The relationship of riboflavin to cancer is intriguing but many gaps remain in our knowledge. Several studies indicate that riboflavin deficiency inhibits tumor growth in experimental animals and possibly in man, but the precise mechanisms involved have not been elucidated. Azo dye carcinogenesis in liver appears to be a special case in that riboflavin deficiency increases the potency of these drugs in tumor causation, probably in large measure because flavin cofactors are involved in their metabolic degradation. Riboflavin influences uptake of chemotherapeutic drugs in at least one instance (methotrexate) into neoplastic cells. The fact that folic acid metabolism depends upon flavin cofactors may have implications for the use of folate antagonists in cancer chemotherapy.

Neoplastic liver appears to lack certain mechanisms that regulate riboflavin metabolism in normal tissues. In addition, it is more resistant than normal liver to riboflavin deficiency, as reflected in the relatively higher concentrations of flavin mononucleotide and flavin adenine dinucleotide measured in samples of tumor than in the host rat liver. By contrast, the concentration of free riboflavin is greatly depressed in Novikoff hepatoma grown in riboflavin-deficient animals. The loss of this relatively dispensable flavin fraction may be one of the mechanisms that enable tumor to retain the more critical flavin mononucleotide and flavin adenine dinucleotide fractions when dietary riboflavin is diminished. The provocative observation that certain patients with cancer excrete less riboflavin than do normal individuals requires further confirmation. Much remains to be learned about the uptake, turnover, binding, and removal of riboflavin and its derivatives from neoplastic tissue.

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Research supported by grants from the USPHS (AM 15265 and CA 12126) and from the Stella and Charles Guttman Foundation. This review is adapted in part from Ref. 55.

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