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Blood, 15 August 2006, Vol. 108, No. 4, pp. 1135-1144. Prepublished online as a Blood First Edition Paper on April 18, 2006; DOI 10.1182/blood-2006-01-013003. This Article Full Text (PDF) All Versions of this Article: blood-2006-01-013003v1 108/4/1135    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Deaglio, S. Articles by Malavasi, F. Search for Related Content PubMed PubMed Citation Articles by Deaglio, S. Articles by Malavasi, F. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted January 20, 2006 Accepted April 2, 2006 In-tandem insight from basic science combined with clinical research: CD38 as both marker and key component of the pathogenetic network underlying chronic lymphocytic leukemia Silvia Deaglio, Tiziana Vaisitti, Semra Aydin, Enza Ferrero, and Fabio Malavasi* Lymphocyte Signaling Unit, Laboratory of Immunogenetics, Department of Genetics,University of Torino * Corresponding author; email: fabio.malavasi{at}unito.it. Absence of mutations in the IgV genes, ZAP-70 and CD38 are the most reliable negative prognostic markers for chronic lymphocytic leukemia (CLL) patients. Several lines of evidence indicate that CD38 may not be merely mere diagnostic marker but also a key element in the pathogenetic network in CLL. First, CD38 is a receptor that induces proliferation and increases survival of CLL cells. Second, CD38 signals start upon interaction with the CD31 ligand expressed by stromal and nurse-like cells. Third, CD38/CD31 contacts upregulate CD100, a semaphorin involved in sustaining CLL growth. Fourth, evidence that nurse-like cells express high levels of CD31 and plexin-B1, the high-affinity ligand for CD100, offer indirect confirmation for this model of receptor cross-talk. Elements of variation in the clinical course of CD38+ CLL patients include i) potential intersection with ZAP- 70, a kinase involved in the CD38 signaling pathway in T and NK cells, and ii) the effects of genetic polymorphisms of the receptors involved, at least of CD38 and CD31. Consequently, CD38 together with ZAP-70 appear to be the key elements of a co-receptor pathway that may sustain the signals mediated by the B cell receptor and potentially by chemokines and their receptors. This would result in acquisition of increased survival potential, providing clues to the poorer prognosis of CD38+ patients. 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