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

Lymph nodes from patients with Hodgkin's disease of the nodular sclerosis or mixed cellularity type were examined by electron microscopy to classify all the cells that occur in these types of lymphoma. Most of the cells showed morphological features that were the same, or nearly the same, as those of cells of normal lymphoid tissue. These included typical interdigitating reticulum cells (IDC), histiocytic reticulum cells, so-called dark reticulum cells, and sinus macrophages. There were also small and medium-sized lymphocytes, immunoblasts, plasma cells, and plasma cell precursors resembling those seen in non-specific lymphadenitis. Germinal center cells, on the other hand, were present in negligible numbers. Special attention was paid to Hodgkin's (H) and Sternberg-Reed (SR) cells. This group of cells proved to be heterogeneous. The only common features were a large cell size, large nuclei, and a prominent nucleolus. Some of the H and SR cells resembled immunoblasts of normal lymphoid tissue. The cytoplasm of these cells contained numerous polyribosomes, and their heterochromatin was coarsely condensed at the nuclear membrane. Other H and SR cells were more similar to histiocytic cells or reticulum cells because of the large number of cell organelles (e.g., lysosome-like granules) and diffuse heterochromatin. Finally, cases of the nodular sclerosis type of Hodgkin's diseases showed another cell type with some resemblance to IDC. The cells of this type are called lacunar cells because of their special light-microscopic appearance.
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PMID:Electron-microscopic aspects of Hodgkin's disease. 727 67

Local tumor growth has been reported after subcutaneous and intraperitoneal injection of Hodgkin's disease (HD) derived cell lines into different immunodeficient mouse strains. An animal model with disseminated growth of tumor cells would be useful for studying the in vivo biology of HD cells as well as for preclinical testing of new therapeutic regimens. For this purpose the HD-derived cell lines L540, L540cy, L428, and KM-H2 were injected intravenously into SCID mice. In contrast to L428 and KM-H2, widespread neoplasia occurred after a period of four to six weeks following injection of L540 and the subline L540cy. Lymph nodes were found to be the preferred site of tumor growth. CD30 surface antigen expression on Hodgkin cells and the karyotype of the tumor cells were preserved in the animal host. Thus, to a large extent, the SCID mouse model mimics the dissemination pattern of Hodgkin's disease in man. To evaluate the role of adhesion molecule expression in the dissemination of HD-derived cell lines, CD44 and members of the immunoglobulin, integrin, selectin, and Fc receptor families were quantified by flow cytometry. CD30 expression was also measured. Although CD44 expression has been correlated with dissemination in non-Hodgkin's lymphoma (NHL), this was not the case in the Hodgkin's SCID mouse model. CD44 was not expressed on the disseminating cell lines L540 and L540cy but was expressed in the nondisseminating lines L428 and KM-H2.
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PMID:Disseminated growth of Hodgkin's-derived cell lines L540 and L540cy in immune-deficient SCID mice. 751 37

Hodgkin's disease is a lymphoma which occurs in man in the lymph nodes or in extra-lymphatic tissue. The disease was first described in 1832 by Thomas Hodgkin, a British physician. The disease develops with different patterns of histology in several types which a varying degree of malignancy: stages of the disease processes may be encountered. Lymph nodes appear phylogenetically first in the mesentery of crocodiles and reach the top of their development in the mammal. Here they are important during the neoplastic development as regional stations thereof. The treatment, depending on the cellular make-up of the type, may vary from advantageous to very toxic. Successful treatment in several cases on the one hand, in contrast to high therapeutic toxicity, and the development of secondary neoplasms on the other, are outlined.
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PMID:Hodgkin's disease: treatment and secondary neoplasms. 772 20

