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T(14;18) translocation in chronic hepatitis C virus infection
Author(s) -
Zignego Anna Linda,
Giannelli Francesca,
Marrocchi Maria Eugenia,
Mazzocca Antonio,
Ferri Clodoveo,
Giannini Carlo,
Monti Monica,
Caini Patrizio,
Villa Giorgio La,
Laffi Giacomo,
Gentilini Paolo
Publication year - 2000
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.510310230
Subject(s) - cryoglobulinemia , lymphoproliferative disorders , hepatitis c virus , pathogenesis , immunology , medicine , chronic liver disease , virus , hepatitis c , lymphoma , cirrhosis
Pathogenic mechanisms of B‐cell lymphoproliferative disorders in chronic hepatitis C virus (HCV) infection are unclear. We studied t(14;18) translocation by polymerase chain reaction in peripheral blood mononuclear cells from 50 patients with HCV‐related liver disease (group A), 7 with mixed cryoglobulinemia syndrome (group B), 55 with HCV‐negative liver disease (group C), and 30 with HCV‐negative chronic rheumatic disorders or chronic infection by nonhepatotropic agents (group D). T(14;18) was significantly more frequent in group A (13/50 patients = 26 %) and group B (5/7 = 71.4%) patients than in group C (1/55 = 3.6%) and group D (1/30 = 3.3%) ones. Immunoblot analysis showed bcl‐2 over‐expression in all t(14;18)‐positive samples. In group A, 10/13 (77%) patients with t(14;18) and 13/37 (35%) without t(14;18) had serum cryoglobulins in the absence of mixed cryoglobulinemia symptoms ( P < .05). These data indicate that t(14;18) and bcl‐2 over‐expression in lymphoid cells are frequent in chronic HCV infection and suggest that this event may contribute to the pathogenesis of HCV‐related lymphoproliferative disorders.