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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 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 Citation Map 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. Related Collections Neoplasia Cell Adhesion and Motility Signal Transduction Free Research Articles Review Articles Clinical Trials and Observations Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  REVIEW IN TRANSLATIONAL HEMATOLOGY 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 From the Lymphocyte Signaling Unit, Laboratory of Immunogenetics, Department of Genetics, Biology and Biochemistry & CeRMS, University of Torino Medical School, Torino, Italy. Abstract The absence of mutations in the IgV genes, together with the presence of 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 be not only a 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 up-regulate CD100, a semaphorin involved in sustaining CLL growth. Fourth, evidence that nurselike cells express high levels of CD31 and plexin-B1, the high-affinity ligand for CD100, offers indirect confirmation for this model of receptor cross-talk. Elements of variation in the clinical course of CD38+ CLL patients include (1) potential intersection with ZAP-70, a kinase involved in the CD38 signaling pathway in T and natural killer (NK) cells, and (2) 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 coreceptor 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. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: D. Rossi, A. Zucchetto, F. M. Rossi, D. Capello, M. Cerri, C. Deambrogi, S. Cresta, S. Rasi, L. De Paoli, C. L. Bodoni, et al. CD49d expression is an independent risk factor of progressive disease in early stage chronic lymphocytic leukemia Haematologica, October 1, 2008; 93(10): 1575 - 1579. [Abstract] [Full Text] [PDF] S. Aydin, D. Rossi, L. Bergui, G. D'Arena, E. Ferrero, L. Bonello, P. Omede, D. Novero, F. Morabito, A. Carbone, et al. 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