الفهرس 
IntroductionOnly 14 pages are availabe for public view
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Abstract
Cancer colon is the second most common cause of cancer in women and the third most common in men. Globally incidences vary 10-fold with the highest rates in Australia, New Zealand, Europe and the US and the lowest rates in Africa and South-Central Asia. However, in Egypt, CRC represents 4.2% in males and 3.8% in females of all cancers.
The biologically active form of the vitamin is obtained by 25-hydroxylation of vitamin D3 in the liver and 1α-hydroxylation in the kidney. 1,25D3 inhibits the growth of tumor cells by inducing the expression of cyclin-dependent kinase inhibitors, such as p21, p27, and cystatin D, and by inhibiting the expression of pro-proliferative genes, including c-my and cyclin D1. In addition, 1,25D3 has been shown to upregulate miR-627, which targets the histone demethylase jumonji domain containing protein 1A, and thereby inhibits proliferation of colon cancer cells in vitro and in vivo through epigenetic regulation. The cellular effects of vitamin D are mediated via binding of 1,25(OH) 2D to vitamin D receptor (VDR), a member of the nuclear receptor superfamily which regulates the transcription of genes, including proto-oncogenes and tumor suppressor genes.
Our study is aimed to assess the relation between vitamin D receptor gene polymorphism and cancer colon occurrence. To our knowledge, this is the first study to evaluate the relation between vitamin D receptor gene polymorphism and the cancer colon occurrence in Egypt. This may help to predict cancer colon in those populations.