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Query: UMLS:C0019829 (Hodgkin's disease)
 30,247 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In recent years, techniques, probes, and reagents became available to reliably visualize individual Epstein-Barr virus (EBV)-infected cells, to assess EBV gene expression, and to analyze the clonal composition of EBV genomes in human tissues. Application of these techniques to more than 1000 lymphoid tissue specimens revealed (1) characteristic cellular and compartmental distribution patterns of EBV-infected cells in normal lymph nodes, reflecting the interference of EBV with physiologic B cell differentiation pathways, (2) an association of EBV with various mono- and oligoclonal lymphoproliferations ranging from benign conditions to overtly malignant lymphomas, and (3) characteristic patterns of EBV gene expression among EBV-associated lymphoproliferations. In the context of the established immortalizing and transforming properties of EBV, the findings support the concept of an etiologic role of EBV for cases of certain lymphomas such as Burkitt's lymphoma, anaplastic large cell lymphoma, Hodgkin's disease, and lymphomas arising in immunocompromised individuals. In contrast, lymphomas harboring EBV in only proportions of the tumor cells (such as cases of peripheral T cell lymphoma and some B cell lymphoma types) argue against an etiologic role in the primary process of malignant transformation for the virus in these instances. Since in many of these cases a proportion of the EBV infected tumor cells express the EBV oncoprotein LMP (latent membrane protein) the virus may influence, however, the proliferative properties as well as the morphological and molecular phenotype of the neoplastic cells.
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PMID:[Epstein-Barr virus associated lymphocyte proliferation]. 128 80

Immunoscintigraphy (IS) using the HRS-3 Hodgkin associated monoclonal antibody (MoAb) was performed in 18 patients with Hodgkin's Disease (HD) at staging or restaging. Either F(ab')2 fragments (14 patients) or whole HRS-3 (4 patients) labeled with 77-260 Mbq 131-I were used. Whole body images, including anterior and posterior views, were taken from a digital gamma camera, within 4 to 8 hours after injection and then daily for 5 days. In one patient IS was discontinued due to iodine intolerance. Seventeen patients were evaluable: 14 showed a true positive result including 2 cases which were reviewed as anaplastic large cell lymphoma (ALCL). Nodal, splenic, bone marrow and muscle involvements were imaged, many of these sites were previously unsuspected. In 7 patients with true positive findings the Pressman Specificity Index, as measured from biopsied material, ranged from 1.5-3 in 4 patients and from 5 to greater than 100 in 3 patients. Imaging was equivocal or failed in 1 patient (lymph nodes). In 2 patients, IS imaging was truly negative due to the absence of active HD, and a false negative result occurred once (inguinal node). In none of the patients a false positive image was observed. In order to rule out non-specific iodine uptake a control, anti-ACE MoAb, labeled with 125-Iodine was injected simultaneously in 10 patients. The evaluation of the study gave a sensitivity of 87% and a good specificity. IS using radioiodine labeled MoAbs is feasible and represents a reliable non-invasive diagnostic method for the staging and follow-up of HD and ALCL.
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PMID:Immunoscintigraphy in Hodgkin's disease and anaplastic large cell lymphomas: results in 18 patients using the iodine radiolabeled monoclonal antibody HRS-3. 133 72

In Hodgkin's disease, Epstein-Barr virus (EBV) is found in CD30-positive Reed-Sternberg cells. We therefore studied 60 CD30-positive non-Hodgkin's lymphomas (NHLs) for the presence of EBV by the polymerase chain reaction (PCR) and DNA in situ hybridization (DISH), and by immunohistochemistry for the latent EBV proteins LMP and EBNA-2. CD30-negative NHLs and reactive lymph nodes served as controls. The CD30-positive cases comprised 17 anaplastic large cell lymphomas (ALCLs) (> 75 per cent CD30-positive cells) and 43 non-ALCLs (with 5-35 per cent CD30-positive cells). By PCR, 40 of 60 CD30-positive NHLs (67 per cent) were EBV-positive; in CD30-negative cases, 6/29 (21 per cent) were EBV-positive, as were 12/50 (24 per cent) reactive lymph nodes. The DISH procedure demonstrated the EBV genome exclusively in the nuclei of tumour cells in 23 of the 37 PCR EBV-positive cases that were tested. PCR-negative cases were always DISH-negative, as were the PCR-positive reactive lymph nodes and CD30-negative NHLs. Immunohistochemistry demonstrated LMP in neoplastic cells of 7/47 (15 per cent) CD30-positive NHLs, both ALCL and non-ALCL always in PCR EBV-positive cases, but never in the two control groups. EBNA-2 staining could not be detected. It is concluded that EBV is present (and transcriptionally active) in a sizeable number of NHLs and an association between the presence of the EBV genome and CD30 expression seems likely.
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PMID:High incidence of EBV genome in CD30-positive non-Hodgkin's lymphomas. 133 46

