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Magnesium in Breast Cancer: What Is Its Influence on the Progression of This Disease?

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Abstract

Breast cancer is a disease of high mortality, characterized by the progressive accumulation of mutations that contribute to the uncontrolled development of breast tissue cells. Literature shows that disturbances in mineral homeostasis, such as magnesium, may interfere with tumor progression. The objective of this study is to provide updated information about magnesium’s role in the pathogenesis of breast cancer. A review of literature was carried out from a search for articles in the PubMed and CAPES Periodicals databases published between 1995 and 2016 with the cross-references of the descriptors “magnesium,” “breast neoplasms,” and “oxidative stress” and the corresponding words in Portuguese. We included studies on the metabolism and bioavailability of magnesium and studies related to breast cancer and excluded articles in which only the abstract was available, dissertations, theses, articles involving adjuvant and/or neoadjuvant therapies, and supplementation of minerals in breast cancer patients. Magnesium is a mineral that participates in the metabolism of various nutrients and nucleic acids. In the presence of breast cancer, neoplastic cells increase the expression of magnesium transport channels, which raises the intracellular concentration of the mineral, contributing to tumor growth through its function of increasing energy demand. The data obtained in this review illustrates the influence of magnesium on the progression of breast cancer. However, the existing data are scarce and inconsistent, which demonstrates a need for further studies on the subject with a goal to have better control of the disease.

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Correspondence to Dilina do Nascimento Marreiro.

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Mendes, P.M.V., Bezerra, D.L.C., dos Santos, L.R. et al. Magnesium in Breast Cancer: What Is Its Influence on the Progression of This Disease?. Biol Trace Elem Res 184, 334–339 (2018). https://doi.org/10.1007/s12011-017-1207-8

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  • DOI: https://doi.org/10.1007/s12011-017-1207-8

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