BER-H2: a new anti-Ki-1 (CD30) monoclonal antibody directed at a formol- resistant epitope

Blood ◽  
1989 ◽  
Vol 74 (5) ◽  
pp. 1678-1689 ◽  
Author(s):  
R Schwarting ◽  
J Gerdes ◽  
H Durkop ◽  
B Falini ◽  
S Pileri ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
B Cell ◽  
Plasma Cells ◽  
Large Cell ◽  
Diagnostic Value ◽  
Paraffin Sections ◽  
Lymphomatoid Papulosis ◽  
Tissue Sections ◽  
Hodgkin's Lymphomas ◽  
Cd30 Antigen

The production and characterization of a monoclonal antibody (MoAb) designated Ber-H2, directed against a new epitope of the Ki-1 (CD30) antigen, are described. In comparison with the formerly reported Ki-1 MoAb whose reactivity with Hodgkin and Reed-Sternberg (H-RS) cells in frozen tissue sections is well-documented, the Ber-H2 MoAb showed new, important features: the labeling intensity of the Ber-H2 MoAb was much stronger, and the number of positively labeled cells was higher. Most important, however, was that the Ber-H2 MoAb could be applied in routinely processed, formaldehyde-fixed, paraffin-embedded tissue sections. Therefore, it was possible to investigate an unprecedented number of tumors received as frozen or formaldehyde-fixed material for expression of the CD30 antigen. Beside Hodgkin's disease, the Ber-H2 MoAb labeled a variable number of cells in lymphomatoid papulosis, peripheral T-cell lymphomas, and angoimmunoblastic lymphadenopathy. Among B-cell non-Hodgkin's lymphomas (NHLs), some cases containing large centroblast-like or immunoblast-like cells or displaying plasma- cellular differentiation were positive. This finding was in keeping with the reactivity of the Ber-H2 MoAb with activated B-cell blasts and a subpopulation of plasma cells in paraffin sections of normal lymphoid tissue. The diagnostic value of the Ber-H2 MoAb was most significant for a group of anaplastic large-cell (ALC) lymphomas (formerly frequently referred to as malignant histiocytosis or regressive atypical histiocytosis), of which more than 50 cases could be investigated, owing to applicability in paraffin sections. Although about one third of these ALC lymphomas did not express the leukocyte common (CD45) antigen, they were consistently reactive with the Ber-H2 MoAb in both frozen and paraffin-embedded tissue sections. Using the Ber-H2 MoAb, these Ki-1 lymphomas could be easily distinguished from other nonlymphoid anaplastic large-cell tumors.

scholarly journals BER-H2: a new anti-Ki-1 (CD30) monoclonal antibody directed at a formol- resistant epitope

Blood ◽  
1989 ◽  
Vol 74 (5) ◽  
pp. 1678-1689 ◽  
Author(s):  
R Schwarting ◽  
J Gerdes ◽  
H Durkop ◽  
B Falini ◽  
S Pileri ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
B Cell ◽  
Plasma Cells ◽  
Large Cell ◽  
Diagnostic Value ◽  
Paraffin Sections ◽  
Lymphomatoid Papulosis ◽  
Tissue Sections ◽  
Hodgkin's Lymphomas ◽  
Cd30 Antigen

Abstract The production and characterization of a monoclonal antibody (MoAb) designated Ber-H2, directed against a new epitope of the Ki-1 (CD30) antigen, are described. In comparison with the formerly reported Ki-1 MoAb whose reactivity with Hodgkin and Reed-Sternberg (H-RS) cells in frozen tissue sections is well-documented, the Ber-H2 MoAb showed new, important features: the labeling intensity of the Ber-H2 MoAb was much stronger, and the number of positively labeled cells was higher. Most important, however, was that the Ber-H2 MoAb could be applied in routinely processed, formaldehyde-fixed, paraffin-embedded tissue sections. Therefore, it was possible to investigate an unprecedented number of tumors received as frozen or formaldehyde-fixed material for expression of the CD30 antigen. Beside Hodgkin's disease, the Ber-H2 MoAb labeled a variable number of cells in lymphomatoid papulosis, peripheral T-cell lymphomas, and angoimmunoblastic lymphadenopathy. Among B-cell non-Hodgkin's lymphomas (NHLs), some cases containing large centroblast-like or immunoblast-like cells or displaying plasma- cellular differentiation were positive. This finding was in keeping with the reactivity of the Ber-H2 MoAb with activated B-cell blasts and a subpopulation of plasma cells in paraffin sections of normal lymphoid tissue. The diagnostic value of the Ber-H2 MoAb was most significant for a group of anaplastic large-cell (ALC) lymphomas (formerly frequently referred to as malignant histiocytosis or regressive atypical histiocytosis), of which more than 50 cases could be investigated, owing to applicability in paraffin sections. Although about one third of these ALC lymphomas did not express the leukocyte common (CD45) antigen, they were consistently reactive with the Ber-H2 MoAb in both frozen and paraffin-embedded tissue sections. Using the Ber-H2 MoAb, these Ki-1 lymphomas could be easily distinguished from other nonlymphoid anaplastic large-cell tumors.