In this session there seemed to be general agreement on the existence of anaplastic large cell lymphoma (ALCL) as an entity defined by a characteristic morphology and by diffuse expression of the Ki-1 (CD30) antigen. The discussion indicated the lack of specific immunophenotypic and genotypic markers for such a neoplasm and the variability of the clinical patterns associated with it: these include a childhood form, an adult cutaneous form, and an adult nodal disease. While typical cases of ALCL are clearly distinct (by pathologic, cytogenetic, and clinical criteria) from Hodgkin's disease (HD), there is a variety of histologic and immunophenotypic patterns that overlap those of ALCL and HD; most of these would be classified as HD, lymphocyte depletion (LD) or nodular sclerosis (NS), syncytial subtype. No agreed-upon criteria were found that could consistently define these patterns, nor was an agreement possible on whether they are part of a continuum unifying ALCL and HD or phenotypically similar expressions of different diseases.
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PMID:The distinction of Hodgkin's disease from anaplastic large cell lymphoma. 148 Aug 51

The final Workshop of the meeting focused on cases of Hodgkin's disease (HD) in combination with non-Hodgkin's lymphoma (NHL), either T, B, or anaplastic large cell (ALC) type. The cases selected for this session fell into five categories: nodular lymphocyte-predominance Hodgkin's disease (NLPHD) with NHL, B cell chronic lymphocytic leukemia (CLL) with HD-like transformation, follicular lymphoma (FL) with HD or anaplastic large cell lymphoma (ALCL) (composite or discordant), HD following mycosis fungoides (MF), and HD following ALCL. Taken together, these cases left the participants with the distinct impression that there is likely to be some biological relationship between HD and a variety of T cell and B cell NHL.
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PMID:The relationship between Hodgkin's disease and non-Hodgkin's lymphoma. 148 Aug 53

Anaplastic large cell lymphoma (ALCL) is a high grade non-Hodgkins lymphoma recognized by the expression of the CD30 marker and by its morphology. We report a patient with a 6-year history of a non-specific erythroderma in whom ALCL developed with rapid and fatal dissemination to the lymph nodes and internal organs.
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PMID:Primary cutaneous anaplastic large-cell lymphoma with a prolonged erythrodermic prodrome. 153 5

Attempts to understand the malignant lymphomas have followed two major lines of investigation: attempts to define the relationship of neoplastic lymphoid cells to stages of normal T- and B-lymphocyte differentiation, and attempts to understand the genetic abnormalities associated with malignant transformation. It is hoped that these two lines of investigation will make it possible to define clinically important entities, so that specific treatment strategies can be developed and tested, and will also point the way to new options for treatment and prevention. Despite the advances in immunology of the last two decades, our understanding of the relationships of lymphoma cells to the normal immune system remains incomplete. Techniques of molecular genetics, which initially promised to resolve questions of clonality and lineage, have proven less definitive than had been hoped. Studies in the field of molecular cytogenetics--the study of chromosomal translocations by molecular techniques--have just begun to unravel some of the mysteries surrounding neoplastic transformation and differentiation. As we enter the last decade of the century, small advances continue to chip away at the uncertainties shrouding the malignant lymphomas. Advances in the past year include the subclassification of low-grade B-cell lymphomas, including so-called intermediate lymphocytic lymphoma and extranodal lymphomas of mucosa-associated lymphoid tissue, the classification of T-cell lymphomas, the definition of Hodgkin's disease and its relationship to anaplastic large cell lymphoma, and new techniques for characterizing lymphoid cells in paraffin-embedded tissue sections.
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PMID:Pathology of malignant lymphomas. 166 Nov 68

