Magnesium: The overlooked electrolyte in blood cancers? Original paper

What was reviewed?

This review examined magnesium as an underrecognized electrolyte in hematology and oncology, with a focus on blood cancers and lymphoma. The authors explained how magnesium supports DNA stability, DNA repair, apoptosis regulation, and control of oxidative stress and inflammation, then connected these mechanisms to cancer risk and outcomes. They also reviewed why magnesium deficiency is common, why routine testing can miss total-body depletion, and how common exposures in cancer care, such as diarrhea, malabsorption, and certain drugs, can worsen magnesium loss.

Who was reviewed?

The authors synthesized evidence from human observational studies, hospitalized patient cohorts, mechanistic cell studies, and animal models rather than enrolling a single study population. The “who” therefore included general adult populations evaluated for magnesium intake and cancer risk, hospitalized and critically ill patients where hypomagnesemia was measured alongside mortality and length of stay, and patients with hematologic malignancies who often receive magnesium-wasting therapies. The review also drew on rare-disease patients with XMEN syndrome and on populations where Epstein–Barr virus burden relates to lymphoma biology.

What were the most important findings?

The review linked low magnesium to worse health outcomes in general and highlighted signals that magnesium status may matter in blood cancers even though lymphoma-specific prognosis data remain limited. It emphasized that serum magnesium is an imperfect proxy because most body magnesium is intracellular or in bone, so “normal” serum values can coexist with deficiency. The authors highlighted a major immune mechanism from XMEN disease: MAGT1 defects reduce intracellular free magnesium, impair T and NK cell activation, lower NKG2D expression, and weaken control of EBV-infected cells, which increases lymphoma risk. They also described inflammatory activation during magnesium deficiency, including NF-κB–linked cytokine signaling, and discussed how cancer cells can upregulate transport pathways such as TRPM7 to favor growth.

What are the greatest implications of this review?

Clinicians should treat magnesium as a clinically meaningful variable in patients with blood cancers, not just a routine electrolyte, because deficiency is common, often silent, and plausibly linked to immune dysfunction, inflammation, and viral control. The review supports more proactive screening in high-risk settings, careful interpretation of “normal” serum magnesium, and thoughtful replacement strategies that avoid rapid peaks that trigger renal wasting. It also argues for better-designed prospective studies to test whether hypomagnesemia independently predicts outcomes in lymphoma and other blood cancers, and whether correcting deficiency improves immune competence and clinical endpoints.