Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019829 (Hodgkin's disease)
 30,247 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

There is growing evidence for a B-cell lineage of lymphocyte-predominant Hodgkin's disease (1). To support this assumption, in situ hybridization techniques were used to detect immunoglobulin light-chain mRNA in 44 formalin-fixed specimens of Hodgkin's lymphoma (22 of lymphocyte-predominant Hodgkin's disease; 22 of mixed-cellularity Hodgkin's disease). In addition, immunoglobulin light chains were evaluated by polyclonal antisera. All specimens had been unequivocally diagnosed histologically by the referees of the German Hodgkin Trial and been immunophenotyped by monoclonal antibodies against CD15, CD20, CD30, and CD45. Light-chain mRNA coding either for kappa or for lambda could be detected by an enhanced in situ hybridization protocol using microwave heating in the lymphocytic and histiocytic cells of 14 (64%) of 22 specimens of lymphocyte-predominant Hodgkin's disease tested. None of the specimens, however, belonging to one of the classic subtypes of Hodgkin's disease (mixed-cellularity Hodgkin's disease) showed positivity for mRNA in the giant tumor cells. Our results support the idea that lymphocyte-predominant Hodgkin's disease represents a B-cell malignancy that is a entity separate from classic Hodgkin's disease. Diverging results of former studies in assessing light-chain mRNA in lymphocytic and histiocytic cells probably reflect problems with the detection threshold, i.e., the sensitivity of the techniques applied.
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PMID:Light-chain mRNA in lymphocyte-predominant and mixed-cellularity Hodgkin's disease. 868 37

Expression of the Epstein-Barr virus (EBV) gene product LMP1 is found in tumour cells in varying proportions of Hodgkin's disease (HD) cases. It is not clear which cellular genes are influenced by EBV in HD. A total of 387 HD cases were tested for differences among LMP1-positive and -negative cases with respect to age, sex, histotype and immunophenotypic parameters (CD2, CD3, CD4, CD15, CD19, CD20, CD21, CD22, CD23, CD25, CD30, CD43, CD45RA, CD45R0, CD70, HLA-DR, T-cell receptor beta-chain, and p53 expression). Comparison of patient age and sex as well as distribution of histotype and tumour cell immunophenotype with published data suggests that the cases in this study are representative of the spectrum of HD in developed countries. LMP1 expression was found in 131/387 HD cases (36.4 per cent) with non-homogeneous distribution among HD histotypes, the mixed cellularity type (HDmc) being most frequently EBV-associated (71/129 cases, 55 percent). No relationship was found to age and sex. Significant phenotypic differences were restricted to the HDmc histotype, where the tumour cells expressed the activation marker CD30 in a larger proportion, and CD20 in a smaller proportion, when harbouring EBV. These results suggest that EBV may influence the tumour cell phenotype in HD.
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PMID:Phenotypic modulation of Hodgkin and Reed-Sternberg cells by Epstein-Barr virus. 869 46

A case of CD5-positive diffuse large cell lymphoma in a patient with autoimmune hemolytic anemia (AIHA) is reported. The patient was diagnosed with AIHA in December 1988. Three and a half years later, the patient complained of fever and left sided flank pain. Abnormal lymphocytes appeared in the peripheral blood and were positive for HLA-DR, CD5, CD19, CD20, and surface immunoglobulin (mu, lambda). The pathological diagnosis of the cervical lymphnode was non-Hodgkin lymphoma; diffuse large cell type with a starry sky-like appearance. Although the 8q24 translocation was not detected by karyotypic analysis of the peripheral blood mononuclear cells (PBMNC), Southern blot analysis revealed that the c-myc rearrangements had occurred. This case showed two rearranged bands with Eco RI, Bam HI, or Bgl II digestion, and a germline band with Hin dIII digestion using a second exon fragment of the c-myc gene as a probe. Despite intensive chemotherapy, this patient died 6 months after being diagnosed with malignant lymphoma. We discuss the c-myc rearrangements in this aggressive CD5-positive diffuse large B cell lymphoma.
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PMID:Aggressive CD5-positive diffuse large B cell lymphoma showing c-myc rearrangements developed in a patient with autoimmune hemolytic anemia. 871 79