scholarly journals Immunolocalization of the ICE/Ced-3–Family Protease, CPP32 (Caspase-3), in Non-Hodgkin's Lymphomas, Chronic Lymphocytic Leukemias, and Reactive Lymph Nodes

Blood ◽  
1997 ◽  
Vol 89 (10) ◽  
pp. 3817-3825 ◽  
Author(s):  
Stanislaw Krajewski ◽  
Randy D. Gascoyne ◽  
Juan M. Zapata ◽  
Maryla Krajewska ◽  
Shinichi Kitada ◽  
...  
Keyword(s):  
B Cells ◽  
Lymph Nodes ◽  
B Cell ◽  
Germinal Center ◽  
Caspase 3 ◽  
Large Cell ◽  
B Cell Lymphomas ◽  
Mantle Zone ◽  
Dynamic Regulation ◽  
Hodgkin's Lymphomas

Immunohistochemical analysis of the apoptosis-effector protease CPP32 (Caspase-3) in normal lymph nodes, tonsils, and nodes affected with reactive hyperplasia (n = 22) showed strong immunoreactivity in the apoptosis-prone germinal center B-lymphocytes of secondary follicles, but little or no reactivity in the surrounding long-lived mantle zone lymphocytes. Immunoblot analysis of fluorescence-activated cell sorted germinal center and mantle zone B cells supported the immunohistochemical results. In 22 of 27 (81%) follicular small cleaved cell non-Hodgkin's B-cell lymphomas, the CPP32-immunopositive germinal center lymphocytes were replaced by CPP32-negative tumor cells. In contrast, the large cell component of follicular mixed cells (FMs) and follicular large cell lymphomas (FLCLs) was strongly CPP32 immunopositive in 12 of 17 (71%) and in 8 of 14 (57%) cases, respectively, whereas the residual small-cleaved cells were poorly stained for CPP32 in all FLCLs and in 12 of 17 (71%) FMs, suggesting that an upregulation of CPP32 immunoreactivity occurred during progression. Similarly, cytosolic immunostaining for CPP32 was present in 10 of 12 (83%) diffuse large cell lymphomas (DLCLs) and 2 of 3 diffuse mixed B-cell lymphomas (DMs). Immunopositivity for CPP32 was also found in the majority of other types of non-Hodgkin's lymphomas studied. Plasmacytomas were CPP32 immunonegative in 4 of 12 (33%) cases, in contrast to normal plasma cells, which uniformly contained intense CPP32 immunoreactivity, implying downregulation of CPP32 in a subset of these malignancies. All 12 peripheral blood B-cell chronic lymphocyte leukemia specimens examined were CPP32 immunopositive, whereas 3 of 3 small lymphocytic lymphomas were CPP32 negative, suggesting that CPP32 expression may vary depending on the tissue compartment in which these neoplastic B cells reside. The results show dynamic regulation of CPP32 expression in normal and malignant lymphocytes.

scholarly journals Immunolocalization of the ICE/Ced-3–Family Protease, CPP32 (Caspase-3), in Non-Hodgkin's Lymphomas, Chronic Lymphocytic Leukemias, and Reactive Lymph Nodes

