Page 225 - Vitamin D and Cancer

212 F.S.G. Cheung and J.K.V. Reichardt

Genetic background: Age, culture, vitamin D UV exposure
VDR Polymorphisms intake, medical condition:,
Elderly
Veiled women
Natural vitamin D intake
Vitamin D Vitamin D supplement
analogues Organ transplant recipients
Xerodoma pigmentosum

Genomic and non genomic pathways:
D -VDR-RXR
Formation of 1,25(OH) 2 3 Vitamin D
complex to induce gene expression levels
Rapid membrane receptor signaling
pathways

Classical functions: Non classical/ Anti- DNA damage:
Maintaining adequate cancer effects: CPD formation
blood calcium levels Anti-proliferation Oxidative damage
Bone mineralization Pro-differentiation
Photoprotection

Skin cancer
development

Fig. 9.3 Vitamin D and skin cancer. UV radiation can cause DNA damage that can lead to skin cancer.
However, the vitamin D level in our body is also dependant on UV radiation induced vitamin D syn-
thesis as well as our vitamin intake from food sources. The amount of vitamin D synthesized from UV
exposure is influenced by the age, culture, and existing medical conditions of the individual. Genetic
variants of the vitamin D receptor (VDR) can influence the ability of vitamin D to elicit its biological
actions. Vitamin D in the body can carry out classical functions such as mineral and bone homeostasis
as well as non classical functions that can result in anti-cancer effects. Thus the balance of UV exposure
in causing DNA damage and vitamin D synthesis determines the risk of skin cancer

Achknowledgments We thank Lucia Musumeci and Cheng Li (The University of Sydney) for
their helpful contributions and Bruce Armstrong (The University of Sydney) for his helpful discus-
sions and comments on this chapter. The work in the lab of JKVR was supported by NCI grant P01
CA108964 (Project 1). JKVR is also a Medical Foundation Fellow at The University of Sydney.

References

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vitamin D analogs (Paricalcitol and QW-1624F2–2) in squamous cell carcinoma cells.
Oncology 70(6):483–492
2. Anderson PH, Hendrix I, Sawyer RK et al (2008) Co-expression of CYP27B1 enzyme with
the 1.5 kb CYP27B1 promoter-luciferase transgene in the mouse. Mol Cell Endocrinol
285(1–2):1–9