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)

Highly malignant non-Hodgkin lymphomas (HM-NHL) may sometimes develop clinical features simulating an epithelial carcinoma with metastatic dissemination. Conventional histopathological study may be insufficient to differentiate between both conditions. Two patients with HM-NHL are reported with a rapid general deterioration; one of them had osteolysis and hypercalcemia. In both cases a diffuse bone marrow infiltration by large sized cells with blastic appearance was found. The initial suspected diagnosis was occult epithelial neoplasia with metastatic dissemination. The morphological study with optic microscopy and the ultrastructural analysis did not establish the origin of these cells. The definitive diagnosis was obtained by immunohistochemical techniques. In both cases, the cells were positive for the CD 45 (common leukocyte antigen) monoclonal antibody (MoAb), and for several MoAbs of lymphoid B differentiation. In one of them, the B lymphoid lineage was confirmed by monoclonal reordering of the gene that synthetises the immunoglobulin heavy chain.
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PMID:[High-degree malignancy non-Hodgkin's lymphoma simulating a disseminated carcinoma. Presentation of 2 cases]. 271 30

Despite intensive efforts using a wide variety of approaches, the cellular lineage and clonality of the abnormal cells of Hodgkin's disease have remained an enigma. In the present study, cell separation techniques that enriched for Reed-Sternberg cells and their variants were used to generate sufficient percentages of abnormal cells to allow detection of rearrangements in these cell fractions. DNA from the involved tissues of eight Hodgkin's disease patients was subjected to Southern blot analysis to detect rearrangements of T cell antigen receptor genes and immunoglobulin genes. Immunoglobulin gene rearrangements were found in three of five cases in which Reed-Sternberg cells and their variants were enriched by cell separation techniques to cell frequencies greater than 1%. Rearrangements of immunoglobulin heavy chain genes occurred in two cases, and a lambda light chain gene rearrangement occurred in a third case. Rearrangements were not detected in lymphocyte fractions or in unseparated cells prepared from the same tissues. The putative Hodgkin's cell line, L428, also contained rearrangements of immunoglobulin heavy and kappa and lambda light chain genes and, in addition, harbored a single T cell receptor beta gene rearrangement. These findings indicate that Reed-Sternberg cell-enriched fractions contain clonal cell populations and provide a lead, at the molecular genetic level, to a possible lymphoid derivation of the Reed-Sternberg cell.
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PMID:Rearranged antigen receptor genes in Hodgkin's disease. 295 98

A study comparing the usage of monoclonal and polyclonal antibodies specific for immunoglobulin light and heavy chains was performed on frozen-tissue sections of 30 B-cell non-Hodgkin's lymphomas. In 16 cases, monotypic staining for an immunoglobulin light chain was demonstrated with monoclonal antibodies using a three-step avidin-biotin peroxidase complex (ABC) method; 13 cases were positive for kappa. In 14 cases, no immunoglobulin light-chain production was demonstrated. Repeat staining of 11 of these 14 cases with polyclonal anti-sera by a direct immunoperoxidase method demonstrated monotypic staining for light chain in 10 cases, 9 of which were positive for lambda. In 22 of 30 non-Hodgkin's lymphomas, an immunoglobulin heavy chain was identified using monoclonal anti-sera. In eight cases, however, no heavy chain was found. Repeated staining with polyclonal sera of additional sections in three of eight cases demonstrated heavy-chain production in each case. Decreased sensitivity, especially for the detection of the lambda light chain, rendered this particular lot of monoclonal antibodies unsuitable for immunophenotyping non-Hodgkin's lymphomas. Variability of antigenic sites on the immunoglobulin molecule seems a likely explanation for these observations.
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PMID:Comparison of monoclonal and polyclonal antibodies directed against immunoglobulin light and heavy chains in non-Hodgkin's lymphoma. 307 27

