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)

Surgeons are involved in the diagnosis and staging of patients with lymphoma. Treatment requires accurate information about histologic classification and the extent of disease. While most patients with non-Hodgkin's lymphoma are treated with systemic chemotherapy, the exact stage of disease in patients with Hodgkin's lymphoma may determine the therapy to be used. The use of minimally invasive surgery in surgical staging of patients with Hodgkin's disease has the potential to decrease the morbidity and mortality of the staging procedure in these patients. All of the components of a staging procedure (liver biopsies, splenectomy, lymph node biopsies, and oophoropexy) can be performed laparoscopically. The procedure is performed with the patient in the supine position. After obtaining several liver biopsies, the splenectomy is completed. Lymph nodes are then sampled from the celiac, portal, iliac, and peri-aortic regions. Lymph nodes identified as abnormal on pre-operative imaging studies are identified and excised. While each of these procedures is technically challenging, the laparoscopic conduct of this diagnostic procedure may afford patients decreased post-operative morbidity and mortality.
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PMID:Laparoscopic evaluation of lymphoma. 977 29

The defects in lymphocyte apoptosis that underlie the autoimmune lymphoproliferative syndrome (ALPS) are usually attributable to inherited mutations of the CD95 (Fas) gene. In this report, we present the histopathological and immunophenotypic features seen in the lymph nodes (n = 16), peripheral blood (n = 10), bone marrow (n = 2), spleen (n = 3), and liver (n = 2) from 10 patients with ALPS. Lymph nodes showed marked paracortical hyperplasia. Interfollicular areas were expanded and populated by T cell receptor-alphabeta CD3+ CD4-CD8- (double-negative, DN) T cells that were negative for CD45RO. CD45RA+ T cells were increased in all cases studied. The paracortical infiltrate was a result of both reduced apoptosis and increased proliferation, as measured by in situ detection of DNA fragmentation and staining with MIB-1, respectively. The paracortical proliferation may be extensive enough to suggest a diagnosis of malignant lymphoma. Many of the paracortical lymphocytes expressed markers associated with cytotoxicity, such as perforin, TIA-1, and CD57. CD25 was negative. In addition, most lymph nodes exhibited florid follicular hyperplasia, often with focal progressive transformation of germinal centers; in some cases, follicular involution was seen. A polyclonal plasmacytosis also was present. The spleens were markedly enlarged, more than 10 times normal size. There was expansion of both white pulp and red pulp, with increased DN T cells. DN T cells also were observed in liver biopsies exhibiting portal triaditis. In the peripheral blood, the T cells showed increased expression of HLA-DR and CD57 but not CD25. CD45RA+ T cells were increased in the four cases studied. Polyclonal B cell lymphocytosis with expansion of CD5+ B cells was a characteristic finding. Taken together, the histopathological and immunophenotypic findings, particularly in lymph nodes and peripheral blood, are sufficiently distinctive to suggest a diagnosis of ALPS. Of note, two affected family members of one proband developed lymphoma (T-cell-rich B-cell lymphoma and nodular lymphocyte predominance Hodgkin's disease, respectively).
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PMID:Pathological findings in human autoimmune lymphoproliferative syndrome. 981 46

Lymph node excision biopsy is commonly carried out for the investigation of lymphadenopathy. The objective of this study is to elucidate the pattern of nodal pathology seen in a private pathology practice. A total of 137 nodal biopsies for primary investigation of nodal enlargement were retrieved from the files in a private diagnostic pathology laboratory in the year 1997. Lymph nodes excised for cancer staging were excluded from this study. The histology was reviewed based on H&E stained sections, and with additional histochemical and immunoperoxidase stains when deemed necessary. Cases of malignant lymphomas were sub-classified with the aid of further immunophenotyping using a panel of monoclonal and polyclonal lymphoid antibodies. One case was excluded from this study due to inadequate tissue for further assessment. There were 58 males and 78 females, giving a ratio of 1:1.3 in the remaining 136 cases. They consisted of 13 Malays (M), 108 Chinese (C), 14 Indians (I) and 1 other ethnic group (O). The ratio of M:C:I:O was 1:8.3:1.1:0.1. The majority of the cases were in the age range of 20 to 50 years. The pathology consisted of 17 (12.5%) malignant lymphomas [6 Hodgkin's lymphoma, 11 non-Hodgkin's lymphoma], 35 (25.7%) metastatic carcinomas, 45 (33.1%) reactive hyperplasia, 19 (13.9%) tuberculosis, 11 (8.2%) Kikuchi's disease and 9 (6.6%) others (Castleman's disease 2, cat scratch disease 2, Kimura's disease 1, sarcoidosis 1, non-specific lymphadenitis 3). All categories of nodal disease showed approximately similar ratio of ethnic and gender distribution as above, except for Kikuchi's disease, for which 100% of the patients were female. The most common site of biopsy was from the head and neck region, particularly the cervical group of nodes. The most common nodal pathology seen in the private laboratory was reactive hyperplasia, followed by metastatic carcinoma. Malignant lymphoma constituted only 12.5% of the cases.
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PMID:Pattern of lymph node pathology in a private pathology laboratory. 1106 12

