Linked Life Data

17376892

Source:http://linkedlifedata.com/resource/pubmed/id/17376892

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pubmed-article:17376892pubmed:abstractTextPrevious studies on apoptosis defects in acute lymphoblastic leukemia (ALL) have focused on chemotherapy-induced, primarily mitochondrial death pathways. Yet, immunologic surveillance mechanisms including sensitization to apoptotic signals mediated via the death receptor CD95 might contribute to leukemic control. Here, we show that primary B-cell precursor ALL cells from children escape from receptor-dependent cell death in 2 ways: Resting ALL blasts are protected from receptor-mediated apoptosis due to the absence of CD95 surface expression. However, even though CD40 ligation results in up-regulation of CD95, ALL blasts, unlike normal B cells, remain resistant to apoptosis. We show that this apoptosis resistance involves the selective up-regulation of the short isoforms of the caspase-8 inhibitor c-FLIP acting directly at the CD95 receptor level. Treatment with cycloheximide during CD40 activation prevents up-regulation of those c-FLIP isoforms and sensitizes ALL cells toward CD95-mediated apoptosis. We therefore propose that induction of the short c-FLIP isoforms inhibits the onset of CD95-induced apoptosis in primary CD40-stimulated ALL cells despite high CD95 expression.lld:pubmed
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pubmed-article:17376892pubmed:pagination384-7lld:pubmed
pubmed-article:17376892pubmed:dateRevised2007-11-15lld:pubmed
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pubmed-article:17376892pubmed:articleTitleUp-regulation of c-FLIPS+R upon CD40 stimulation is associated with inhibition of CD95-induced apoptosis in primary precursor B-ALL.lld:pubmed
pubmed-article:17376892pubmed:affiliationClinic for Pediatric Hematology, Heinrich Heine University of Duesseldorf, Germany. troeger@med.uni-duesseldorf.delld:pubmed
pubmed-article:17376892pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:17376892pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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