BACKGROUND: Magnesium plays a role in a large number of cellular metabolic reactions. Cetuximab, by the inhibition of epidermal growth factor (EGR), is able to induce hypomagnesaemia by interfering with magnesium transport in the kidney. OBJECTIVE: To investigate the interactions between magnesium homeostasis and EGF receptor (EGFR) inhibition. METHODS: We performed an updated literature search using the MEDLINE database for articles published from 1 January 1966 to 15 February 2008. We comprehensively reviewed all the data published in abstract form during the most significant international meetings (American Society of Clinical Oncology, American Association for Cancer Research, European Society for Medical Oncology and European Cancer Organisation). RESULTS/ CONCLUSION: We propose that EGFR inhibition may reduce cancer proliferation and also decrease magnesium levels. These reduced magnesium levels in turn contribute to the inhibition of angiogenesis by directly acting on endothelial cells and indirectly affecting EGFR signalling and the production of angiogenic molecules.
BACKGROUND:Magnesium plays a role in a large number of cellular metabolic reactions. Cetuximab, by the inhibition of epidermal growth factor (EGR), is able to induce hypomagnesaemia by interfering with magnesium transport in the kidney. OBJECTIVE: To investigate the interactions between magnesium homeostasis and EGF receptor (EGFR) inhibition. METHODS: We performed an updated literature search using the MEDLINE database for articles published from 1 January 1966 to 15 February 2008. We comprehensively reviewed all the data published in abstract form during the most significant international meetings (American Society of Clinical Oncology, American Association for Cancer Research, European Society for Medical Oncology and European Cancer Organisation). RESULTS/ CONCLUSION: We propose that EGFR inhibition may reduce cancer proliferation and also decrease magnesium levels. These reduced magnesium levels in turn contribute to the inhibition of angiogenesis by directly acting on endothelial cells and indirectly affecting EGFR signalling and the production of angiogenic molecules.