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burkitt lymphoma/arginina
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Effect of arginine-deficient media on the herpes-type virus associated with cultured Burkitt tumor cells.
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After incubation at 37 C for 2 or more days, Basal Medium Eagle (BME) supplemented with 25% fetal calf serum (FCS) was not able to support adequate growth of EB3 and other lines of Burkitt tumor cells. The medium did, however, increase, by a factor of about 10, the number of cells synthesizing
Effect of arginine deficiency on synthesis of DNA and immunoglobulin receptor of Burkitt lymphoma cells.
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Mechanisms of cell death induced by arginase and asparaginase in precursor B-cell lymphoblasts.
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Arginase has therapeutic potential as a cytotoxic agent in some cancers, but this is unclear for precursor B acute lymphoblastic leukaemia (pre-B ALL), the commonest form of childhood leukaemia. We compared arginase cytotoxicity with asparaginase, currently used in pre-B ALL treatment, and
Endothelium derived relaxing factor release from canine coronary artery by leukocytes.
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Lectins, known to recognize endothelial cell adhesion molecules, have been shown to release endothelium-derived relaxing factor (EDRF) from blood vessels. We investigated the effects of different leukocyte-type cells to determine if these cells, by interacting with the endothelium, could release
The gene encoding the p53-regulated inhibitor of cdks (pic1) is not expressed in the molt-4 leukemia-cell line with p53 truncated at the carboxyl-terminus, and harbors a nucleotide substitution at codon-31 in several other cancer cell-lines.
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Entry into the cell cycle is governed by cyclins, cyclin-dependent kinases (CDKs) and CDK-inhibitors (CDKIs). The p53-regulated inhibitor of CDKs (PIC1) is a universal CDKI whose gene expression is directly induced by the p53 tumor suppressor protein. Reverse transcription and polymerase chain
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