Hypothesis for the Mechanism of Elevated Serum Copper in Cancer Patients

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Abstract
Neoplastic growths seem to interfere with normal processes regulating the serum level of ceruloplasmin, a Cu-containing oxidase, which accounts for 96% of serum Cu. Normal catabolism of ceruloplasmin in the liver follows desialylation. In patients with tumors, ceruloplasmin may be resialylated at the tumor cell surface or in peripheral blood. Decreased catabolism due to resialylation of asialo-ceruloplasmin could account for the increased concentration of serum Cu noted in patients with neoplasia.