Concordant loss of heterozygosity of DNA repair gene, hOGG1, in melanoma in situ and atypical melanocytic hyperplasia

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Abstract

Background

One major risk factor for cutaneous melanoma is chronic sun-exposure and oxidative stress. Among various oxidative DNA damages, 8-oxoquanine is the most abundant and is potentially mutagenic if not sufficiently repaired. The human 8-oxoquanine DNA glycosylase 1 (hOGG1) gene specifically repairs 8-oxoguanine, and this gene shows frequent loss of heterozygosity (LOH) in human tumors. In this study, we investigate whether hOGG1LOH occurs in melanoma in situ(MIS) and adjacent atypical melanocytic hyperplasia (AMH).

Methods

Twelve skin biopsies with MIS and adjacent AMH were included. DNA samples derived from manual microdissection of tissues were subjected to polymerase chain reaction amplification using three fluorescent-labeled microsatellite makers, followed by fragment analysis.

Results

Five of 12 cases were informative for both telomeric (3S1297) and centromeric (3S1289 or 3S1300) markers, bordering the hOGG1locus. Among them, four (80%) MIS and three (60%) AMH showed hOGG1LOH at both markers.

Conclusions

These results shows that LOH at hOGG1gene is associated with MIS and AMH and suggest that the hOGG1gene may play a role in melanocytic tumor progression.

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