Vitamin D and the mammary gland
a review on its role in normal development and breast cancer
Nair Lopes, Joana Paredes, José L Costa, Bauke Ylstra and Fernando Schmitt*
* Corresponding author: Fernando Schmitt fschmitt at ipatimup.pt
Breast Cancer Research 2012, 14:211 doi:10.1186/bcr3178
Published: 31 May 2012
Breast cancer is a heterogeneous disease, associated with diverse biological behaviours and clinical outcome. Although some molecular subgroups of breast cancer have a targeted therapy, the most aggressive tumours still lack a molecular target. Despite Vitamin D being classically associated with the physiological role of calcium regulation and phosphate transport in bone metabolism, several studies have been demonstrating a wide range of functions for this hormone, which are particularly important in the field of cancer. The mechanisms underlying the protective actions of Vitamin D in cancer development are only sparsely understood, but evidence shows that Vitamin D participates in cell growth regulation, apoptosis and cell differentiation. In addition, Vitamin D has been implicated in the suppression of cancer cell invasion, angiogenesis and metastasis. Most of Vitamin D biological actions are mediated by the Vitamin D receptor (VDR) and the synthesis and catabolism of this hormone are regulated by the enzymes CYP27B1 and CYP24A1. In the present review we highlight research data concerning the function of this hormone in the mammary gland, with a special focus on breast carcinogenesis. Hence, and although the available data are controversial, we considered not only updated information on epidemiology of Vitamin D in breast cancer and its potential value as a therapeutic agent or prophylactic (with an emphasis on molecular mechanisms and effectors of Vitamin D action), but we included data on its role in other stages of breast cancer progression as well. Accordingly, we review data on the influence of Vitamin D in the development of normal breast and the expression of Vitamin D-related proteins (VDR, CYP27B1 and CYP24A21) in benign mammary lesions and ductal carcinomas in situ.
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Press Release by the authors
Breast cancer is a heterogeneous disease, associated with diverse biological behaviours and clinical outcome. Although some molecular subgroups of breast cancer have a targeted therapy, the most aggressive tumours still lack a molecular target.
Despite Vitamin D being classically associated with the physiological role of calcium regulation and phosphate transport in bone metabolism, several studies have been demonstrating a wide range of functions for this hormone, which are particularly important in the field of cancer. The mechanisms underlying the protective actions of Vitamin D in cancer development are only sparsely understood, but evidence shows that Vitamin D participates in cell growth regulation, apoptosis and cell differentiation.
In addition, Vitamin D has been implicated in the suppression of cancer cell invasion, angiogenesis and metastasis. Most of Vitamin D biological actions are mediated by the Vitamin D receptor (VDR) and the synthesis and catabolism of this hormone are regulated by the enzymes CYP27B1 and CYP24A1.
In the present review we highlight research data concerning the function of this hormone in the mammary gland, with a special focus on breast carcinogenesis. Hence, and although the available data are controversial, we considered not only updated information on epidemiology of Vitamin D in breast cancer and its potential value as a therapeutic agent or prophylactic (with an emphasis on molecular mechanisms and effectors of Vitamin D action), but we included data on its role in other stages of breast cancer progression as well.
Accordingly, we review data on the influence of Vitamin D in the development of normal breast and the expression of Vitamin D-related proteins (VDR, CYP27B1 and CYP24A21) in benign mammary lesions and ductal carcinomas in situ.
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See also Vitamin D Life
- Category Breast Cancer and Vitamin D
223 items - Compelling evidence – Breast Cancer and vitamin D – Dissertation June 2012
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