To optimize the immunohistochemical detection of the multidrug resistance (MDR)-associated P-glycoprotein (P-gp) in chronic lymphoid disorders, the authors compared the sensitivity of three different monoclonal antibodies (MoAb) directed against P-gp (C219, JSB-1, and MRK 16) by using the APAAP technique on four tissue preparations obtained from lymphoid tumors: Cryostat sections, ModAMEX processed sections, frozen cytospin preparations, and fresh cytospin preparations. Tumor samples were obtained from patients with previously treated chronic lymphocytic leukemia (6 cases) or non-Hodgkin's malignant lymphoma (4 cases). Lymph nodes (n = 9), spleen (n = 3), and blood (n = 5) were analyzed. JSB-1 MoAb detected P-gp in 4 of 12 cases (33.3%) on either frozen sections or ModAMEX processed sections, and in 6 of 17 cases (35.3%) on frozen cytospin preparations. The sensitivity of JSB-1 was significantly improved when fresh cytospin preparations were used with an incidence of P-gp positive samples as high as 70.6% (P < .05). C219 MoAb was unreactive with lymphoid cells whatever the technique used, whereas this antibody stained stromal cells. MRK 16 MoAb was equally reactive to JSB-1 on fresh cytospin preparations, but unreactive when the other preparations were used. The specificity of JSB1 MoAb was confirmed by both Western blot analysis and Rhodamine 123 efflux assay. The authors used JSB-1 MoAb on fresh cytospin smears prepared from 28 CLL patients. Overall incidence of P-gp positive cases was 39.2%. Univariate analysis showed that P-gp expression was correlated with prior therapy, refractoriness to treatment, Rai stratification, and time of tissue storage after diagnosis. The authors recommend the use of JSB-1 on fresh cytospin preparations for the immunocytochemical detection of P-gp in chronic lymphoid disorders.
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PMID:Optimization of immunohistochemical detection of P-glycoprotein in chronic lymphoid disorders. 780 2

We describe nine patients who initially developed non-Hodgkin's lymphoma and subsequently developed Hodgkin's disease. The median interval from the diagnosis of non-Hodgkin's lymphoma (NHL) to the diagnosis of Hodgkin's disease (HD) was 5 years (range, 2-12 years). The median age of the patients at time of diagnosis of NHL was 54 years (range, 27-81 years). Seven of nine cases (78%) of NHL were primarily nodal. According to the Working Formulation, seven NHL were follicular (two small cleaved cell, three mixed small and large cell, two large cell), one was diffuse large cell, and one was large cell immunoblastic. All NHL had histologic or immunophenotypic findings indicative of B-cell lineage. Seven of the nine patients were treated in a nonuniform manner: four with chemotherapy and three with chemotherapy and radiation therapy. At the time of HD, the median age of the patients was 59 years (range, 35-85 years). Lymph nodes were involved in all patients. Six HD biopsies were subclassified as nodular sclerosis, one as mixed cellularity, and two cases were not further subclassified. Immunophenotypic studies revealed that the Reed-Sternberg and Hodgkin cells were LeuM1 or BerH2 positive and LCA negative in eight of nine biopsies, supporting the histologic diagnosis. These results further demonstrate that patients with NHL may subsequently develop HD. The NHLs are usually of B-cell lineage. The results also emphasize the need for rebiopsy in patients with NHL who experience an apparent clinical relapse.
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PMID:Hodgkin's disease following non-Hodgkin's lymphoma. A clinicopathologic and immunophenotypic study of nine cases. 827 24

Castleman's disease (CD) is characterized by lymph node enlargement due to hyperplasia of abnormal lymphoid follicles and paracortical lymphocytic hyaline vascular (HV) stroma or plasmacytosis (PC). The lymphoid follicles in CD show involuted germinal centers and prominent mantle zone lymphocytes. Ninety-seven cases clinically suspected to be CD were analyzed according to conventional histologic criteria established by Castleman and Keller for diagnosis. Twenty-two cases were excluded as nonspecific hyperplasia (12); Hodgkin's and non-Hodgkin's lymphoma (9); and multiple myeloma involving lymph node paracortex (1). The 75 remaining cases, consisting of 51 cases of CD and 24 with altered follicles or paracortex suggestive of CD, were further analyzed immunohistologically for changes in follicular dendritic reticulum cells (FDRC) using the monoclonal antibody Ki-M4p, for germinal center proliferation with Ki-S5, for mantle zone immunophenotype with Ki-B3 and Ki-B5, for paracortical plasmacytoid monocytes with Ki-M1p, and for plasma cell clonality by applying antibodies to kappa and lambda immunoglobulin light chains. Lymph nodes showing nonspecific follicular and paracortical hyperplasia were included as controls. Hyaline vascular CD and plasma cell CD showed enlarged, polyploid FDRC with prominent nucleoli, decreased germinal center proliferation, and mantle zone populations of immunophenotypically aberrant, Ki-B3-negative B lymphocytes. Thirty-seven percent of hyaline vascular CD and plasma cell CD contained plasmacytoid monocytes, and 15% showed interstitial areas of lambda predominant plasma cells. Plasmacytoid monocytes were common in hyaline vascular CD but rare in plasma cell CD. Cases suspected to be CD that demonstrated a mantle zone population of Ki-B3-negative B lymphocytes had clinical finding of POEMS (polyneuropathy, organomegaly, endocrinopathy, monoclonal paraprotein, and skin changes or sclerotic bone lesions) syndrome and were reclassified as hyaline vascular CD, plasma cell CD, and mantle zone CD with an aberrant mantle zone immunophenotype only (lacking follicular center and paracortical histologic or immunohistologic abnormalities). Immunohistochemistry was valuable for identification of dysplastic FDRC, decreased germinal center proliferation, and plasmacytoid monocytes. In addition, immunohistochemistry was essential for detection of plasma cell clonality, an aberrant mantle zone immunophenotype, and mantle-zone-restricted CD that was devoid of diagnostic alterations of germinal center or paracortex.
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PMID:Diagnosis of Castleman's disease by identification of an immunophenotypically aberrant population of mantle zone B lymphocytes in paraffin-embedded lymph node biopsies. 860 6

