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)

Although Epstein-Barr virus (EBV) is commonly present in the neoplastic Reed-Sternberg and Hodgkin cells of the mixed cellularity, nodular sclerosis, and lymphocyte depletion types of Hodgkin's disease (HD), EBV is rare in the neoplastic cells of the nodular lymphocyte predominance type of HD, particularly in the United States. We describe a 19-year-old Hispanic man in whom nodular lymphocyte predominance HD involved a cervical lymph node. Epstein-Barr virus was identified in the neoplastic L & H cells by using in situ hybridization for EBV RNA and immunohistochemical staining for EBV latent membrane protein-1. Polymerase chain reaction studies demonstrated the type A strain of EBV. The presence of EBV in this case may be related to drainage of the virus from the oropharynx to the cervical lymph node. The presence of EBV also may be related to this patient's Hispanic ethnic origin.
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PMID:Detection of Epstein-Barr virus in the L & H cells of nodular lymphocyte predominance Hodgkin's disease: report of a case documented by immunohistochemical, in situ hybridization, and polymerase chain reaction methods. 938 51

Extensive diagnostic and scientific investigations are often restricted by limited availability of material. Therefore, methods like multiplex PCR strategies are needed to conserve as much sample as possible. Unfortunately, the establishment of such procedures poses several difficulties. Here we describe the advantages of a new enzyme, AmpliTaq Gold DNA Polymerase, in multiplex and time-release PCR. The application of this thermostable recombinant Taq DNA polymerase allows the specific amplification of DNA/cDNA targets with very high sensitivity. With our protocol, the specific amplification of 13 different cDNAs of cytokines and cytokine receptors can be realized in three multiplex PCRs (IL-2R alpha, IL-2/15R beta, gamma c-chain, IL-4 and IL-4R alpha; IL-10, IL-15 and IL-15R alpha; and IL-2, IFN gamma, IL-7, IL-7R alpha and IL-9R alpha). The novel application of AmpliTaq Gold DNA Polymerase in a time-release PCR protocol allows specific amplification of target DNA/cDNA when only limited amounts of material are available or only low-copy-number DNA/cDNA is suspected. No IL-9 cDNA can be detected in peripheral blood mononuclear cells (PBMC) in the absence of any stimulation, thus it was difficult to amplify this target with routine PCR protocols. Here we demonstrate the reliable and reproducible amplification of IL-9 cDNA in the Hodgkin's lymphoma cell line KM-H2, in PBMC and in stimulated PBMC. Results with AmpliTaq Gold DNA Polymerase were more sensitive and specific compared with AmpliTaq DNA Polymerase, with and without manual hot-start procedure.
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PMID:Advantages of a new Taq DNA polymerase in multiplex PCR and time-release PCR. 945 68

Subclassification of malignant non-Hodgkin's lymphoma is important to be able to choose the right treatment. However, this subclassification can be difficult, and immunohistochemistry and polymerase chain reaction are used to improve diagnostic safety. We have investigated the value of immunohistochemistry and polymerase chain reaction in the subclassification of 49 low grade non-Hodgkin's lymphomas of B-cell type. Immunohistochemistry showed B-cell phenotype in all biopsies, and 23 (85%) of 27 follicular lymphomas showed positive reaction for bcl-2 antibodies in follicles. Polymerase chain reaction demonstrated a monoclonal pattern for IgH in 36 (73%) of 49 biopsies, and 10 (37%) of 27 follicular lymphomas demonstrated translocation (14; 18). Immunohistochemistry and polymerase chain reaction contributed to subclassification or confirmation of the diagnosis of 46 (94%) of 49 biopsies. Our conclusion is that immunohistochemistry and polymerase chain reaction have a natural place in the diagnosis of lymphomas.
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PMID:[Low grade non-Hodgkin lymphoma of B-cell type. What is the benefit of polymerase chain reaction and immunohistochemical examination?]. 949 31

Abundant evidence has led to the clinical and biological separation of lymphocyte predominance from other types of Hodgkin's disease. However, it is still not clear whether lymphocyte predominance represents a polyclonal reactive lesion (possibly representing an abnormal immune disorder), a polyclonal or oligoclonal preneoplastic disorder or a monoclonal neoplastic disorder. The clinical and histological features are distinctive, but they do not provide clear indications of the nature of lymphocyte predominance. Some immunohistochemical and in situ hybridization studies have shown monotypic light chain restriction in the L&H cells, almost always of kappa type, implying a monoclonal process. Southern blotting studies are of limited utility, given their relatively low sensitivity and the rarity of L&H cells within involved tissues. Polymerase chain reaction studies have yielded conflicting results. Some, but not all, have demonstrated monoclonal populations in tissue extracts. Single cell PCR studies have generally not found monoclonal populations, although one case stands as an exception. Cases of large cell lymphoma complicating lymphocyte predominance have been monoclonal by polymerase chain reaction and clonospecific primers derived from these clones have demonstrated similar populations in the corresponding lymphocyte predominance tissues in some, but not all, studies.
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PMID:Clonality in lymphocyte predominance Hodgkin's disease. 954 90

