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 Blood, 15 June 2008, Vol. 111, No. 12, pp. 5646-5653.
Prepublished online as a Blood First Edition Paper on April 18, 2008; DOI 10.1182/blood-2008-01-129726.

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NEOPLASIA

CD38 gene polymorphism and chronic lymphocytic leukemia: a role in transformation to Richter syndrome?

Semra Aydin1,2, Davide Rossi3, Luciana Bergui4, Giovanni D'Arena5, Enza Ferrero1,2, Lisa Bonello2, Paola Omedé4, Domenico Novero6, Fortunato Morabito7, Antonino Carbone8, Gianluca Gaidano3, Fabio Malavasi1,2, and Silvia Deaglio1,2

1 Department of Genetics, Biology, and Biochemistry, 2 Research Center for Experimental Medicine (CeRMS), University of Torino Medical School, Turin; 3 Division of Hematology, Department of Clinical and Experimental Medicine & Biotechnologie Ricerca Medica Applicate (BRMA), Amedeo Avogadro University of Eastern Piedmont and Ospedale Maggiore della Carità, Novara; 4 Department of Medicine and Experimental Oncology, University of Torino Medical School, Turin; 5 Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS) Casa Sollievo della Sofferenza Hospital, San Giovanni Rotondo; 6 Laboratory of Pathology, Department of Pathology, Molinette Hospital, Turin; 7 Hematology Unit, Department of Internal Medicine, Azienda Ospedaliera di Cosenza, Cosenza; and 8 Department of Pathology, Istituto Nazionale Tumori, Milan, Italy

CD38 rules proliferation signals in chronic lymphocytic leukemia (CLL) cells, suggesting that the molecule is not merely a prognostic marker but also a key element in the pathogenetic network underlying the disease. CD38 has a genetic polymorphism, characterized by a C>G variation in the regulatory region of intron 1. The working hypothesis is that the presence of different alleles in CLL patients marks (or accounts for) some of the clinical heterogeneity. CD38 allele distribution in 248 Italian patients overlapped with that of the controls (n = 232), suggesting that susceptibility to CLL is not influenced by CD38 genotype. Stratification of patients according to markers of unfavorable prognosis constantly resulted in a significantly higher frequency of the rare G allele. Furthermore, analysis of clinical parameters showed that G allele is independently associated with nodal/splenic involvement. The highest G allele frequency was observed in the 16 patients of the cohort that developed Richter syndrome (RS). Five-year cumulative incidence of transformation was significantly higher in G allele carriers than in CC homozygotes. Multivariate analysis on a total of 30 RS patients confirmed that the probability of transformation is strongly associated with G allele, likely representing an independent risk factor for RS development.


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