In Vitro and in Vivo Effect of Deoxycoformycin in Human T Cell Leukemia
The success of anti-cancer chemotherapy is often limited by the toxicity of chemotherapeutic agents toward normal bone marrow cells and other rapidly dividing cells. It is most desirable, but it has been difficult to find anti-cancer agents that are selectively toxic to neoplastic cells. Approaches to the achievement of such chemotherapeutic selectivity were developed out of the recent elucidation of the causal association of severe combined immunodeficiency with hereditary deficiency of adenosine deaminase (ADA) (1,2). ADA, an enzyme that catalyzes the deamination of adenosine and deoxy-adenosine to inosine and deoxy-inosine, is widely distritubed in mammalian tissue (3,4). However, inherited deficiency of ADA activity is associated with selective impairment of lymphoid functions, particularly T cell functions, although the enzyme is virtually absent from all tissues examined (4).
KeywordsHigh Pressure Liquid Chromatography Adenosine Deaminase Severe Combine Immunodeficiency Purine Metabolism Drastic Alteration
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