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

Histologic and paraffin immunohistologic studies were carried out on 32 patients with lymphocyte-predominance Hodgkin's disease (LPHD) seen from 1970 through 1982. While nodular histology was accurately predictive of B-cell phenotype (Leu M1 -/L26+), diffuse histology corresponded to either B-cell or Hodgkin's (Leu M1 +/L26-) phenotype, not invariably predictable even when attention was paid to subtle paragranuloma cytology. Clinical characteristics were compared between histologic (diffuse v nodular) and immunophenotypic (Leu M1 +/L26-, Hodgkin's phenotype, v Leu M1 -/L26+, B-cell phenotype) subgroups. Ten patients have since died, and the median follow-up of the living patients was 14 years (range, 6 to 31). Of the several clinical parameters compared, only axillary nodal presentation was strongly associated with both B-cell phenotype and nodular histology, while male predominance related more to B-cell phenotype than nodular histology. No significant difference in overall survival or relapse rate was apparent among either the histologic or the immunophenotypic subgroups. However, very late but salvageable relapses were associated with nodular histology. The incidences of secondary malignancies and death from Hodgkin's disease (HD) were also comparable between the subgroups. Although difference in clinical presentation may exist, neither the histologic nor the immunophenotypic subcategories of LPHD could be demonstrated to correlate with differences in clinical outcome.
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PMID:Clinical correlates of distinct immunophenotypic and histologic subcategories of lymphocyte-predominance Hodgkin's disease. 223 Aug 88

Five cases of nodular, lymphocyte predominant Hodgkin's disease (nLP HD), in which an association with (n = 3) and transformation to (n = 2) large cell lymphoma (LCL) were found, were studied with monoclonal antibodies against B-, T-, and Reed-Sternberg (R-S) cell-associated antigens and epithelial membrane antigen (EMA) on paraffin sections. Both lymphocytic (L) and histiocytic (H) cells of nLP HD and lymphoma cells of LCL expressed multiple B-cell-associated antigens (detected by LN-1/CDw75, L26, MB2, DBB.42, DBA.44, DND.53, DNA.7 antibodies) but did not react with antibodies against T-cell-associated (MT1, UCHL1/CD45RO) (one exception for CD45RO in LCL) and R-S cell-associated (Leu-M1/CD15, Ber-H2/CD30) antigens. EMA was expressed by L and H cells in all cases and conserved in LCL cells, emphasizing the frequent expression of EMA by the diagnostic cells of nLP HD. An antibody (BNH9) against blood group-related antigens (H and Y oligosaccharide antigens) that does not normally react with lymphoid cells was found to be reactive with few L and H cells in two of five and most LCL cells in four of five cases. The finding might be indicative of abnormal activation of lymphoid cells. The data reinforce current implications that nLP HD is a B-cell malignancy in evolution and that it is not truly representative of Hodgkin's disease in terms of biological and clinical behavior.
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PMID:Further phenotypic evidence that nodular, lymphocyte-predominant Hodgkin's disease is a large B-cell lymphoma in evolution. 224 Mar 55

Patients with Hodgkin's Disease (HD) occasionally develop monomorphic lymphomas in which mononuclear cells, usually large in size, grow in sheets, and in which there are few reacting cells or classic Reed-Sternberg (RS) cells. Twelve patients of this type were reviewed to determine the nature of the monomorphic growth. Paraffin-embedded tissue sections from the original diagnostic HD and the monomorphic growths were stained for Leu-M1 (CD15), leukocyte common antigen (LCA, CD45), pan B-cell markers LN1, LN2, and L26, and pan T-cell marker UCHL1 (CD45R) reactive in paraffin-embedded tissues. Cases were included only if the original diagnostic material had the classic histopathologic features of HD, if there was a separate monomorphic growth (in place or time), and if sufficient materials from both phases were available for study. Original diagnoses of HD included nodular sclerosing (NS; 8 cases); lymphocyte predominant (LP; 2 cases); mixed cellularity (MC; 1 case); and lymphocyte depleted (LD: 1 case) types. RS cells in the eight cases of NS HD and one case of MC HD were generally Leu-M1 and LN2 positive, and L26, LN1, UCHL1, and LCA negative. RS cells in one case of NS HD were LCA positive in addition to Leu-M1, LN1, and LN2. Two cases of NS HD showed L26 positive RS cells. Conversely, RS cells and lymphocytic-histiocytic (L and H) variants in the cases of LP HD were Leu-M1 and LN2 negative, and LCA and LN1 positive. The one case of LD HD possessed RS cells that were negative for Leu-M1, but positive for LCA, L26, LN1, and LN2. In seven cases (4 NS, 2 LP, 1 LD) the monomorphic growths possessed a B-cell phenotype (LCA, L26, and LN1 positive; Leu-M1 and UCHL1 negative). In the remaining cases (4 NS, 1 MC), the monomorphic growths were Leu-M1 positive, and displayed phenotypes similar to the RS cells of the original NS HD. Southern blot analysis was performed on the monomorphic components of five cases and showed some form of immunoglobulin gene rearrangement in each (4 cases: rearranged heavy chain-joining region gene; 1 case: rearranged Mu chain-constant region gene). Two of these cases expressed L26 and LN1 in the monomorphic phases. Despite apparent immunoglobulin gene rearrangement, one case expressed T-cell antigens Leu-4 (CD3) and Leu-1 (CD5), in addition to Leu-M1 (CD15).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Monomorphic lymphomas arising in patients with Hodgkin's disease. Correlation of morphologic, immunophenotypic, and molecular genetic findings in 12 cases. 229 52

