Activity of 2-Chloro-2′-Deoxyadenosine in Chronic Lymphocytic Leukemia, Hairy Cell Leukemia, and Autoimmune Hemolytic Anemia
Interest in the pathways of nucleotide metabolism in human lymphocytes was stimulated by the serendipitous observations of Giblett, et al., who found that two inborn errors of purine nucleoside metabolism cause severe impairment of lymphocyte function, while sparing other cell types (1, 2). A genetic deficiency of adenosine deaminase engenders a combined immunodeficiency syndrome (1). A similar deficiency in purine nucleoside phosphorylase is associated with a selective cellular immune deficit (2).
KeywordsChronic Lymphocytic Leukemia Adenosine Deaminase Chronic Lymphocytic Leukemia Patient Hairy Cell Leukemia Chronic Lymphocytic Leukemia Cell
Unable to display preview. Download preview PDF.
- 9.D.A. Carson, D.B. Wasson, J. Kaye, B. Ullman, D.W. Martin, Jr., R.K. Robins, and J.A. Montgomery, Deoxycytidine kinase-mediated toxicity of deoxyadenosine analogs toward malignant human lymphoblasts in vitro and toward murine L1210 leukemia in vivo, Proc. Natl. Acad. Sci. USA 77: 6865 (1980).PubMedCrossRefGoogle Scholar
- 12.L.D. Piro, C.J. Carrera, E. Beutler, and D.A. Carson, 2-chlorodeoxyadenosine: An effective new agent for the treatment of chronic lymphocytic leukemia, Blood, in press.Google Scholar