This study compares the histologic and immunophenotypic features of 71 cases of primary CD30+ diffuse large-cell lymphomas (DLCL) and 128 cases of Hodgkin's disease (HD) and discusses the clinical features of 52 patients with CD30+ DLCL. It includes analysis of sites of involvement, staging, response to treatment, sites and treatment of recurrences, and disease-free and overall survival. Diagnostic immunophenotypic differences were found between CD30+ DLCL and HD. All cases of CD30+ DLCL were positive for one or more common or lineage-specific lymphocyte antigens or for EMA. In contrast, 96.9% of HD cases were negative for CD45, CD45-RO, CD43, and CD20. The four exceptions are discussed. All cases of HD were negative for EMA. In patients with CD30+ DLCL, a T-cell phenotype was found in 60%, a null-cell type in 22%, and a B-cell type in 18% of the cases. The median age of patients with T- and null-cell phenotype was 22 years (range, 4 to 72). Fifty-two percent of them had high-stage (III and IV) disease and 61% had extranodal involvement at presentation, including 25% with skin lesions. Lymph nodes draining the skin lesions became involved in seven of 11 patients. No patient had initial bone marrow involvement. Most patients were treated with chemotherapy, and 83% had a complete remission. Fifty-four percent remain free of disease with a median follow-up of 47 months. Thirteen patients (29%) had one or more recurrences and five of them remain free of disease after salvage therapy, with a median follow-up period of 79 months. The clinical stage did not affect survival, probably as a result of different therapy. The t(2;5) translocation was found in five of 15 patients who had cytogenetic abnormalities. Of the other 10 cases, the translocation was detected by reverse transcriptase-polymerase chain reaction (RT-PCR) in four of five cases studied. All nine cases were of T- or null-cell phenotype. The cases of B-cell CD30+ DLCL had a characteristic immunophenotype. All were negative for EMA. These patients were older and had frequent bone marrow involvement but no skin infiltration by lymphoma. All three patients who were human immunodeficiency virus-positive (HIV+) had lymphomas of B-cell lineage. Detection of the t(2;5) translocation by molecular genetics is a useful and highly specific marker in the differential diagnosis between HD and CD30+ DLCL.
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PMID:CD30 (Ki-1)-positive malignant lymphomas: clinical, immunophenotypic, histologic, and genetic characteristics and differences with Hodgkin's disease. 863 11

