Malignant lymphomas of the gastro-intestinal tract: a reappraisal on the basis of the newly proposed Revised European American Lymphoma Classification.
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Europe↗
Biomedical subjects
E Sabattini
Publications and source records attributed to E Sabattini.
[Considerations in Hodgkin's disease].
The Authors critically review the problem of Hodgkin's disease (HD) in the light of the most recent findings obtained by means of immunohistochemistry and molecular biology. The following topics are discussed in details: 1) the definition of the borders between HD and non-Hodgkin's lymphomas, 2) the histogenesis of Hodgkin's and Reed-Sternberg cells, 3) the relationships between neoplastic cells and microenvironment, and 4) the pathogenetic role of Epstein-Barr virus in the onset of HD.
Biomarkers, Tumor↗
Lymphoproliferation in type II mixed cryoglobulinemia.
OBJECTIVE: The role of the hepatitis C virus (HCV) in the etiology of type II mixed cryoglobulinemia (MC) has been well established, but the pathogenetical relationships among the virus, the immune system, the natural history of MC, and lymphoproliferation in the bone marrow and liver need to be further elucidated. METHODS: Eighty-two patients with HCV positive type II MC and 20 subjects with chronic hepatitis C without MC were studied: bone marrow and liver specimens were examined by routine histology and immunohistochemistry, particularly focusing on parameters related to disease behaviour, such as the expression of the bcl-2 oncogene product and the proliferation-associated Ki67 antigen. RESULTS: In most MC patients there were lymphoid infiltrates within the bone marrow showing a monomorphic cytology, frequent immunoglobulin light chain monotypic restriction, expression of the anti-apoptotic bcl-2 oncogene product, and a low proliferative capacity (Ki-67 < 3%). On the other hand, in all non-cryoglobulinemic patients a bone marrow picture of reactive lymphoplasmacytosis was found. In both MC and chronic hepatitis patients, the liver biopsy showed portal infiltrates consisting of T-cells, associated with a significant B-cell component; the latter was particularly abundant in MC, where it was frequently arranged in pseudo-follicles. The B-cell component expressed the bcl-2 oncogene product and CD5 antigen, thus suggesting that the immune system is actively involved in the production of liver damage both in MC and non-cryoglobulinemic patients. It is worth noting that in MC patients (but not in the non-cryoglobulinemic patients) these CD5+/bcl-2+ B-cells frequently also exhibited a monotypic restriction bearing an IgM kappa. CONCLUSION: Our findings in these liver and bone marrow studies further support the role of a lymphoproliferative disorder in the pathology of type II MC: the B cells involved accumulate due to the inhibition of apoptosis, and their low proliferative index justifies the indolent course of the disease. HCV probably interacts with these B-cells, facilitating their clonal expansion.
Adult↗