Lymph nodes with Hodgkin disease (HD) harbor few neoplastic cells in a marked leukocytic infiltrate. Since chemokines are likely to be involved in the recruitment of these leukocytes, the expression of potentially relevant chemokines and chemokine receptors were studied in lymph nodes from 24 patients with HD and in 5 control lymph nodes. The expression of regulated on activation, normal T cell expressed and secreted (RANTES), monocyte chemotactic protein (MCP)-1, macrophage inflammatory protein (MIP)-1alpha, and MIP-1beta was analyzed by in situ hybridization and that of CCR3 and CCR5 by immunohistochemistry and flow cytometry. It was found that, overall, the expression of all 4 chemokines was markedly enhanced, but the cellular source was different. RANTES was expressed almost exclusively by T cells whereas the expression of MCP-1, MIP-1alpha, and MIP-1beta was confined largely to macrophages. In control lymph nodes, chemokine expression was low, with the exception of MIP-1alpha in macrophages. CCR3 and CCR5 were highly expressed in T cells of HD involved but not of control lymph nodes. CCR3 was equally distributed in CD4+ and CD8+ cells, but CCR5 was associated largely with CD4+ cells. In HD lymph nodes, CCR3 and CCR5 were also expressed in B cells, which normally do not express these receptors. All these chemokines and receptors studied, by contrast, were absent in the neoplastic cells. It was concluded that chemokines are involved in the formation of the HD nonneoplastic leukocytic infiltrate. Expression of CCR3 and CCR5 appears to be characteristic of HD, but the roles of these receptors' up-regulation for the disease process remain unclear.
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PMID:CC chemokines and the receptors CCR3 and CCR5 are differentially expressed in the nonneoplastic leukocytic infiltrates of Hodgkin disease. 1123 88

The etiology of classical Hodgkin lymphoma (cHL) is largely unknown. High serum CD30-levels are associated with increased risk of cHL. Epstein-Barr virus (EBV) is detectable in the tumor cells in 1/3 of cHL cases in the Western world. The PD-1 pathway (T-cell inflamed immune response) might contribute to the pathogenesis by enabling pre-malignant CD30+ or EBV + cells to evade immune surveillance. We aimed to investigate if high infiltrations of CD30+, PD-1+, PD-L1+ and EBV + cells in benign lymph nodes from patients that later develop cHL (cases) (n = 15) were associated with risk of cHL compared to controls (n = 45) with benign lymph nodes from patients that did not develop cHL. Pathology registries including 3500 cH L patients were screened. Lymph nodes were stained with immunohistochemistry and in situ hybridization and the risk for cHL calculated with logistic regression. High CD30-expression by B- and T-cells was associated with a decreased risk of cHL [(OR = 0.10, 95 % CI:0.03-0.39) and (OR = 0.13, 95 % CI:0.01-0.71), respectively], which remained significant for CD30 + B-cells (OR = 0.15, 95 % CI:0.03-0.60) in multivariate analyses. Amount of PD-1+, PD-L1+ and EBV + cells were not statistically significantly associated with risk of cHL. However, the amount of PD-L1+ leukocytes tended to be higher in cases later developing cHL (OR = 2.84, 95 % CI:0.61-12.61). High proportions of potential precursors to cHL, i.e. CD30 + B-cells in benign lymph nodes are not associated with an increased risk of cHL, while a tendency for a T-cell inflamed immune response, i.e. abundant PD-L1+ cells, was observed in biopsies taken prior to the cHL diagnosis.
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PMID:Precursor cells and implications of a T-cell inflamed immune response in the pre-malignant setting in Hodgkin lymphoma. 3178 52

The case of 70-year-old man with mantle cell lymphoma (MCL) carrying t(11;14) translocation that relapsed as nodal lymphoma combining MCL and classic Hodgkin lymphoma (cHL) 9 years after autologous peripheral blood stem cell transplant (auto-PBSCT) is reported. Lymph nodes contained two separate areas of MCL and cHL-like components. Hodgkin and Reed-Sternberg (HRS)-like cells were accompanied by a prominent histiocyte background. HRS-like cells were CD5- , CD15+ , CD20- , CD30+ , PAX5+ , Bob.1- , Oct2- and EBER+ . The MCL component expressed cyclin D1 and SOX11, whereas cyclin D1 and SOX11 expressions were reduced and lost, respectively, in HRS-like cells. Polymerase chain reaction results showed a single clonal rearrangement of the IGH gene in MCL and cHL-like components. CCND1 break apart fluorescence in situ hybridization showed split signals in both MCL and HRS-like cells, suggesting that MCL and cHL-like components were clonally related. Acquisition of p53 expression and Epstein-Barr virus (EBV)-positivity was seen in HRS-like cells. The patient died of disease progression with elevated hepatobiliary enzymes. The autopsy showed both MCL and cHL-like components around the bile ducts, splenic white pulp and bone marrow. The two components were phenotypically distinct, but genetically related, suggesting that transformation of MCL to HRS-like cells during the course of MCL in association with EBV infection.
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PMID:Mantle cell lymphoma with EBV-positive Hodgkin and Reed-Sternberg-like cells in a patient after autologous PBSCT: Phenotypically distinct but genetically related tumors. 3307 23


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