In this report we analyze the morphological and immunohistochemical findings observed in 5 cases of CD30/Ki-1 positive anaplastic large cell lymphoma, a recently recognized neoplastic entity. In comparison with the Ki-1 lymphomas so far described, these cases showed a fairly large number of Reed-Sternberg-like cells, often admixed with small lymphocytes and occasional eosinophils. Moreover, in all our cases immunohistochemical reactions detected the CD15/Leu-M1 antigen, together with markers of the T-lineage and of lymphoid activation. In previous studies the CD15/Leu-M1 antigen has been found in the majority of cases of Hodgkin's disease, but has been stated to be absent typically in Ki-1 lymphomas. Our results indicate that this antigen cannot be considered a reliable tool to distinguish between Ki-1 lymphomas and Hodgkin's disease. Furthermore, the morphological and immunohistochemical findings reported suggest that in some cases Ki-1 cell lymphoma and Hodgkin's disease may be closely related. They may represent different steps in the progression of the same lymphoproliferative disorder.
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PMID:Anaplastic large cell lymphoma, CD30/Ki-1 positive, expressing the CD15/Leu-M1 antigen. Immunohistochemical and morphological relationships to Hodgkin's disease. 196 60

The authors have examined cellular areas of lymphoma tissue in 28 cases of Hodgkin's disease (HD) or anaplastic large cell lymphoma (ALCL, 'Ki-1 cell lymphoma') to evaluate the boundaries between the two entities. Methods applied included conventional histology; test point analysis; semiautomated morphometry of nuclear profile features of Reed-Sternberg and other atypical large cells (RSALCs); and immunohistochemistry of these elements on all paraffin sections and, in 15 cases, on frozen sections. Mean nuclear profile morphotypes of RSALCs per case varied independently of immunophenotype and histologic diagnosis. Conversely, immunohistochemistry demonstrated significant, although not consistent, preferential positivities of these CD30+ elements for CD15 in HD, and for epithelial membrane antigen (EMA) and CD43 in ALCLs. In the latter, RSALCs also exhibited a tendency for CD45 and CD45RO positivity and for the expression of T-cell-associated antigens. However, there were considerable overlaps. This continuous spectrum of RSALC nuclear profile morphotypes and immunophenotypes, ranging from HD over questionable cases, intermediate between HD and ALCL, to ALCLs, was paralleled by differences in the reactive component of lymphomas. Lymphocytes and granulocytes were significantly deficient in ALCLs.
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PMID:Hodgkin's disease and CD30-positive anaplastic large cell lymphomas--a continuous spectrum of malignant disorders. A quantitative morphometric and immunohistologic study. 217 9

The CD30 antigen has been reported as the immunophenotypic hallmark of a recently described category of non-Hodgkin's lymphoma, termed anaplastic large cell lymphoma. From a series of approximately 500 lymphomas, 17 cases showing typical anaplastic features have been identified. They were strongly labelled by monoclonal antibodies recognizing CD30 (Ki-1 or BerH2). However, 36 other lymphomas, mainly high-grade, of non-anaplastic cytology also expressed CD30, either diffusely or focally, with a staining pattern identical to that seen in anaplastic large cell lymphomas. This clearly suggests that such lymphomas cannot be identified solely on the basis of being high-grade non-Hodgkin's lymphomas showing CD30 positivity. From the present results, the distinction between the anaplastic and non-anaplastic types would be better made with antibodies to epithelial membrane antigen than to CD30. Clinical data, available for 48 of the patients (16 with anaplastic large cell lymphomas and 32 with non-anaplastic) revealed no significant differences with regard to age at presentation, sex or clinical signs. A short-term follow-up study of 25 patients revealed that for the first 2 years after diagnosis there were no significant differences in patient survival between anaplastic large cell lymphoma, other CD30+ high-grade lymphomas and all high-grade non-Hodgkin's lymphomas considered together. These findings, which must be confirmed by larger studies, suggest that in a general lymphoma clinic there is probably little justification for differentiating anaplastic large cell lymphomas or CD30+ lymphomas from other high-grade non-Hodgkin's lymphomas.
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PMID:CD30 expression in non-Hodgkin's lymphoma. 217 74


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