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Monoclonal lymphocyte proliferation and bcl-2 rearrangement in essential mixed cryoglobulinaemia
1Department of Hematology, Sackler Faculty of Medicine, Tel Aviv University, Israel.
Insights
Essential mixed cryoglobulinaemia (EMC) type II and hepatitis C virus (HCV) infection in a patient led to a clonal B-lymphocyte proliferation. Genetic analysis revealed oncogene translocations, including bcl-2 and myc, linked to disease progression.
Area of Science:
- Hematology
- Oncology
- Virology
Background:
- Essential mixed cryoglobulinaemia (EMC) type II is a condition associated with B-cell abnormalities.
- Hepatitis C virus (HCV) infection is a known risk factor for lymphoproliferative disorders.
- Understanding the genetic underpinnings of B-cell malignancies in HCV-positive patients is crucial.
Abstract:
A patient with essential mixed cryoglobulinaemia (EMC) type II and hepatitis C virus (HCV) infection, in whom immunophenotypic and genotypic studies demonstrated a clonal proliferation of B lymphocytes, is described. Fluorescent in situ hybridization with probes to Ig heavy chain gene and to the oncogene bcl-2 demonstrated a translocation of bcl-2 to the immunoglobulin heavy chain locus on chromosome 14. A sharp rise in the level of the monoclonal IgM was associated with a second genetic aberration [t(8:22) (q24:q11)]. No other clinical evidence of disease progression could be demonstrated. Low grade lymphoproliferative disorder with typical cytogenetic abnormalities developed on the background of EMC and HCV. Clinical progression was associated with a second genetic abnormality involving the myc oncogene. It is possible that HCV chronic infection may indirectly influence oncogenes associated with lymphoma.