Philadelphia chromosome without breakpoint cluster region rearrangement in a case of Lennert's lymphoma of suppressor phenotype.

A 60-year-old woman presented with diffuse lymphadenopathy. Diagnostic and staging work-up showed that the patient had diffuse small cleaved cell lymphoma (diffuse poorly differentiated lymphocytic lymphoma) with associated histiocytes (lymphoepithelioid cell lymphoma) by the Kiel classification system. Immunohistologic staining showed a T suppressor cell tumour phenotype. Cytogenetic studies revealed the Philadelphia chromosome (Ph1). On DNA studies, the breakpoint cluster region (BCR) gene was not rearranged suggesting that the Ph1 involvement was not identical to that seen in chronic myelogenous leukemia (CML). This case is presented because of the rarity of Ph1 in lymphoid malignancies, particularly in those of T-cell origin, and because of its potentially adverse implications.

Expression of interleukin-2 receptor beta subunit in hematopoietic malignancies.

The expression of the interleukin-2 (IL-2) receptor was studied in neoplastic cells derived from acute leukemias, T-cell lymphoblastic lymphomas, peripheral T-cell lymphomas, chronic lymphocytic leukemias, well-differentiated lymphocytic lymphomas, and established cell lines by both flow cytometric analysis and sodium dodecyl sulfate/polyacrylamide gel electrophoresis (SDS-PAGE) after affinity crosslinking of radiolabeled IL-2. Cells from most acute leukemias (19 of 22), irrespective of their subtype (T, common or nonlymphoid leukemias), as well as T-cell lymphoblastic lymphomas and peripheral T-cell lymphomas expressed only the p70-75 beta subunit of the IL-2 receptor. Cells from the more mature B-cell neoplasms, chronic lymphocytic leukemia, and well-differentiated lymphocytic lymphoma, expressed predominantly alpha beta IL-2 receptors (11 of 14). In contrast to these results, most cell lines established from hematopoietic malignancies do not express either chain of the IL-2 receptor. Further studies are necessary to determine the exact function of the IL-2R p70-75 beta subunit in immature hematopoietic cells, but its wide distribution throughout the hematopoietic system suggests that IL-2 may play a role in the early stages of hematopoiesis.

Alpha-2b interferon in the treatment of advanced chronic lymphocytic leukemia.

In four patients treated for progressive B-CLL, stage C, with alpha-2b interferon a detailed analysis of the distribution of surface molecules characterizing both the leukemic and the residual populations of peripheral blood lymphocytes as evaluated by flow cytometry did not reveal any significant changes during and after the interferon therapy. With the dosage of 3 x 10(6) IU of interferon injected subcutaneously three times per week, no effect on progression of the disease was detected. The treatment was well tolerated, thrombocytopenia was the only side-effect observed.

Differential expression of LFA-1 molecules in non-Hodgkin's lymphoma and lymphoid leukemia.

We investigated the expression of adherence molecules lymphocyte function-associated antigens-1 alpha and -beta (LFA-1 alpha, -beta) and p150, 95 in 103 well-characterized non-Hodgkin's lymphomas (NHLs) and lymphoid leukemias (LLs). We found that NHLs and LLs differentially express LFA-1 molecules according to their lineage derivation, degree of clinical aggressiveness, and anatomic site of involvement. Specifically, (a) T-cell neoplasms nearly always express these molecules; (b) diffuse aggressive B-cell NHLs and mature LLs often lack LFA-1 alpha molecules; and (c) B-cell chronic lymphocytic leukemia (CLL) is often LFA-1 alpha-negative while B-cell small lymphocytic lymphomas (SLLs) are nearly always LFA-1 alpha-positive. Furthermore, the low expression of LFA-1 alpha in CLL is related to the low degree of homotypic lymphocyte adhesion after tumor promoter antigen stimulation that does not modulate the expression of LFA-1 alpha in vitro. The differential expression of LFA-1 by B-cell CLL and SLL and their degree of homotypic lymphocyte adhesion may account for the distinct anatomic compartmentalization and characteristic clinical behavior of these two morphologically and immunologically similar lymphoid malignancies.

A histogenesis of malignant lymphoma, small cleaved cell of the B cell type and intermediate lymphocytic lymphoma (mantle zone lymphoma). An immuno- and enzymehistochemical study.

We have studied the histogenesis of malignant lymphoma (ML), small cleaved cell of the B-cell type and intermediate lymphocytic lymphoma (mantle zone lymphoma) by comparing immunophenotypes and ALP-activity of neoplastic cells with those of germinal center cells (follicular center cells) and mantle zone (MZ) cells of secondary follicles in non-neoplastic lymphoid tissues. The neoplastic cells in 3 cases of ML, follicular, small cleaved cell and 1 case of ML, small cleaved cell expressed the phenotypes similar to those of germinal center (GC) B lymphocytes (SIgM+, B1+, B2+, CALLA+, SigD-, IL-2R-, Leu-1- and ALP-). The neoplastic cells in 2 cases of ML, follicular, small cleaved cell and 12 cases of ML, diffuse, small cleaved cell displayed the characteristic phenotypes of MZ B lymphocytes (SIgM+, SIgD+, BA-1+, IL-2R+, Leu-1+ and ALP+). The phenotypes of 2 cases of mantle zone lymphoma were closely comparable with those of MZ B lymphocytes. These findings indicate that the histogenesis of ML, small cleaved cell of the B-cell type is heterogeneous and can be divided phenotypically into 2 types (GC B lymphocyte origin and MZ B lymphocyte origin). It is also apparent that intermediate lymphocytic lymphoma (mantle zone lymphoma) is derived from MZ B lymphocytes of secondary follicles.