The relationship between T cell receptor (TCR) beta and gene immunoglobulin heavy chain locus was investigated in 25 cases of unselected human lymphomas as well as in normal and non-neoplastic lymphoid tissues. Hybridizing our blots with Jurkat 2, a clone specific for the beta chain gene of TCR, did not demonstrate extra bands in non-neoplastic tissues composed of 50-95% T-cells. On the contrary, rearranged bands were detected in six out of six cases of T-cell lymphomas. No TCR beta gene rearrangements were detected in 11 B-cell lymphomas, which in turn presented modification of the immunoglobulin heavy chain gene germline configuration. Our results suggest that TCR beta chain gene rearrangements are a good marker for human T-cell neoplasias in humans and complement the analysis with immunoglobulin genes probes. Eighth samples were devoid of any rearrangements: this group comprises cases of Hodgkin's disease T-lymphoblastic lymphomas in clinical remission and malignancies of unknown origin, as discussed in the text. We conclude that the analysis using DNA probes specific for TCR beta and IgH genes can be of aid to the pathologist in the diagnosis and classification of human lymphomas.
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PMID:The contribution of molecular biology in the diagnosis of human lymphomas. 309 91

To study the pathogenesis of Hodgkin's disease (HD), which today remains obscure, we have undertaken a combined experimental approach: determination of TdT and molecular analysis of rearrangements of immunoglobulin heavy chain (IgH), T-cell receptor (TCR) beta chain and the T-cell rearranging gamma (TRG) genes. TdT determination indicate would the presence of immature cells that are not detected in the normal lymphnode; molecular analysis of the rearrangements of these genes would reveal the presence of even a small monoclonal population of both T and B lineages in the lymphnodes. We believe that the combination of these two types of analysis can indicate whether an expanding lymphoid clone is responsible for this disease. TdT determination was negative in all 41 cases tested. Gene rearrangements were studied in 10 cases for IgH and TCR beta genes and in 5 cases for the TRG gene. No abnormal band beside the germ-line ones was detected in any of our cases, ruling out the presence of a minor neoplastic population. We can explain these results in at least three ways: first, the neoplastic population could represent less than 1% of the total, thus escaping detection by current techniques; second, the neoplastic population is not lymphoid in nature or is composed of mature cells that do not rearrange Ig and TCR genes and therefore belongs to a true non-B, non-T lineage; third, the pathogenesis of HD is completely different from that of non-Hodgkin's lymphomas (NHL) and does not involve the clonal expansion of a cell frozen at a particular maturative stage as is thought to happen in most NHL.
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PMID:Lack of TdT and immunoglobulin and T-cell receptor gene rearrangements in Hodgkin's disease. 313 16

We have shown that the human cellular oncogene c-myc is composed of three exons and is transcribed from two initiation sites separated by 175-base-pair DNA in HeLa cells. For both resulting mRNA species, exon 1 composes the 5' untranslated region and the initiator methionine is located 16 base pairs down-stream from the 5' splice acceptor of exon 2. In a non-Hodgkin lymphoma, Manca, harboring a t(8; 14) translocation, c-myc gene is broken within intron 1, and its exons 2 and 3 are translocated to a site between the heavy chain joining region cluster and C mu-coding DNA segment of the immunoglobulin heavy chain locus. The translocated c-myc gene is transcribed from points within intron 1 but is apparently still translated from the same methionine codon as the mRNA from the unrearranged c-myc gene. The nucleotide sequence of the c-myc gene shows that a region of exon 1 is highly complementary to a region of exon 2. Thus the mRNA from the untranslocated c-myc gene, as opposed to that of the translocated c-myc gene, could form a stable stem-loop structure (delta Go = -90 kcal/mol; 1 cal = 4.184 J) where the initiator AUG would be located within the loop. In view of the bind-and-scan model for the initiation of eukaryotic translation, we propose that such a secondary structure will severely hinder the translation. We further propose that the c-myc gene is often activated by translocation through the escape from such a translational suppression.
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PMID:Activation of the c-myc gene by translocation: a model for translational control. 632 75