Lymph node biopsies from 57 local and referred cases, previously diagnosed at Southampton between 1978 and 1987 as lymphocyte predominance Hodgkin's disease were examined using the monoclonal antibodies MT1, UCHL1, L26, LN-1, E29/68 (EMA), Leu-M1 (CD15) and Ber-H2 (CD30). Of the 34 cases with a nodular architecture, 21 (19 male, two female) contained polylobated Reed-Sternberg cell variants with a B-cell phenotype, which lacked expression of CD15. In all cases, the polylobated cells showed positive staining with L26 and LN-1. Six cases expressed EMA and three showed positive staining with Ber-H2. Two cases lacking polylobated cells were reclassified as reactive follicular hyperplasia with progressive transformation of germinal centres. The remaining 11 cases had an atypical immunophenotype and were reclassified, mainly as mixed cellularity Hodgkin's disease. In six cases, the lymph node architecture showed a mixture of nodular and diffuse growth patterns. Five of these cases contained polylobated cells with the typical morphology and immunophenotype of those seen in nodular lymphocyte predominance Hodgkin's disease. The sixth case contained cells expressing CD15, and was reclassified as nodular sclerosing Hodgkin's disease. Of the fifteen biopsies with a diffuse architecture, four contained polylobated B-cells lacking expression of CD15. These were considered to be diffuse lymphocyte predominance Hodgkin's disease. The remaining 11 cases were reclassified as either Hodgkin's disease, mixed cellularity or as T-cell lymphomas.
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PMID:Lymphocyte predominance Hodgkin's disease--an immunohistochemical study. 232 37

The histologic and immunologic features of an unusual morphologic expression of nodular sclerosing Hodgkin's disease, which ahs been termed the "syncytial variant," are described. In biopsy material from 18 cases, numerous Reed-Sternberg cell variants were observed in sheets and cohesive clusters, and at least focal evidence of nodular sclerosis was present in each case. The granulocyte antibody anti-Leu M1 reacted with antigenic determinants in Reed-Sternberg cells and atypical variants thereof in 13 of the 18 cases; the lack of staining with antibodies reactive with the leukocyte common (T200) antigen (PD7/26), keratin (AE1), and S100 protein (polyclonal anti-S100) was helpful in excluding non-Hodgkin's lymphoma, carcinoma, and melanoma, respectively. This unusual form of nodular sclerosing Hodgkin's disease is important to recognize, since it may simulate metastatic neoplasms, thymoma, and non-Hodgkin's lymphoma.
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PMID:The "syncytial variant" of nodular sclerosing Hodgkin's disease. 242 45

Leu-M1, or MMA, originally was proposed as a differentiation antigen on myelomonocytic cells and was said to be useful as an aid in distinguishing lymphoid from myeloid leukemias. Subsequently, it was proposed by Hsu and Jaffe as a useful marker of Reed-Sternberg cells and their variants in paraffin-embedded sections in Hodgkin's disease and as an aid in the differential diagnosis among Hodgkin's disease, non-Hodgkin's lymphomas, and reactive lymphoid proliferations. In order to test the usefulness of this antibody in classifying acute leukemias and to investigate the spectrum of its positivity on B5 and/or formalin-fixed, paraffin-embedded tissue sections, a variety of benign and neoplastic hematopoietic and lymphoid disorders were studied, using Leu-M1 and the ABC immunoperoxidase technic. Definite positivity in neoplastic cells was present in 4 of 16 patients with acute nonlymphocytic leukemias, 0 of 9 patients with acute lymphocytic leukemias/lymphoblastic lymphoma, 11 of 13 patients with Hodgkin's disease, and 0 of 18 patients with non-Hodgkin's lymphomas. Granulocyte staining could be identified in many cases. Although not identified in tonsillar sections from three patients, variable numbers of sometimes large mononuclear and rare binucleate cells were identified in some of the 14 reactive lymph nodes studied as well. These data, together with other data recently reported, suggest that in routinely processed tissue sections, Leu-M1 is a relatively sensitive marker for Hodgkin's disease, but it does not appear to be specific for that diagnosis. Although marking some acute nonlymphocytic leukemias in tissue sections, its lack of sensitivity and possible lack of specificity severely limits its usefulness in classifying the acute leukemias.
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PMID:The spectrum of Leu-M1 staining in lymphoid and hematopoietic proliferations. 242 38

