User:Victoria Berger/sandbox: Difference between revisions
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====Mechanisms==== | ====Mechanisms==== | ||
=====Genes===== | =====Genes===== | ||
Two important genes relating to the vitamin D pathway are CYP24A1 and CYP27B1. CYP24A1 is responsible for [[metabolizing]] both calicidiol and calcitriol. The other gene, CYP27B1, is responsible for converting calcidiol into the more active metabolite calcitriol. Both of the genes are responsible for the local concentration of vitamin D in the breast tissue. As the breast tumor progresses, the expression of CYP24A1 is increased whereas the expression of CYP27B1 is decreased. The result is that less calcidiol is converted to the active form and also that [[catabolism]] of vitamin D is increased. This result has detrimental effects on the cells in the breast tissue and favors tumor progression and formation. | |||
=====Calcidiol and Calcitriol===== | =====Calcidiol and Calcitriol===== | ||
Calcidiol is important in protecting breast cells against [[cellular stress]].<ref name=Peng> XJ Peng, A Vaishnav, G Murillo, F Alimirah, KEP Torres, RG Mehta (2010). "Protection Against Cellular Stress by 25-Hydroxyvitamin D-3 in Breast Epithelial Cells". "Journal of Cellular Biochemistry" "'110"': 1324-1333 </ref> Cellular stress is implicated in starting the tumor process. Calcitriol, once bound to the vitamin D receptor, is involved with modulation of [[cell proliferation]], [[differentiation]], cancer [[metastasis]] and [[angiogenesis]]. The effective concentration of calcitriol for cell protection is 10nmol/L whereas the most effective concentration for calcidiol is 250nmol/L.<ref name=Peng/> The difference in effective concentrations is caused by how tightly the two [[ligands]] bind to the vitamin D receptor with calcitriol binding tighter to the vitamin D receptor. | |||
=====Vitamin D Receptor===== | =====Vitamin D Receptor===== | ||
Revision as of 19:10, 7 November 2010
Vitamin D
In recent years, vitamin D has been shown to decrease the risk of getting breast cancer. When different mechanisms of the vitamin D pathway are inhibited, breast cancer formation is favored. The two major forms of vitamin D, calcidiol and calcitriol, play a role in prevention. Vitamin D in the body can be measured by the serum concentration of calcidiol.
Mechanisms
Genes
Two important genes relating to the vitamin D pathway are CYP24A1 and CYP27B1. CYP24A1 is responsible for metabolizing both calicidiol and calcitriol. The other gene, CYP27B1, is responsible for converting calcidiol into the more active metabolite calcitriol. Both of the genes are responsible for the local concentration of vitamin D in the breast tissue. As the breast tumor progresses, the expression of CYP24A1 is increased whereas the expression of CYP27B1 is decreased. The result is that less calcidiol is converted to the active form and also that catabolism of vitamin D is increased. This result has detrimental effects on the cells in the breast tissue and favors tumor progression and formation.
Calcidiol and Calcitriol
Calcidiol is important in protecting breast cells against cellular stress.[1] Cellular stress is implicated in starting the tumor process. Calcitriol, once bound to the vitamin D receptor, is involved with modulation of cell proliferation, differentiation, cancer metastasis and angiogenesis. The effective concentration of calcitriol for cell protection is 10nmol/L whereas the most effective concentration for calcidiol is 250nmol/L.[1] The difference in effective concentrations is caused by how tightly the two ligands bind to the vitamin D receptor with calcitriol binding tighter to the vitamin D receptor.