We reviewed our experience with six T-cell-rich B-cell lymphomas (TRBL) presenting in skin. Immunohistochemical studies were performed on all biopsies. The lymphoid population consisted mainly of CD3 and/or UCHL-1 (CD45RO) positive T cells. 5 to 15% of the lymphoid cells stained for the B-cell marker L26 (CD20). Monoclonality of the B-cell component was demonstrated in all cases, utilizing either light chain restriction (5 cases) or clonal immunoglobulin heavy chain gene rearrangement by polymerase chain reaction (PCR) (2 cases). One case was confirmed to be monoclonal by both techniques. Additionally, no clonal rearrangements of the T-cell receptor gamma gene were observed. There was considerable morphological variety in these cases. In H&E stained sections, the differential diagnosis included pseudolymphoma, peripheral T-cell lymphoma, Hodgkin's disease, Lennert's lymphoma and a MALT lymphoma. A significant component of monoclonal plasma cells was present in 3 of 6 cases, suggesting a possible origin from cutaneous immunocytoma. In fact, one of our cases was a biphasic lymphoma displaying TRBL with a small focus of immunocytoma. We conclude that immunophenotypic analysis is necessary for the diagnosis of TRBL. Pathologists should be aware of this type of cutaneous B-cell lymphoma to avoid misinterpretation as a pseudolymphoma.
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PMID:T-cell-rich B-cell lymphoma presenting in skin. A clinicopathologic analysis of six cases. 872 43

Possible associations between the immunophenotype of Hodgkin (H) and Sternberg-Reed (S-R) cells, the expression of CD57 (Leu 7) antigen, and the presence of Epstein-Barr virus (EBV) were investigated in lymph node specimens from 50 cases of Hodgkin's disease (HD), including 26 cases of mixed cellularity and 24 cases of nodular sclerosis. Tissues were fixed in 10% neutral formalin, or/and B5 solution. H and S-R cells were CD30+, CD15+ (85% of the cases) and LCA (CD45). A proportion of neoplastic cells positive for either T-cell markers (CD3) or B-cell markers (CD20) was observed in 10% and 34% of the cases, respectively. Membrane positivity for CD57 antigen was found in H and S-R cells in 10 cases (8 cases of mixed cellularity, and 2 cases of nodular sclerosis). Such immunopositivity was only observed in B5-fixed sections. No staining for CD57 antigen was identified in H and S-R cells of any case with CD20 positive neoplastic cells. H and S-R cells of both CD57-positive and CD57-negative cases were further studied by immunohistochemistry for LMP1, by in-situ hybridization for EBER and by polymerase chain reaction (PCR) for EBV-DNA. No association was identified between the expression of CD57 antigen and the presence of EBV sequences, transcripts or proteins. Our findings do not support a B-cell origin for H and S-R cells in CD57-positive cases of Hodgkin's disease and suggest that these neoplastic cells may be related to natural killer (NK) or T-cells expressing CD57 antigen.
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PMID:Phenotype of Hodgkin and Sternberg-Reed cells and expression of CD57 (LEU7) antigen. 875 Jun 33

