Quantitative Aspects of the Binding of Folie Acid by Folate Antiserum1

units for the synthesis of the purine ring and the methylation of uridylate to thymidylate is a fundamental requirement for cell replication. The mammalian cell cannot synthesize the basic pteroylglutamate structure and, consequently, growth and maturation of both normal and neoplastic cells require an exogenous source of this vitamin. For this reason, the folate coenzymes have been the target of intensive investigation, particularly as related to tumor growth. Indeed, the objective of cancer and leukemia chemotherapy with antagonists of folie acid is to interfere with the biological function of this vitamin and thereby inhibit neoplastic cell growth. It has long been known that folate deficiency frequently accompanies the disordered growth of neoplasia. Morphological evidence of erythroid megaloblastosis, low serum and red cell folate (10, 14), decreased urinary excretion of folie acid following a loading dose (6), and increased urinary excretion of formiminoglutamic acid (3) has been observed in patients with a variety of cancers and with leukemia, suggesting that these cancers preferentially utilize available folate. Of considerable interest in this regard is the observation that folate deficiency may retard the leukemic process. Where