We report 51 cases of a previously undescribed tumor of the distal extremities that is often mistaken for an inflammatory or infectious process, Hodgkin's disease, or various sarcomas. These lesions developed in patients of all ages (range, 4-81 yr; median, 40 yr) and affected the sexes nearly equally (27 men, 24 women). They presented as a painless mass of the fingers (14 cases), hand (11 cases), wrist or arm (10 cases), toe or foot (8 cases), or lower leg (5 cases), usually within the subcutaneous tissues. Grossly, they were infiltrative, multinodular masses characterized by a dense chronic inflammatory infiltrate that merged with a stroma, which varied from densely hyaline to focally myxoid and contained sheets of short spindled to rounded epithelioid cells. Focally, the epithelioid cells were extremely large with bizarre, vesicular nuclei and macronucleoli resembling Reed-Sternberg cells or virocytes. Despite the level of atypia, mitotic activity was low. The tumor cells consistently expressed vimentin but lacked a variety of other mesenchymal, epithelial markers, e.g., S100 protein, desmin, actin, neuron-specific endolase, epithelial membrane antigen, HMB-45, CD34) and leukocyte markers (CD15, CD30, CD45). Keratin was noted focally and weakly in four cases and CD68 focally in six cases, the latter suggesting that the cells had acquired phagocytic properties. Immunostains for cytomegalovirus were negative. Polymerase chain reaction for Epstein-Barr virus showed amplification levels consistent with latent infection in 4 of 10 cases, but no cases showed levels consistent with active infection. All of the bacterial and viral cultures were negative. Follow-up information was available in 27 cases. Recurrences developed in six patients (interval, 15 mo-10 yr), but there were no metastases or tumor-related deaths. In one patient, progressive proximal extension up the arm was noted. Although the most common submitting diagnosis was that of an inflammatory or infectious process, the negative studies for infectious agents, clinical behavior with local recurrences, immunophenotypic profile, and cytologic atypia support the idea that these are unusual mesenchymal neoplasms with at least the potential for local recurrence. It remains to be investigated whether with time these lesions will prove to have metastatic potential.
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PMID:Inflammatory myxohyaline tumor of distal extremities with virocyte or Reed-Sternberg-like cells: a distinctive lesion with features simulating inflammatory conditions, Hodgkin's disease, and various sarcomas. 957 90

The role of oncogene or tumor supressor gene in Epstein-Barr virus (EBV) associated malignant lymphomas (MLs) is poorly understood. We examined 36 MLs (21 EBV positive and 15 EBV negative) and 6 reactive hyperplasias for the presence of myc gene amplification. Polymerase chain reaction (PCR) technology was used to examine the state of amplification of the proto-oncogene c-myc in formalin-fixed paraffin-embedded tissues. Variable degrees of myc gene amplification were detected in reactive hyperplasias and MLs. However, significant increase of c-myc copy numbers above 3 times were only found in 12 out of 31 non-Hodgkin's MLs (38.7%), in which 6 cases were EBV positive and 6 cases were EBV negative. In conclusion, myc gene amplification appears to play a part in MLs but no correlation was found between EBV infection and myc gene amplification.
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PMID:Detection of MYC gene amplification in malignant lymphomas. 961 Jun 16

The use of allogeneic BMT in patients with relapsed non-Hodgkin lymphoma (NHL) offers the advantage of tumor-free bone marrow and possibly a 'graft-versus-lymphoma effect' which may decrease the risk of recurrence. However, allogeneic BMT also poses an increased risk of death due to graft-versus-host disease (GVHD) which can be ameliorated by T cell depletion. We performed a retrospective review of 37 patients who underwent T cell-depleted allogeneic BMT for aggressive and indolent NHL between 1988 and 1996. Polymerase chain reaction (PCR) was used to identify indolent NHL patients with the BCL2/IgH translocation which served as a marker of residual disease. Sixteen of 37 patients (44%) are alive and progression-free with a median follow-up of 4.4 years (range 1-10.3). The incidence of grade 2-4 acute GVHD was 36% and extensive chronic GVHD developed in 12%. Patients with aggressive NHL have an overall PFS of 33% (12-54%); those with chemotherapy-resistant and sensitive disease have PFS of 17% (0-47%), and 40% (15-65%) respectively at 5 years. Patients with indolent histologies have overall PFS of 62% (37-86%); those with chemotherapy-resistant and sensitive disease have PFS of 55% (25-85%) and 80% (45-100%) respectively at 5 years. Eight patients with indolent disease had a BCL2/IgH translocation detectable by PCR. Five of these eight patients remain alive and progression free at a median of 6.5 years after BMT (range 2.1-7.4 years), four of whom remain PCR positive from 1.7 to 2.9 years after transplantation. We conclude that T cell-depleted allogeneic BMT poses a low risk for death due to GVHD, and should be considered for patients with relapsed and refractory indolent NHL.
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PMID:T cell-depleted allogeneic bone marrow transplantation for high-risk non-Hodgkin's lymphoma: clinical and molecular follow-up. 961 81