We report a novel strategy, called end-product (EP) amplification, capable of enhancing the sensitivity of immunohistochemical procedures by about an order of magnitude or more. The strategy employs an antibody (anti-EP) to the product generated by the action of horseradish peroxidase on 3,3'-diaminobenzidine (DAB), and can be extended to the products of other enzymes as well, e.g., alkaline phosphatase. Amplification is the consequence of the ability of anti-EP to detect the multiplicity of product moelcules resulting from the turnover of substrate by a single enzyme molecule. The subsequent detection of anti-EP was by biotinylated goat anti-rabbit antibody, followed by avidin-peroxidase and DAB or by avidin-alkaline phosphatase and Vector Red. Further amplification can be accomplished by repeated cycles of the protocol. Anti-EP was produced by immunization with a bovine serum albumin (BSA) conjugate of a soluble polymer of DAB, prepared by a carefully controlled reaction of DAB with horseradish peroxidase and hydrogen peroxide. Coupling to BSA (and to RSA) was accomplished with glutaraldehyde. The titer of anti-EP was established by ELISA. Formalin-fixed, paraffin-embedded sections of five cases of Hodgkin's disease and five tonsils with follicular hyperplasia were immunolabeled for the following lymphoid markers: CD3, CD20, CD30, CD45RA, and CD68. EP amplification with anti-EP was also applied to cases of CMV pneumonia and cerebral toxoplasmosis to determine whether this procedure could improve detection of the infectious agents. Immunolabeling of the primary antibody was performed by the avidin-biotin-peroxidase technique with DAB as the reaction substrate. The specificity of EP amplification was tested by demonstrating binding of anti-EP with Vector Red with the generation of a fluorescence end-point. There was complete congruence in the distribution of the DAB signal and the red immunofluorescence representing EP amplification. The intensity of the DAB signal was increased as much as 16-fold by EP amplification, making possible a reduction in the amount of the primary antibody by as much as 85-90%. Sensitivity also increased with respect to weakly expressed antigens and low concentrations of infectious agents.
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PMID:A strategy for immunohistochemical signal enhancement by end-product amplification. 875 54

Lymphocyte predominance Hodgkin's disease (LPHD) is a B-cell lymphoproliferative disorder; patients with LPHD have an increased risk of developing synchronous or metachronous B-cell non-Hodgkin's lymphoma. The synchronous presence of LPHD and B-cell lymphoma in the same lymph node in some cases lends support to the argument that the B-cell lymphoma arises as a consequence of transformation or progression of LPHD. We have recently identified three cases of LPHD occurring simultaneously with T-cell lymphoma in a series of 76 cases of LPHD in the files of the Nebraska Lymphoma Study Group Registry. In large areas of the lymph nodes, atypical T cells with large, irregular, and hyperchromatic nuclei were admixed with Reed-Sternberg variants characteristic of LPHD (L&H cells). However, in all cases, areas of typical nodular LPHD without obvious T-cell lymphoma were also evident. In one case, frozen-section immunohistochemistry demonstrated the absence of expression of CD5, CD4, or CD8 by the T-cell lymphoma. The L&H cells in all cases expressed CD45 and CD20, as expected. In all three cases, clonal T-cell receptor (TCR)-gamma gene and TCR-beta gene rearrangements were documented by polymerase chain reaction analysis and Southern blotting, respectively. No clonally rearranged immunoglobulin genes were detected by either technique. To our knowledge, this represents the first report of the simultaneous occurrence of LPHD and T-cell lymphoma. Although B-cell lymphoma occurring in the setting of LPHD is a well-recognized phenomenon, previous reports of T-cell lymphoma occurring after a diagnosis of LPHD, as well as our cases with synchronous disease, suggest that the association of T-cell lymphoma and LPHD may not be uncommon as well. Furthermore, our cases indicate that T-cell lymphoma occurring in LPHD is not therapy related. However, the underlying mechanisms by which these composite lymphomas occur remain unknown.
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PMID:Concurrent lymphocyte predominance Hodgkin's disease and T-cell lymphoma. A report of three cases. 877 90

