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

We studied 11 cases of malignant lymphoma diagnosed concurrently with or following lymph node infarction. Cases included seven B-cell lymphomas, three T-cell lymphomas, and one case of Hodgkin's disease. Sections of viable and infarcted tissue were immunostained in parallel using a panel of antibodies effective in routinely processed, wax-embedded tissue. The panel included anti-leucocyte-common antigen (CD45), T-cell-associated antigens (UCHL1, MT1), B-cell-associated antigens (MB1, 4KB5 (CD45R), MT2, LN1), a B-cell-specific antigen (L26), C3D-1 (CD15), and BER-H2 (CD30). Antibodies to intermediate filament cytoskeletal proteins, epithelial membrane antigen, and Factor VIII-related antigen were also used. In eight cases, staining of the infarcted material gave evidence of a lymphoid proliferation of either T- or B-cell type; an in the case of Hodgkin's disease, the results supported this diagnosis. The immunophenotype derived in the infarcted tissue mirrored the findings in the viable material in these eight cases of non-Hodgkin's lymphoma. A case of testicular infarction with concurrent intraosseous lymphoma was also examined. Staining in this case provided evidence of infarcted lymphoma. Thus, immunostaining of infarcted lymphoid tissue with these novel antibodies provides valuable information that conventional light microscopy cannot offer.
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PMID:Antigen preservation in infarcted lymphoid tissue. A novel approach to the infarcted lymph node using monoclonal antibodies effective in routinely processed tissues. 326 14

Reagents that recognize antigens on lymphoid cells in fixed and wax-embedded sections have been applied to a series of cases of non-Hodgkin's lymphomas. The panel consisted of MB1, 4KB5 (CD45r), LN1, L26 and MB2 which recognize antigens expressed predominantly on B-lymphocytes; UCHL1 and MT1 which recognize antigens expressed on T-lymphocytes and myeloid cells; antibodies recognizing the non-lineage antigens LeuM1 (CD15), BerH2 (CD30), anti-EMA; anti-lysozyme and MAC 387 which detect antigens present on some macrophages; and finally TAL1B5 (class II MHC), CAM 5.2 (low molecular weight cytokeratin) and PD7/26 + 2B11(CD45). Two hundred and four cases of non-Hodgkin's lymphoma have been studied, of which 158 had been fully characterized on frozen sections. The series was biased towards high-grade (n = 108) and T-cell (n = 44) tumours and these were largely prospectively accrued. It was found that discrimination between B-cell and T-cell lymphomas can be reliably achieved using these reagents and that a small panel (CD45, L26, MB2, MT1, UCHL1) is adequate for this purpose. Using the full range of reagents it is not possible to subdivide cases into groups that correspond with morphological subtypes of lymphoma. Although paraffin section immunohistochemistry is of value, the diagnosis of lymphoproliferative disorders must still be based upon the assessment of well fixed, carefully prepared tissue sections using conventional tinctorial methods.
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PMID:Paraffin section immunohistochemistry. I. Non-Hodgkin's lymphoma. 326 64

The role of antibodies of CD15 as diagnostic markers of Hodgkin's disease was assessed from a review of the literature. A total of 571 cases of Hodgkin's disease and 386 cases of non-Hodgkin's lymphoma were included. The sensitivity of CD15 in detecting cases of Hodgkin's disease was 80% or 91% if cases of lymphocyte predominant Hodgkin's disease were excluded. The specificity of CD15 was only 80.6%, or in other words, 19.4% of cases of non-Hodgkin's lymphoma were CD15 positive. In an ideal test both the sensitivity and specificity would be 100% and if the test performance were no better than chance then they would both be 50%. It is concluded that CD15 immunostaining cannot be regarded as a sensitive or specific marker of Hodgkin's disease. Application of this formal method of analysis to other immunohistological reagents and panels of antibodies is discussed.
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PMID:Value of CD15 immunostaining in diagnosing Hodgkin's disease: a review of published literature. 332 93

A variant of lymphadenitis mimicking interfollicular Hodgkin's disease is described. The morphology, immunohistochemistry and clinical course of 25 cases are reported. The morphology is characterized by changes in the interfollicular region within a well-preserved lymph node architecture. These changes include variegated hyperplasia of the pulp with epithelioid cells, mature eosinophilic granulocytes and immunoblasts occasionally resembling Hodgkin cells. In contrast to Hodgkin's disease no typical Sternberg-Reed cells could be found. Immunohistochemically, neither positive reactions with Hodgkin cell markers (anti-CD15: LeuM1; 3C4; C3D-1) nor B-cell monoclonality could be detected. Transition to malignancy, in particular Hodgkin's disease, did not occur in our cases.
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PMID:Lymphadenitis mimicking Hodgkin's disease. 336 42