The clinical and pathological features of eight cases of feline T-cell-rich B-cell lymphoma are described. The disease occurred in older cats (mean age 11.4 +/- 3.9 years), which on initial examination generally showed enlargement of a single submandibular or cervical lymph node. After excision, there was no recurrence of the lesions at 6 months in three cats. In one further case, however, the lesion had recurred 6 months later; it was again excised but recurred after an additional 6 months. Microscopically, there was effacement of normal lymph node architecture by a nodular (n = 4) or diffuse (n = 4) proliferation of small to blastic lymphocytes, accompanied by a characteristic population of bizarre giant, or multinucleate, cells. The mitotic rate was low and mitoses were restricted to the atypical population. Immunophenotyping revealed the smaller lymphocytes to be a mixture of CD3+ MHC Class II+ T lymphocytes and BLA36+CD79variable MHC Class IIvariable B lymphocytes. The atypical cells were of the B-cell lineage (BLA36+MHC Class IIvariable). Polymerase chain reaction analysis revealed no proviral DNA products of feline leukaemia virus or feline immunodeficiency virus in tissue from any tumour, confirming that these neoplasms were not associated with either virus. The clinical, histological and immunophenotypic findings in these cats were identical with those of "nodular lymphocyte predominance (lymphocytic and histiocytic/L&H) Hodgkin's disease" in man.
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PMID:T-cell-rich B-cell lymphoma in the cat. 1008 89

Although follicle center cell lymphoma and mantle cell lymphoma are both B cell non-Hodgkin's lymphomas (NHL), they are regarded as separate entities with distinct clinical, morphological, immunophenotypic and molecular characteristics. To our knowledge, the coexistence of these 2 lymphomas in the same patient has never been reported. We describe a 70-year-old woman with a long-standing history of follicle center cell lymphoma, cytological grade I, who subsequently developed a composite lymphoma consisting of well-demarcated foci of persistent follicle center cell lymphoma surrounded by mantle cell lymphoma. This morphological interpretation was supported by the presence of both bcl-1 and bcl-2 gene rearrangements, which are molecular genetic hallmarks of mantle cell lymphoma and follicle center cell lymphoma, respectively. Polymerase chain reaction (PCR) analysis for rearranged immunoglobulin heavy chain (IgH) genes showed a dominant band identical in size in microdissected tumor cells of the follicle center cell and mantle cell lymphomas. Cloning and sequence analysis of the PCR products revealed a common clone-specific IgH gene rearrangement in these 2 lymphomas. These findings suggest that this composite lymphoma represents the unusual evolution of a malignant B-cell clone that resulted in the development of 2 morphologically distinct but clonally related B-cell NHLs. These findings also show the importance of integrating morphological, immunophenotypic, and molecular data to enhance our understanding of the complex pathogenic interrelationships in lymphomagenesis.
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PMID:A distinctive composite lymphoma consisting of clonally related mantle cell lymphoma and follicle center cell lymphoma. 1083 5

We report three cases of nodal peripheral T-cell lymphoma (PTCL) with Reed-Sternberg-like (RS-like) cells of B-cell pheno- and/or genotype. Histologic analysis in all cases revealed diffuse nodal effacement by atypical lymphoid cells of variable size. Two of the three cases had features of angioimmunoblastic T-cell lymphoma (AILT). Large mononuclear and binucleated cells with prominent eosinophilic nucleoli and abundant cytoplasm resembling classic RS cells and mononuclear variants were scattered throughout all biopsies. The lymphoma cells in the three cases were of T-cell lineage (CD3+, CD43+, and CD45RO+). The RS-like cells from all cases were CD30 and CD15 positive. In contrast to the neoplastic T cells, the RS-like cells lacked all T-cell markers and in two cases were positive for CD20. Epstein-Barr virus (EBV) latent membrane protein 1 (LMP1) and EBER 1 (2/2) were detected in the RS-like cells in all cases. The neoplastic T cells were negative for EBV. Polymerase chain reaction (PCR) analysis demonstrated clonal rearrangements of the T-cell receptor gamma chain gene in the three cases. PCR analysis of microdissected RS-like cells for immunoglobulin heavy chain gene rearrangements in cases 1 and 3 showed an oligoclonal pattern. The presence of RS-like cells in PTCL represents a diagnostic pitfall, because in one case this observation led to a misdiagnosis of Hodgkin's disease (HD). The oligoclonal expansion of EBV-infected cells may be related to underlying immunodeficiency associated with T-cell lymphomas and AILT in particular. This phenomenon may provide the basis for some cases of Hodgkin's disease after T-cell lymphomas and suggests that they are clonally unrelated neoplasms. The expression of LMP1 appears to be crucial for the immunophenotype and probably for the morphology of the RS and RS-like cells appearing in diverse lymphoid malignancies, including HD, chronic lymphocytic leukemia, and PTCL.
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PMID:Peripheral T-cell lymphoma with Reed-Sternberg-like cells of B-cell phenotype and genotype associated with Epstein-Barr virus infection. 1052 24


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