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S Pileri

Publications and source records attributed to S Pileri.

223 records · Page 13Linked to original sources
PubMedDate not supplied

Primary T-cell lymphoma of the central nervous system.

A series of 6 patients with primary T-cell lymphomas of the central nervous system (PTCLCNS) is presented. The clinical, histological and immunohistological findings are shown. The lesions were infratentorial in the 34% and sopratentorial in the 66% of the cases. Of the 5 cases with an available follow-up only one died in the first year after diagnosis and one is alive and well after 42 months. These data agree with those of others series of PTCLCNS in the literature. In conclusion our data and those of the literature suggest that immunophenotyping should routinely be carried in primary non-Hodgkin's lymphomas of the CNS (PNHLCNS), because the T-cell forms run a more favourable course than the B-cell varieties.

Adult↗
PubMedDate not supplied

Controversies on Hodgkin's disease and anaplastic large cell lymphoma. Hematopathology Study Group of the Società Italiana di Anatomia Patologica.

Just one year ago the Italian Society of Pathology (S.I.A.P.) created a Study Group which included members of the most active Italian hematopathology teams. Prof. Pasquale Calapso was asked to chair the Group and Prof. Stefano Pileri to take care of secretarial duties. The aim of the Group is to spread hematopathologic knowledge among young pathologists and to promote activities that can contribute to updating Italian pathologists on topics of both speculative and diagnostic interest. The first Workshop of the S.I.A.P. Hematopathology Group was held at the Palazzo dei Congressi in Bologna, November 20, 1993. About 150 pathologists from all over Italy took part in the meeting, which consisted of two sections devoted to: a) discussion of the boundaries between Hodgkin's disease and non-Hodgkin's lymphomas, and b) a case seminar illustrating the impact of immunohistochemistry in the diagnosis of bone-marrow biopsy. The first section included 5 presentations and a Round Table chaired by Prof. Luciano Fiore-Donati. Below, the contributors to this section summarize the content of their presentations, which were aimed at answering specific questions the Organizers had put to them.

Hodgkin Disease↗
PubMedDate not supplied

Expression of multidrug resistance gene (MDR-1) in human normal leukocytes.

BACKGROUND: The mdr-1 gene, which codes for a 170-kd transmembrane glycoprotein (P170), is frequently overexpressed in multidrug resistant (MDR) tumor cell lines and in spontaneous tumors, including leukemia and lymphoma. However, it is also constitutively expressed as a normal gene in normal tissues. METHODS: We used human mdr-1 cDNA and three anti-P170 monoclonal antibodies (MoAbs: MRK-16, C-219 and JSB-1) to investigate the normal peripheral blood leukocyte content of mdr-1 specific mRNA and of P170 through immunocytochemistry and flow cytometry. RESULTS: We did not find any increase in mdr-1-specific mRNA, while small amounts of P170 were easily detectable in about two thirds of the lymphocytes and monocytes and in about one third of the granulocytes. The level of P170 expression in leukocytes was similar to that found in non-MDR tumor cell lines. CONCLUSIONS: mdr-1 is constitutively expressed in human normal leukocytes at levels that cannot significantly affect drug resistance. Accordingly, low-level mdr-1 expression in leukemic cells should not be considered a label of pleiotropic drug resistance.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMedDate not supplied

[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↗
PubMedDate not supplied

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↗