The clonality of Reed-Sternberg cells is still a matter of controversy. In Hodgkin's disease, these cells rarely constitute more than 2% of all cells in tissue biopsies of lymph node lesions, the rest being a large collection of various reactive cells. To determine in which cells the abnormal karyotype occurs, we studied two patients with Hodgkin's disease by a cytogenetic method allowing simultaneous analysis of cell morphology, immunologic phenotype, and karyotype in the same mitotic cell. The Ber-H2 (CD30) and Leu-M1 (CD15) monoclonal antibodies were used to identify mitotic Reed-Sternberg cells. In 24-48-hour cultures of lymph node cells from Hodgkin's lesions, there was a mixture of cells with an abnormal clonal karyotype and a normal karyotype. The abnormal clonal karyotype was restricted to Ber-H2- and Leu-M1-positive cells, i.e., the Reed-Sternberg cells. In keeping with these findings, most of the clonal atypical karyotypes occurred in kappa- and lambda-positive large cells, i.e., Reed-Sternberg cells. Mitotic cells with T markers (CD3,4,8) or B markers (CD22) had the normal karyotype. There were no mitoses in cells expressing the antigens recognized by Leu11 (CD16) or Leu11 + Leu7. These findings provide strong evidence suggesting that in Hodgkin's disease only the Reed-Sternberg cells possess a clonal karyotypic abnormality and thus are most probably the only neoplastic component in Hodgkin's disease.
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PMID:Unique display of a pathologic karyotype in Hodgkin's disease by Reed-Sternberg cells. 340 2

Waldeyer's ring is an uncommon, rarely reported primary site for Hodgkin's disease. We report a series of 16 such cases culled from the files of the Armed Forces Institute of Pathology and the National Cancer Institute. The patients' median age was 41 years (range, 14-74), and they presented with airway obstruction or unilateral tonsillar enlargement. The disease was localized to the Waldeyer's ring (stage I) in 46% of patients and extended to the cervical lymph nodes (stage II) in 39% and to the spleen (stage III) in 15%. Local radiation therapy, with or without chemotherapy, obtained a complete response in all but two patients. There was local recurrence in one patient and distant spread in three others. All patients for whom follow-up is available are alive without evidence of disease at 9 to 216 months (median, 20 months) except two who died of widespread Hodgkin's disease and two others who died of other causes. Histologically, eight cases were classified as mixed cellularity type (50%), four as nodular sclerosis (25%), and one as lymphocyte predominance, nodular (LPn; 6.3%); three others that showed interfollicular involvement were unclassified (18.7%). The Reed-Sternberg (RS) and atypical mononuclear cells in most cases of mixed cellularity and interfollicular types and all cases of nodular sclerosis had the classic immunophenotype (CD45-, CD20- and/or CD45RO-, CD15+ and/or CD30+). In the single case of LPn, they were of B-cell lineage (CD45+, CD20+, CD45RO-, CD15-, CD30-). In situ hybridization performed on routinely processed sections revealed Epstein-Barr virus (EBV) EBER1 mRNA in RS cells of eight of 12 cases studied (67%) only in mixed cellularity and nodular sclerosis, but not in LPn. We conclude that, however rarely, Hodgkin's disease of typical morphology and immunophenotype can originate in Waldeyer's ring. The incidence of EBV detection in the RS cells in our study is greater than that usually seen in nodal Hodgkin's disease in the United States. The greater prevalence of EBV-related Hodgkin's disease at this site is probably a reflection of the fact that the Waldeyer's ring is a reservoir for EBV.
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PMID:Hodgkin's disease of Waldeyer's ring. Clinical and histoimmunophenotypic findings and association with Epstein-Barr virus in 16 cases. 750 65

Epstein-Barr virus (EBV) has been demonstrated in the Reed-Sternberg cells and their mononuclear variants (Hodgkin cells; H-RS cells) in a substantial number of Hodgkin's disease (HD) cases. Moreover, EBV can modulate both in vivo and in vitro the expression of several cellular genes, including lymphoid differentiation markers. Therefore we investigated, in 64 cases of HD, the relationship between the presence of EBV and the expression of lymphoid (CD45RB), T- (CD3, CD45RO), B- (CD20, MB2 antigen, CDw75), and myeloid-cell lineage markers (CD15), and of activation markers (CD30, EMA, and the 115D8 antigen) on the H-RS cells. EBV-positive cases, as demonstrated by the presence of EBER-1 and -2 RNA and LMP-1 protein expression, showed a significant reduction in the expression on H-RS cells of T-cell lineage (CD3, P < 0.02), B-cell lineage (CD20; P < 0.005), and activation markers (EMA; P < 0.002 and the 115D8 antigen; P < 0.001) as compared with EBV-negative cases. No differences were found in the expression of CD15, CD30, CD45RO, CD45RB, CDw75, or the MB2 antigen on H-RS cells in EBV-positive and EBV-negative HD cases. Interestingly, in 11 cases of EBV-negative HD, B- as well as T-cell lineage markers could be found on some H-RS cells. These data suggest that EBV in H-RS cells is able to down-regulate the expression of T- (CD3) and B- (CD20) cell lineage markers and lymphoid activation markers (EMA and the 115D8 antigen).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Decreased expression of cellular markers in Epstein-Barr virus-positive Hodgkin's disease. 752 10

