{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,30]],"date-time":"2026-05-30T01:01:55Z","timestamp":1780102915060,"version":"3.54.0"},"reference-count":35,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2005,3,15]],"date-time":"2005-03-15T00:00:00Z","timestamp":1110844800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J of Cellular Biochemistry"],"published-print":{"date-parts":[[2005,5]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>An enhanced linkage\u2010specific 9\u2010<jats:italic>O<\/jats:italic>\u2010acetylated sialic acid (9\u2010<jats:italic>O<\/jats:italic>\u2010AcSA) on peripheral blood mononuclear cells (PBMC) of children with acute lymphoblastic leukaemia, ALL (PBMC<jats:sub>ALL<\/jats:sub>, 9\u2010<jats:italic>O<\/jats:italic>\u2010AcSA<jats:sup>+<\/jats:sup> cells) was demonstrated by using a lectin, Achatinin\u2010H, whose lectinogenic epitope was 9\u2010<jats:italic>O<\/jats:italic>\u2010AcSA\u03b12\u20106GalNAc. Our aim was to evaluate the in vitro contributory role of this glycotope (9\u2010<jats:italic>O<\/jats:italic>\u2010AcSA\u03b12\u20106GalNAc) towards the survival of these 9\u2010<jats:italic>O<\/jats:italic>\u2010AcSA<jats:sup>+<\/jats:sup> cells in ALL patients. For direct comparison, 9\u2010<jats:italic>O<\/jats:italic>\u2010AcSA<jats:sup>\u2212<\/jats:sup> cells were generated by removing <jats:italic>O<\/jats:italic>\u2010acetyl group of 9\u2010<jats:italic>O<\/jats:italic>\u2010AcSA present on PBMC<jats:sub>ALL<\/jats:sub> using <jats:italic>O<\/jats:italic>\u2010acetyl esterase. An elevated level of serum interferon gamma (IFN\u2010\u03b3) in affected children led us to think that PBMC<jats:sub>ALL<\/jats:sub> are continuously exposed specifically to this cytokine. Accordingly, 9\u2010<jats:italic>O<\/jats:italic>\u2010AcSA<jats:sup>+<\/jats:sup> and 9\u2010<jats:italic>O<\/jats:italic>\u2010AcSA<jats:sup>\u2212<\/jats:sup> cells were exposed in vitro to IFN\u2010\u03b3. A twofold increased NO release along with inducible NO synthase (iNOS) mRNA expression by the 9\u2010<jats:italic>O<\/jats:italic>\u2010AcSA<jats:sup>+<\/jats:sup> cells was observed as compared to the 9\u2010<jats:italic>O<\/jats:italic>\u2010AcSA<jats:sup>\u2212<\/jats:sup> cells. The decreased viability of IFN\u2010\u03b3 exposed 9\u2010<jats:italic>O<\/jats:italic>\u2010AcSA<jats:sup>\u2212<\/jats:sup> cells as compared to 9\u2010<jats:italic>O<\/jats:italic>\u2010AcSA<jats:sup>+<\/jats:sup> cells were reflected from a 5.0\u2010fold increased caspase\u20103\u2010like activity and a 10.0\u2010fold increased apoptosis in the 9\u2010<jats:italic>O<\/jats:italic>\u2010AcSA<jats:sup>\u2212<\/jats:sup> cells when production of NO was lowered by adding competitive inhibitor of iNOS in reaction mixture. Therefore, it may be envisaged that a link exists between induction of this glycotope and their role in regulating viability of PBMC<jats:sub>ALL<\/jats:sub>. Taken together, it is reasonable to hypothesise that <jats:italic>O<\/jats:italic>\u2010acetylation of sialic acids on PBMC<jats:sub>ALL<\/jats:sub> may be an additional mechanism that promotes the survival of lymphoblasts by avoiding apoptosis via IFN\u2010\u03b3\u2010induced NO production. \u00a9 2004 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/jcb.20382","type":"journal-article","created":{"date-parts":[[2005,3,15]],"date-time":"2005-03-15T21:16:45Z","timestamp":1110921405000},"page":"206-216","source":"Crossref","is-referenced-by-count":28,"title":["Interferon gamma promotes survival of lymphoblasts overexpressing 9\u2010<i>O<\/i>\u2010acetylated sialoglycoconjugates in childhood acute lymphoblastic leukaemia 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