Blood ◽  
1997 ◽  
Vol 89 (10) ◽  
pp. 3817-3825 ◽  
Author(s):  
Stanislaw Krajewski ◽  
Randy D. Gascoyne ◽  
Juan M. Zapata ◽  
Maryla Krajewska ◽  
Shinichi Kitada ◽  
...  
Keyword(s):  
B Cells ◽  
Lymph Nodes ◽  
B Cell ◽  
Germinal Center ◽  
Caspase 3 ◽  
Large Cell ◽  
B Cell Lymphomas ◽  
Mantle Zone ◽  
Dynamic Regulation ◽  
Hodgkin's Lymphomas

Abstract Immunohistochemical analysis of the apoptosis-effector protease CPP32 (Caspase-3) in normal lymph nodes, tonsils, and nodes affected with reactive hyperplasia (n = 22) showed strong immunoreactivity in the apoptosis-prone germinal center B-lymphocytes of secondary follicles, but little or no reactivity in the surrounding long-lived mantle zone lymphocytes. Immunoblot analysis of fluorescence-activated cell sorted germinal center and mantle zone B cells supported the immunohistochemical results. In 22 of 27 (81%) follicular small cleaved cell non-Hodgkin's B-cell lymphomas, the CPP32-immunopositive germinal center lymphocytes were replaced by CPP32-negative tumor cells. In contrast, the large cell component of follicular mixed cells (FMs) and follicular large cell lymphomas (FLCLs) was strongly CPP32 immunopositive in 12 of 17 (71%) and in 8 of 14 (57%) cases, respectively, whereas the residual small-cleaved cells were poorly stained for CPP32 in all FLCLs and in 12 of 17 (71%) FMs, suggesting that an upregulation of CPP32 immunoreactivity occurred during progression. Similarly, cytosolic immunostaining for CPP32 was present in 10 of 12 (83%) diffuse large cell lymphomas (DLCLs) and 2 of 3 diffuse mixed B-cell lymphomas (DMs). Immunopositivity for CPP32 was also found in the majority of other types of non-Hodgkin's lymphomas studied. Plasmacytomas were CPP32 immunonegative in 4 of 12 (33%) cases, in contrast to normal plasma cells, which uniformly contained intense CPP32 immunoreactivity, implying downregulation of CPP32 in a subset of these malignancies. All 12 peripheral blood B-cell chronic lymphocyte leukemia specimens examined were CPP32 immunopositive, whereas 3 of 3 small lymphocytic lymphomas were CPP32 negative, suggesting that CPP32 expression may vary depending on the tissue compartment in which these neoplastic B cells reside. The results show dynamic regulation of CPP32 expression in normal and malignant lymphocytes.

scholarly journals A monoclonal antibody that recognizes B cells and B cell precursors in mice.

1981 ◽  
Vol 153 (2) ◽  
pp. 269-279 ◽  
Author(s):  
R L Coffman ◽  
I L Weissman
Keyword(s):  
Monoclonal Antibody ◽  
Bone Marrow ◽  
B Cells ◽  
B Cell ◽  
Plasma Cells ◽  
Bone Marrow Cells ◽  
Cell Lineage ◽  
Hematopoietic Stem ◽  
B Cell Precursors

The monoclonal antibody, RA3-2C2, appears to be specific for cells within the B cell lineage. This antibody does not recognize thymocytes, peripheral T cells, or nonlymphoid hematopoietic cells in the spleen or bone marrow. Nor does it recognize the pluripotent hematopoietic stem cells, the spleen colony-forming unit, All sIg+ B cells and most plasma cells are RA3-2C2+. In addition, approximately 20% of nucleated bone marrow cells are RA3-2C2+ but sIg-. This population contains B cell precursors that can give rise to sIg+ cells within 2 d in vitro.

scholarly journals A rare case of nodular lymphocyte predominant Hodgkin lymphoma, which developed 5 years after successful treatment of diffuse large B-cell lymphoma

2021 ◽  
Vol 20 (1) ◽  
pp. 162-167
Author(s):  
M. A. Senchenko ◽  
D. S. Abramov ◽  
A. E. Rudneva ◽  
E. V. Volchkov ◽  
G. A. Nasirdinova ◽  
...  
Keyword(s):  
B Cell ◽  
Hodgkin Lymphoma ◽  
World Literature ◽  
Cell Lymphoma ◽  
Pediatric Population ◽  
B Cell Lymphoma ◽  
Large Cell ◽  
Frequent Relapses ◽  
Ann Arbor ◽  
Hodgkin's Lymphomas