This retrospective work aims to analyse the incidence and the radiologic features of initial thoracic involvement of lymphomas, observed in 320 patients selected among 1,153 lymphomas (640 Hodgkin's diseases and 513 non-Hodgkin's lymphomas). Thoracic involvement was not observed in 833 (72%) patients with lymphoma. In Hodgkin's disease (HD) (n = 200) thoracic involvement was observed in 31% (200/640). The mediastinal lymph nodes were noted in 99.5% and predominated in the superior and mid mediastinum in 84.5%. Mediastino-thoracic ratio was superior to 0.33 in 33.5%. Unilateral paratracheal nodes were involved in 26% and the hilar groups in 39.5%. The lung involvement was present in 26.5%, such as nodules in 11% and alveolar infiltration in 6.5%. In the cases with lung involvement, there were concomitant mediastinal lymph nodes. Pleural and pericardial effusions were seen in 23.5% and 4%. Parietal involvement was noted in 1%. In non-Hodgkin's lymphomas (NHL) (n = 120) thoracic involvement was observed in 23% (120/513). The mediastinal lymph nodes were seen in 82.5%, located in superior and mid mediastinum in 60%. Mediastino-thoracic ratio was superior to 0.33 in 47%. Lymph nodes were unilateral paratracheal in 7.5% and hilar in 18%. The posterior mediastinal lymph nodes group was involved in 2%. Lung involvement was noted in 24%, pleural effusion in 48%, pericardial effusion in 4% and parietal involvement in 2.5%. In the cases of thoracic involvement in HD, mediastinal lymph nodes involvement is constant, affecting commonly the anterior mediastinal, paratracheal and hilar groups. Involvement of the posterior mediastinum and paracardiac groups is more common in NHL. Thoracic computed tomography is helpful in the detection of the abnormalities misdiagnosed on the chest X-ray. Computed tomography is valuable in the initial stages of HD because it can modify the treatment in 15%.
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PMID:[Radiological features of thoracic localizations of lymphomas]. 903 3

Tumor necrosis factor-alpha (TNF-alpha) is a potent pro-inflammatory cytokine and mediator of the inflammatory response. It has been implicated in the pathogenesis of many inflammatory disorders, including rheumatoid arthritis (RA), septic shock, and Crohn's disease. Using a specific anti-human TNF-alpha antibody we detected immunoreactivity for this cytokine in the cytoplasm of inflammatory cells in several chronic inflammatory disorders, including RA, scleritis, and polyarteritis nodosa. These cells were identified predominantly as IgG-expressing plasma cells. Lymph nodes from patients with Hodgkin's lymphoma and breast cancer, but not from control subjects, were also found to contain TNF-alpha-positive plasma cells. Cultured EBV-B lymphocytes and a human plasma cell line (ARH-77) when stimulated with phorbol myristate acetate demonstrated cytoplasmic TNF-alpha immunoreactivity. Western blot analysis of cell membranes and conditioned media from both cell types revealed the presence of the 26-kDa membrane-bound from and the 17-kDa soluble from of TNF-alpha, respectively. TNF-alpha was quantitated by enzyme-linked immunosorbent assay and found to be biologically active as determined by the L929 cytotoxicity assay. This is the first demonstration that plasma cells may be capable of modulating immune and inflammatory responses, not only by antibody production, but also by their secretion of a key inflammatory mediator, TNF-alpha.
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PMID:Expression of TNF-alpha by human plasma cells in chronic inflammation. 920 Dec 57

Lymph nodes from the incipient or early neoplastic phase of adult T-cell leukemia/lymphoma (ATLL) histologically resemble Hodgkin's disease. Integrated proviral human T-lymphotrophic virus type I (HTLV-I) has been demonstrated in such lesions. We studied 18 patients with this disease, and about half of the cases developed typical ATLL within 2 or 3 years. In all cases, either mono- or oligoclonal cell populations with proviral HTLV-I DNA were detected by Southern blot analysis and/or inverse polymerase chain reaction (IPCR). In addition, either a mono- or oligoclonal rearrangement of T-cell receptor genes was demonstrated. Giant cells with Reed-Sternberg-like histological features revealed CD15 and CD30 positivity. The background infiltrating lymphocytes represented either no or only minimal nuclear abnormalities with a CD4+ T-cell phenotype. In less than half of all cases, Epstein-Barr virus (EBV) infected the giant cells. A mixed EBV-A and -B type was found in 3, and a multiple genotype of EBV lymphocyte-determined membrane antigen (LYDMA) was found in 6 cases. These results could have been due to the immunodeficient status of the patients. A single-cell PCR of the giant cell, B cell, CD4+ or CD8+ T cells could be performed after cell sorting in 4 cases. HTLV-I infection was frequently found in the CD4+ T cells, but in neither the giant cells nor the B cells. The CD4+ T cells exhibited clonality. The giant cells showed various PCR products of IgH, and also expressed recombination activating genes (RAG). In summary, the giant cells were reactive cells, which resembled the immature B-lineage cells, while HTLV-I infected the CD4+ T cells, which demonstrated clonality. Based on these above findings, we consider CD4+ cells to play an important role in ATLL tumorigenesis.
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PMID:Clonal HTLV-I-infected CD4+ T-lymphocytes and non-clonal non-HTLV-I-infected giant cells in incipient ATLL with Hodgkin-like histologic features. 925 96


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