Abstract
Exposure to sunlight is the major source of vitamin D and the main environmental cause of non-melanocytic skin cancers. Vitamin D, partly mediated through the vitamin D receptor (VDR), has potential therapeutic applications in skin cancer. The aim of this study was to investigate the association of BsmI and ApaI VDR polymorphisms among patients with non-melanoma cancers and controls. An observational case-control study was conducted in a sample of 154 subjects. We observed no significant effects between these polymorphisms and skin cancer risk. When stratified for gender, GG and AG BsmI polymorphisms significantly increased the risk of basal cell carcinomas in males. In relation to ApaI, all three polymorphisms significantly increased the risk of basal cell carcinoma in males. When stratified for age, we found that being 70 years of age or younger was a protective factor against both skin cancers. Being a female and 70 years old or younger was a protective factor for basal cell carcinoma. A comparison of the frequencies of the VDR genotypes in patients older than 70 years vs. 70 years or younger also revealed age-dependent variations in patients with non-melanoma skin cancer. Our study suggests a role for VDR polymorphisms in non-melanoma skin cancer development.
Highlights
To bone mineralization and maintenance of calcium balance, 1α25(OH)2D3 exerts physiological functions, including the regulation of growth and differentiation in a broad variety of normal and malignant cells [1,2].The major source of vitamin D for most humans is exposure to sunlight [3]
The patient group consisted of 81 subjects with non-melanoma skin cancer, and 73 healthy individuals were enrolled to serve as controls
If the BsmI and ApaI polymorphisms were stratified for gender and skin cancer risk, we found that the GG and AG BsmI polymorphisms significantly increased the risk of basal cell carcinoma (BCC) in males (OR: 7.01; IC 95%: 2.35–20.92 and odds ratios (OR): 4.59; IC 95%: 1.60–13.18, respectively)
Summary
To bone mineralization and maintenance of calcium balance, 1α25(OH)2D3 exerts physiological functions, including the regulation of growth and differentiation in a broad variety of normal and malignant cells [1,2].The major source of vitamin D for most humans is exposure to sunlight [3]. To bone mineralization and maintenance of calcium balance, 1α25(OH)2D3 exerts physiological functions, including the regulation of growth and differentiation in a broad variety of normal and malignant cells [1,2]. It is known that vitamin D requires two obligate hydroxylations, first in the liver and in the kidney, to create the active form of vitamin D, 1α25(OH)2D3. Most tissues and cells in the body, including skin, have nuclear receptors for 1α25(OH)2D3, called vitamin D receptors (VDRs). The VDR is an intracellular hormone receptor that binds the active form of vitamin D and interacts with target-cell nuclei to produce a variety of biological effects. VDR binds specific nucleotide sequences in target genes to activate or repress their expression
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