Ten cases of "undifferentiated" large-cell tumors were ultrastructurally characterized by cells with abundant filiform cytoplasmic projections without intercellular junctions. These cases were studied by means of the avidin-biotin-peroxidase complex (ABC) technique applied to formalin-fixed, paraffin-embedded sections using antibodies against high- and low-molecular weight keratins (Ker), vimentin (Vi), epithelial membrane antigen (EMA), S-100 protein, leucocyte common antigen (LCA), kappa (K) and lambda (L) light chains, Leu-M1, lysozyme (Ly), alpha-1 antitrypsin (A1AT) and alpha-1 antichymotrypsin (A1ACT). All 10 cases were negative for Ker and EMA but positive for Vi. S-100 was present only in scattered dendritic cells. LCA was identified in seven cases. In the three LCA-negative cases, two stained for Leu-M1, and one of these also showed intracytoplasmic L; one was negative for all markers but Vi. None of the tumors showed any significant staining for Ly, A1AT, or A1ACT. Our findings indicate that these tumors are nonepithelial and nonneuroectodermal, and that they are best classified as non-Hodgkin's lymphomas. The possibility that some of the filiform large-cell lymphomas may be derived from dendritic reticular cells cannot be excluded.
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PMID:Filiform large-cell lymphomas. An ultrastructural and immunohistochemical study. 243 14

An increased incidence of high-grade malignant non-Hodgkin's lymphomas has been reported in homosexual men. This phenomenon appears to represent another facet of the acquired immunodeficiency syndrome (AIDS). Histologically, the majority of these lymphomas have been small noncleaved cell lymphomas or immunoblastic lymphomas, subtypes most commonly associated with a B-cell phenotype, but immunologic data supporting this have been limited. Using a plastic embedding technique, we have examined a series of 31 malignant lymphomas, including nine from the central nervous system (CNS), in patients with AIDS or at high risk for AIDS. All 31 of the lymphomas were positive with one or more of the following B-cell markers: HLA-DR/la, Pan B, Leu 12, Leu 14, and IgM. All 31 were negative for the pan-T reagent Leu 4 and myeloid-macrophage markers (Leu M1, nonspecific esterase). In addition, seven of the nine CNS lymphomas showed strong plasma membrane staining for adenosine triphosphatase, a B-associated marker. These findings provide strong immunologic evidence for a B-cell origin in the lymphomas of AIDS.
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PMID:Malignant lymphomas in the acquired immunodeficiency syndrome. Additional evidence for a B-cell origin. 245 89

Malignant lymphomas occurring in patients with AIDS are usually derived from the B-cell lineage while T-cell malignant lymphomas are very rare in these patients. We report a HIV seropositive 29-year-old homosexual man in whom cervical lymph node biopsy showed an atypical lymphoproliferative process. On morphological and paraffin section immunohistochemical grounds the possibility of Hodgkin's disease (HD) mixed cellularity was initially suggested, but frozen section immunohistochemical studies revealed that the cellular infiltrate exhibited an aberrant pan T immunophenotype and consequently the diagnosis of peripheral T-malignant lymphomas (T-ML) was made. However, genotypic studies would be required to definitely confirm this diagnosis, in such cases. In our case, varying numbers of small and medium-sized cells were positive for both Leu 3/CD4 and Leu 2/CD8 whereas some large cells reacted only with Leu 3/CD4 antibody. Some medium-sized, large and giant cells showed cytoplasmic positivity for Leu M1/CD15. Furthermore, the positivity of many large and giant cells with the activation markers BerH2/CD30, Ki-1/CD30, Tac/CD25 and HLA-DR suggested an activation state for these cells. Our findings emphasize the usefulness of frozen section immunohistochemical methods in order to investigate the spectrum of lymphoid malignancies occurring in HIV seropositive patients, and confirm results of previous studies which stressed the diagnostic difficulties that may appear in distinguishing HD from peripheral T-ML.
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PMID:Peripheral T-cell lymphoma or Hodgkin's disease in a HIV seropositive patient: a histopathological study. 248 99

We report an autopsy case of malignant histiocytosis. The clinical course was rapidly progressive and terminated with jaundice and respiratory failure. Histologically, there was diffuse infiltration of large atypical cells in the liver, spleen, lymph nodes and bone marrow. It was of interest that these tumor cells contained a number of bizarre multinucleated cells histologically indistinguishable from Reed-Sternberg cells of Hodgkin's disease, and that these atypical cells expressed DAKO M1 (identical to Leu M1) and Ki-1 antigens and also showed binding to peanut agglutinin (PNA), representative markers of Reed-Sternberg cell. An absence of epithelial membrane antigen and presence of Leu M1 antigen in the tumor cells made a diagnosis of Ki-1 lymphoma unlikely. This case study showed that giant or pleomorphic cells indistinguishable histologically and phenotypically from Reed-Sternberg cells occur in malignant histiocytosis.
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PMID:An autopsy case of malignant histiocytosis with Reed-Sternberg-like cells. 254 Jun 13


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