Carcinogenesis, Vol. 23, No. 7, 1149-1153, July 2002
© 2002 Oxford University Press

MOLECULAR EPIDEMIOLOGY AND CANCER PREVENTION

Association of chromosome 19q13.2-3 haplotypes with basal cell carcinoma: tentative delineation of an involved region using data for single nucleotide polymorphisms in two cohorts

Eszter Rockenbauer1, Mette H. Bendixen1, Zuzanna Bukowy1,2, Jiaoyang Yin1,3, Nicklas R. Jacobsen4, Mohammad Hedayati5, Ulla Vogel4, Lawrence Grossman5, Lars Bolund1 and Bjørn A. Nexø1,6

1 Institute of Human Genetics, The Bartholin Building, University of Aarhus, DK-8000 Aarhus C, Denmark,
2 Department of Biology and Environmental Protection, University of Silesia, Katowice, Poland,
3 Department of Medical Genetics, Shenyang Medical College, Shenyang 110034, Liaoning Province, P. R. China,
4 Institute of Occupational Health, DK-2100 Copenhagen O, Denmark and
5 Department of Biochemistry, Bloomberg School of Public Health, The Johns Hopkins University, Baltimore, MD 21205, USA

We have previously used single nucleotide polymorphisms to detect an association of basal cell carcinoma (BCC) in Caucasian Americans and Danes with the genome region 19q13.2-3, which contains several genes involved in the nucleotide excision repair of DNA. In this exploratory paper we have extended the data and used them in a chromosomal scan. The results indicate the presence of a gene variation modulating the risk of developing BSS in a submegabase region including and surrounding the gene RAI. Specifically, persons that are homozygous for the haplotype RAI intron 1A RAI exon 6A appear at increased risk for BCC. In addition, we have looked for possible synergisms between all pairs of markers. We find that a marker in GLTSCR1, presumably separated from RAI by several million bases, supplements the most significant marker in RAI in separating cases from controls, which may suggest the presence of an independent, risk-modulating variation in this second gene region.


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