Recent nucleic acid hybridization studies have implied that Reed-Sternberg/Hodgkin (RS/H) cells are infected with Epstein-Barr virus (EBV) before malignant transformation, and hence, that Hodgkin's disease could develop as a consequence of malignant transformation of an EBV-infected cell. This study is a detailed immunohistochemical and in situ hybridization characterization of the various lymphoid cells in nine cases of infectious mononucleosis (IM), the acute manifestation of EBV infection. The RS/H-like cells of IM were similar in most respects to their morphologically identical counterparts in Hodgkin's disease; they expressed the EBV-encoded protein LMP1, EBV EBER1 transcripts, and CD30 and rarely, if ever, expressed CD45/LCA or T cell markers. Dissimilarities were limited to CD15 negativity and the absence of a collarette of T cells around the RS/H-like cells of IM compared with their Hodgkin's counterparts. Expression of the immortalizing bcl-2 oncoprotein was variable in the RS/H-like cells of IM, as has been demonstrated in the RS/H cells of Hodgkin's disease by other investigators. An apoptosis assay suggested that many apoptotic cells in IM were EBV-infected T cells, in keeping with the previous in vitro observation that IM-derived T cells succumb to apoptosis. Additionally, the apoptosis assay suggested that RS/H-like cells of IM can succumb to programmed cell death, reminiscent of the mummified RS/H cells seen in Hodgkin's disease. The accumulation of evidence suggests that RS/H-like cells of IM are more similar to true RS/H cells than previously recognized.
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PMID:New characterization of infectious mononucleosis and a phenotypic comparison with Hodgkin's disease. 753 53

The origin of the Reed-Sternberg cell, the neoplastic cell of Hodgkin's disease, has not been defined. We evaluated a case of Hodgkin's disease, mixed cellularity type, which presented in the retroperitoneum of a 45-year-old woman. Reed-Sternberg cells and Hodgkin's cells expressed the characteristic markers CD15 and CD30. In addition, they expressed the B-cell antigens CD19 and CD20, as well as CD45/leukocyte common antigen. Clonal rearrangement of the immunoglobulin heavy chain gene was detected by Southern blot analysis. These results suggest that some cases of Hodgkin's disease are derived from an activated cell of lymphoid origin. This case documents a close relationship between Hodgkin's disease and non-Hodgkin's lymphoma, and it demonstrates that even when newer ancillary techniques are employed these two entities can have overlapping features.
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PMID:Hodgkin's disease, mixed cellularity type, with a B-cell immunophenotype. Report of a case and literature review. 753 89

The mouse monoclonal antibody anti-Leu-M1 (CD15) recognizes the carbohydrate determinant lacto-N-fucopentaose III, an oligosaccharide believed to be involved in cell-cell interactions. Anti-Leu-M1 is used in surgical pathology as an aid in the diagnosis of Hodgkin's disease. Additionally, adenocarcinomas derived from various organs stained positively with anti-Leu-M1 at the light microscopic level. Since mesotheliomas do not display positive reactivity to this antibody, Leu-M1 is clinically useful as part of a panel of antibodies in distinguishing adenocarcinomas from mesotheliomas. Previous work was carried out using post-embedding protein A-gold immunocytochemistry on thin sections embedded in Lowicryl K4M from a patient with Hodgkin's disease of the nodular sclerosing type; intense and precise labeling by gold particles was revealed in cytoplasmic granules, which were often clustered in a perinuclear location, in the Golgi apparatus, and focally along the plasma membrane of Reed-Sternberg cells. Moreover, polymorphonuclear leukocytes demonstrated similar labelling along the plasma membrane and over cytoplasmic granules. To define precisely the intracellular localization of Leu-M1 in human adenocarcinomas, we have performed post-embedding immunoelectron microscopy with the protein A-gold technique on sections embedded in Lowicryl K4M from neoplasms of the lung, stomach, colon, and breast. The pattern of labeling by gold particles indicative of Leu-M1 binding varied in adenocarcinomas of the different organs.
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PMID:Comparison of the pattern of expression of Leu-M1 antigen in adenocarcinomas, neutrophils and Hodgkin's disease by immunoelectron microscopy. 755 31


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