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ADI inhibited cell proliferation and induced apoptosis in human leukemic CEM cells in a dose\u2010dependent manner. Simultaneous treatment with ADI and DEX showed synergistic effects on DNA fragmentation and LDH release. In addition, ADI exerted its anti\u2010proliferative activity against DEX\u2010resistant CEM cells. ADI suppressed expression of c\u2010myc, a potential key regulator of cell proliferation and apoptosis, and increased expression of p27<jats:sup>Kip1<\/jats:sup>cyclin\u2010dependent kinase inhibitor. These results suggest that ADI efficiently increases the anti\u2010cancer effect of DEX on human leukemic CEM cells through G<jats:sub>1<\/jats:sub>cell cycle arrest involving downregulation of c\u2010myc and upregulation of p27<jats:sup>Kip1<\/jats:sup>. \u00a9 2004 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/ijc.20435","type":"journal-article","created":{"date-parts":[[2004,6,29]],"date-time":"2004-06-29T19:00:49Z","timestamp":1088535649000},"page":"502-508","source":"Crossref","is-referenced-by-count":33,"title":["Arginine deiminase enhances dexamethasone\u2010induced cytotoxicity in human T\u2010lymphoblastic leukemia CCRF\u2010CEM 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