Nodular lymphocyte predominant Hodgkin lymphoma (NLHLP) – B-cell lymphoma, which has been historically added to the group of Hodgkin's lymphomas, despite the peculiarities of the clinical course, treatment and prognosis, as well as morphological and immunophenotypical differences. In 75% of cases, the disease is detected at early stages (I–II according to Ann Arbor classification), has an indolent course and a favorable prognosis with 10-years an overall survival rate, more than 80%. Despite this, with long-term follow-up and the development of frequent relapses, transformation into diffuse large-cell B-cell lymphoma (DCBCL) or T-lymphocyte/histiocyte-rich DCBCL can occur, isolated cases in children. In the world literature, there are isolated cases of the development of NLHLP after treatment of DCBKL in adults, while among the pediatric population, cases have not been described. This article presents a clinical case of DCBKL in a 10-year-old child who, 5 years after the end of treatment, developed nodular Hodgkin's lymphoma with lymphocytic predominance. The patient's parents agreed to use the information, including the child's photo, in scientific research and publications. 

scholarly journals Amplification of genomic DNA demonstrates the presence of the t(2;5) (p23;q35) in anaplastic large cell lymphoma, but not in other non- Hodgkin's lymphomas, Hodgkin's disease, or lymphomatoid papulosis

Blood ◽  
1996 ◽  
Vol 88 (5) ◽  
pp. 1771-1779 ◽  
Author(s):  
AH Sarris ◽  
R Luthra ◽  
V Papadimitracopoulou ◽  
M Waasdorp ◽  
MA Dimopoulos ◽  
...  
Keyword(s):  
Anaplastic Large Cell Lymphoma ◽  
Hodgkin's Disease ◽  
Genomic Dna ◽  
Cell Lymphoma ◽  
Hodgkin’S Disease ◽  
Large Cell ◽  
Lymphomatoid Papulosis ◽  
Large Cell Lymphoma ◽  
Hodgkin's Lymphomas ◽  
Dna Pcr

Anaplastic large cell lymphoma (ALCL) is a distinct clinicopathologic variant of intermediate grade non-Hodgkin's lymphomas (NHL) composed of large pleomorphic cells that usually express the CD30 antigen and interleukin (IL)-2 receptors, and is characterized by frequent cutaneous and extranodal involvement. With variable frequency ALCL bear the t(2;5)(p23;q35) chromosomal translocation that fuses the nucleophosmin (NPM) gene on chromosome 5q35 to a novel protein kinase gene, Anaplastic Lymphoma Kinase (ALK), on chromosome 2p23. We determined the frequency of this translocation with a novel DNA polymerase chain reaction (PCR) technique using 0.5 microgram of genomic DNA, 5′-primers derived from the NPM gene and 3′-primers derived from the ALK gene and hybridization with internal probes. The presence of amplifiable DNA in the samples was tested with the inclusion in the PCR reaction of oligonucleotide primers designed to amplify a 3016-bp fragment from the beta-globin locus. NMP-ALK fusion amplicons were detected using DNA isolated either from all three ALCL cell lines tested, or from all four primary ALCL tumors known to contain the t(2;5)(p23;q35) translocation. Nested amplicons were detected by hybridization in 100% of specimens diluted 10(4)-fold and in 20% of those diluted 10(5)-fold. We subsequently examined archival genomic DNA from 20 patients with ALCL, 39 with diffuse large cell, 2 with mantle cell, 20 with peripheral T cell, 13 with low-grade NHL, 31 with Hodgkin's disease (HD), and 6 with lymphomatoid papulosis. Fusion of the NPM and ALK genes was detected in three of 18 patients with ALCL who had amplifiable DNA (17%, 95% confidence intervals 4% to 41%), but not in any patients with other NHL, HD, or lymphomatoid papulosis. The amplicon sizes were different in all cell lines and patients reflecting unique genomic DNA breakpoints. We conclude that with genomic DNA-PCR the rearrangement of the NPM and ALK loci is restricted to patients with ALCL. Further studies are needed to determine the prognostic significance of the NPM-ALK rearrangement, to determine whether its detection can aid in the differential diagnosis between ALCL. Hodgkin's disease, and lymphomatoid papulosis, and to establish the usefulness of the genomic DNA PCR in the monitoring of minimal residual disease in those patients whose tumors bear the t(2;5).

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