Abstract
The recognition that human combined immune deficiency is associated with inborn adenosine deaminase (ADA) deficiency has focused attention on the importance of purine nucleoside metabolism and toxicity in the lymphoid system1. This has been reinforced by the development of drugs which inhibit ADA, in particular deoxy-coformycin (DCF), now used in the treatment of T cell and other leukemias2. Cultured human T leukemic lymphoblasts (in the presence of ADA inhibitors) are highly sensitive to dAdo induced cytotoxicity; while Epstein-Barr Virus (EBV) transformed B cell lines are resistant. These cell lines have proven valuable models to study dAdo metabolism and toxicity3.
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Fox, R.M., Tripp, E.H., Taylor, I.W. (1984). Deoxyadenosine Induced G1 Phase Arrest in Leukemic T Cells. In: De Bruyn, C.H.M.M., Simmonds, H.A., Müller, M.M. (eds) Purine Metabolism in Man-IV. Advances in Experimental Medicine and Biology, vol 165. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-0390-0_63
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DOI: https://doi.org/10.1007/978-1-4757-0390-0_63
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