Based on the presence of T cell receptor-beta (TcR-beta) gene rearrangements in L428 and HDLM-1 cells, the expression of CD2 in HDLM-1 cells, and the presence of immunoglobulin heavy-chain (IgH) gene rearrangement in KM-H2 cells, some researchers have concluded that these long-term cell lines derived from patients with Hodgkin's disease are lymphoid in nature. The information obtained from these cell lines has also been used in arguments for a lymphoid origin of H-RS cells in tissue despite the frequent absence of lymphoid markers and Ig/TcR gene rearrangements in these cells. We questioned whether one can use the limited expression of lymphoid markers or the limited gene rearrangement to conclude that H-RS cells have a lymphoid origin, because these markers may be aberrant in tumor cells. In this study, we examined the expression of two T-cell-specific transcription factors (TCF-1 and GATA-3) and one B-cell-specific transcription factor (BSAP) in cultured H-RS cells by using a gel mobility shift assay. The sensitivity and specificity of this assay for determination of cell lineage have been established in a large number of cultured human and murine cell lines. All three types of H-RS cell lines were consistently negative for BSAP, TCF-1, and GATA-3. The absence of GATA-3 was confirmed in H-RS cells in tissues by an in situ hybridization technique. Virtually all B-cell lines, with the exception of some myeloma cell lines, are positive for BSAP, which is the transcription factor for promoters for several B-cell markers, including VpreB1, lambda 5, CD19, and CD20. All T-cell lines tested were positive for TCF-1 and GATA-3, which are the transcription factors for promoters for several T-cell-restricted markers, including CD2, CD3, TcR, and lck. The absence of BSAP, TCF-1, and GATA-3 clearly indicates an underlying difference between H-RS cells and lymphoid cells.
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PMID:Absence of T-cell- and B-cell-specific transcription factors TCF-1, GATA-3, and BSAP in Hodgkin's Reed-Sternberg cells. 878 Jan 59

A patient is described with angioimmunoblastic T-cell lymphoma (AIL) (angioimmunoblastic lymphadenopathy with dysproteinemia [AILD]-type T-cell lymphoma), which was later followed by Hodgkin's disease. At the time of the initial diagnosis, histological examination of a cervical lymph node showed a typical picture of AIL with abundant clear cells which were CD45RO+, CD43+, and CD20-, and there was no evidence of a monoclonal B-cell proliferation by immunohistochemical analysis. In situ hybridization for Epstein-Barr virus (EBV) was negative. Interposed by a bout of recurrence, the patient developed, 16 years later, a left subparotid mass which showed histologic features of Hodgkin's disease, mixed cellularity type. Diagnostic Reed-Sternberg cells and their variants were CD30+, CD15- and CD20+. Neither rearrangement of TCR beta and gamma chain genes nor of immunoglobulin heavy chain and kappa light chain genes was detected in DNA extract from fresh material. In situ hybridization showed the presence of EBV within the Reed-Sternberg cells. The data show that EBV was not etiologically related to AIL in this case. Further, the deficit in cellular immunity that accompanied AIL conceivably permit primary EBV infection or reactivation of latent infection, which eventuated in development of Hodgkin's disease, but the exact pathogenesis remains uncertain.
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PMID:Angioimmunoblastic T-cell lymphoma (angioimmunoblastic lymphadenopathy with dysproteinemia [AILD]-type T-cell lymphoma) followed by Hodgkin's disease associated with Epstein-Barr virus. 880 2

The nature of the Hodgkin/Reed-Sternberg (H/RS) cells in Hodgkin's disease (HD) is still unclear. We have studied isolated H/RS cells from four cases of lymphocytic predominance (LP) HD and six cases of nodular sclerosis (NS) HD and assayed the cells for immunoglobulin heavy chain (IgH) gene rearrangement by the polymerase chain reaction (PCR). The H/RS cells in all four cases of LPHD had rearranged their IgH gene in a polyclonal pattern. The H/RS cells of three cases of NSHD where at least a fraction of the cells expressed the B-cell marker CD20 had also rearranged their IgH gene. In two of the cases, the rearrangements were totally unrelated while in one case, two out of six rearrangements were identical in sequence indicating the presence of a clonal subpopulation amid a polyclonal background. Clonality was assessed independently in one NSHD case by determining the pattern of X-chromosome inactivation. This technique also failed to show that the H/RS cells were monoclonal. Our studies suggest that in both LPHD and NSHD, the H/RS cells may be a polyclonal proliferation at presentation and clonal populations may emerge from this polyclonal background. There is also some evidence of a correlation between the immunophenotype and the genotype of the H/RS cells. Single cell assays show great potential in elucidating the cell lineage and clonality of H/RS cells, as well as their in vivo evolution during the disease process.
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PMID:Single cell analysis of H/RS cells. 883 8


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