The interrelationships between histomorphologic classification, cell surface marker phenotype and prognosis were prospectively studied in 130 adults with non-Hodgkin's lymphomas. Within each of the classification schemes used there were certain histologic variants that exhibited heterogeneity of cell lineage as well as those that were extremely uniform. Diffuse lymphomas with cell populations consisting of large cells, or mixtures of large and small cells were the most heterogeneous phenotypically and were most resistant to precise definition of immunologic cell lineage. The new Working Formulation for Clinical Usage likewise exhibited considerable heterogeneity of phenotype even within well defined histomorphologic categories. Two immunologic phenotypic variables that conferred a significant favorable prognosis were the expression of surface membrane immunoglobulin (B derivation) and the simultaneous expression of a membrane mu and delta immunoglobulin heavy chain. The results of this study suggest that cell surface marker phenotypic determinations have well defined and potentially useful correlations with histomorphologic classification schemes, and are useful in predicting biologic behavior and prognosis. It is suggested that a knowledge of both immunologic phenotype and histomorphologic characteristics is necessary in formulating therapeutic decisions.
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PMID:Adult non-Hodgkin's lymphoma. Correlation of cell surface marker phenotype with prognosis, the new working formulation, and the Rappaport and Lukes-Collins histomorphologic schemes. 664 May 1

The distribution of Bcl-2 oncoprotein was studied immunohistochemically in formaldehyde-fixed and paraffin-embedded reactive and neoplastic lymphoid tissue. The potential of Bcl-2 for the differential diagnosis of follicular lesions was emphasized, and the results on follicular lesions were correlated with those of polymerase chain reaction (PCR) assay of the immunoglobulin heavy chain gene rearrangement. In hyperplastic lymphoid tissue, Bcl-2 reactivity was widespread, including germinal center surroundings, scattered cells within the germinal centers, and the T-cell areas in general. Distinctively negative lymphoid populations included the majority of germinal center cells, and the negative staining pattern was maintained in cases of florid hyperplasia. In contrast, follicular lymphoma cells were consistently Bcl-2 positive. The immunohistochemical Bcl-2 reactivity of lymphoma follicles correlated with the clonal PCR amplification pattern of the immunoglobulin heavy chain gene; all Bcl-2-negative hyperplasias revealed a non-clonal pattern. Clusters of monocytoid B cells were Bcl-2 negative, whereas monocytoid B-cell lymphomas and closely related MALT lymphomas were positive. All other small cell non-Hodgkin's lymphomas of B-cell types showed nearly uniform Bcl-2 reactivity, whereas large cell B-cell lymphomas were variably positive (74%). In Hodgkin's cells, Bcl-2 reactivity was seen in the neoplastic populations of most cases of nodular sclerosis and mixed cellularity types, whereas the L&H and Reed-Sternberg cells in lymphocyte predominance Hodgkin's disease were negative in most cases. Bcl-2 immunohistochemistry thus appears very valuable in the differential diagnosis of follicular hyperplasia and neoplasia, and it may help to distinguish between reactive and neoplastic monocytoid B cells. However, Bcl-2 immunohistochemistry is not useful in the subtyping of B-cell lymphomas.
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PMID:Bcl-2 oncoprotein is widespread in lymphoid tissue and lymphomas but its differential expression in benign versus malignant follicles and monocytoid B-cell proliferations is of diagnostic value. 748 87

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

We have correlated histologic type of Hodgkin's disease, degree of Hodgkin and Reed-Sternberg cell infiltration, percentage of Hodgkin and Reed-Sternberg cell positivity for latent membrane protein, immunophenotype of Hodgkin and Reed-Sternberg cells, and immunoglobulin heavy chain (IgH) gene rearrangements detected by polymerase chain reaction (PCR) in 56 unselected Hodgkin's disease cases. Two protocols were used for amplification of IgH gene using Fr2 or Fr3 V-region primers, in conjunction with nested primers directed to the JH region. PCR products were run on polyacrylamide gels. Immunohistochemical studies were performed on paraffin sections using monoclonal antibodies for CD20 and latent membrane protein, and polyclonal antibody to CD3. Using both primer combinations we detected a definitive clonal band in 23.2% of the Hodgkin's disease cases. Clonal IgH rearrangements were detected in 23.6% of nodular sclerosis type and in 28.5% of mixed cellularity type. Using a highly sensitive method such as PCR, more than 20% of unselected cases of Hodgkin's disease were found to contain B-cell clonal proliferations, but there was no correlation between histological and immunological parameters and molecular analysis results.
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PMID:Evaluation of clonal immunoglobulin heavy chain rearrangements in Hodgkin's disease using the polymerase chain reaction (PCR). 755 2


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