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

Like other immunodeficient populations, HIV-infected individuals are at risk for developing high grade B-cell malignancies. The aetiology of these lymphomas remains unknown. While the tumours share many of the features of B-cell lymphomas seen in immunosuppressed transplant recipients, unlike transplant recipients, Epstein-Barr virus genomic sequences are identified in only a small minority of peripheral lymphomas from HIV-infected individuals. The majority of lymphomas are classified as diffuse, large-cell tumours of either the intermediate grade type or the high grade immunoblastic type. However, approximately one-third of patients present with high grade, small, non-cleaved cell lymphomas. Patients typically present with widespread extranodal disease, often at unusual sites. Lymphoma confined to the central nervous system has been observed in approximately 25% of HIV-infected patients with non-Hodgkin's lymphoma. The therapeutic outcome and survival in these patients has been disappointing. Complete response is achieved less frequently, relapse rates are higher and survival generally shorter than those observed in non-HIV-infected patients with non-Hodgkin's lymphoma. Prognosis is better for those patients without a prior AIDS diagnosis, who have higher total CD4 cell counts, good performance score, absence of an extranodal site of disease, and treatment with more moderate doses of chemotherapy. Hodgkin's disease, while not causally linked to the presence of immunodeficiency, appears to have a more aggressive natural history in the patient with HIV infection. Advanced disease at presentation is the rule, and the response to therapy has been poor with associated short survivals. Poor bone marrow reserve and the occurrence of intercurrent opportunistic infections has made it difficult to administer many of the standard chemotherapeutic regimens now used for the treatment of Hodgkin's disease.
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PMID:AIDS-associated lymphoma. 218 38

Congenital and acquired states of immunodeficiency have long been associated with an increased incidence of malignant lymphoma. An increased incidence of non-Hodgkin's lymphomas was recognized early in the epidemic immunodeficiency state associated with the human immunodeficiency virus (HIV) infection AIDS. Although the precise etiologic mechanism of these lymphomas remains speculative, the presence of Epstein-Barr viral proteins or sequences and characteristic chromosomal translocations giving rise to altered expression of the c-myc oncogene have frequently been observed. It has been suggested that HIV infection leading to disordered T-lymphocyte function (possibly in conjunction with Epstein-Barr infection) leads to the emergence of polyclonal populations of stimulated B lymphocytes. These cells, which undergo physiologic immunoglobulin gene rearrangement, may provide the background for the occurrence of characteristic chromosomal translocations that lead to the emergence of malignant lymphomas. These lymphomas tend to present clinically with high-grade histopathologic subtype, advanced stage, and a propensity for the involvement of otherwise unusual extranodal sites, including the central nervous system. The experience with therapy for HIV-associated lymphomas has indicated that highly aggressive, dose-intensive chemotherapy regimens may be associated with inferior results. More recent regimens have stressed less myelosuppressive therapy combined with prophylaxis for central nervous system disease and pneumocystis infection. The dominant prognostic factors in the HIV-associated lymphomas appear to be primarily related to the underlying HIV infection and include total CD4 lymphocyte count, performance status, and prior AIDS diagnosis.
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PMID:Acquired immunodeficiency syndrome-associated lymphomas. 218 76

T-lymphocyte subgroups and the percentage and the activity of Human Natural Killer cells (HNK) were investigated by the authors in their 24 patients suffering with low grade and 24 with high grade malignancies of non-Hodgkin lymphoma (NHL). According to their observations, the ratio of CD3, CD4, Leu-7, and HNK cells as well as the release by HNK cells of 51Cr bound to target cells decreased, depending on the pathological stage. The tests were performed with monoclonal antibodies. A significant change could also be observed in the reactivity of bone marrow cells to monoclonal sera, which showed complete correspondence in character with the behavior of lymphocytes isolated from peripheral blood. No significant changes could be observed in the quantitative relations of immunoglobulins. Discussing the supposed immunological relation in detail, the role of plasma factor that reduces the formation of T-lymphocytes, is assumed to have primary importance in this phenomenon.
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PMID:[T-lymphocyte subgroups and the activity of human natural killer cells in non-Hodgkin lymphoma of moderate and high malignancy]. 219 10

A case of lymphocyte-depletion Hodgkin's disease is described for the purpose of reviewing the criteria currently used to distinguish this disease from other pleomorphic large-cell malignancies. A 76-year-old man with a 3-month history of daily fevers underwent extensive evaluation and exploratory laparotomy, which revealed only two large, separate splenic tumor nodules. Postoperatively, the patient remained asymptomatic. Histologically, the tumor was composed of giant cells, including both typical Reed-Sternberg forms and mononuclear variants with inflammatory stromal response along its borders. Immunoperoxidase showed tumor cells to be strongly reactive for Leu-M1 (CD15), BER-H2 (CD30), Leu-3 (CD4), and T11 (CD2) and weakly reactive for Leu-4 (CD3) but nonreactive for EMA, LCA, lysozyme, Leu-9, Leu-M3, Leu-M5, and immunoglobulin light chains. Southern blot analysis revealed an isolated clonal band for kappa light chain only. Included in the discussion of this case of primary splenic lymphocyte-depletion Hodgkin's disease is a review of clinical, histologic, immunohistochemical, and gene-rearrangement characteristics of what can be defined as lymphocyte-depletion Hodgkin's disease.
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PMID:Primary splenic lymphocyte-depletion Hodgkin's disease. 222 Jun 73

In order to elucidate the pathological and epidemiological features of malignant lymphoma (ML), particularly of adult T-cell lymphoma/leukemia (ATLL) in the Kagoshima district, age-adjusted and age-specific incidence rates of malignant lymphomas were estimated on 3239 histologically confirmed cases between the years 1963 and 1987. There was a marked increase in the incidence rate from 1976 (4.9) to 1982 (8.5) due to the increase of T-cell lymphomas. The increase was not conspicuous after 1982. Immunohistochemically, all of the 429 MLs found in 1985 and 1986 were examined on paraffin sections and 70 ATLL cases on fresh frozen sections. T-cell ML comprised 65.3%, B-cell ML 30.5%, Hodgkin disease 2.6%, and histiocytic ML 1.2%. Most of ATLL cells were phenotypically CD4+ CD8-, 14% of ATLL cases showed CD4+ CD8+, 6% were CD4- CD8+, and 7% were CD4- CD8-. The simulataneous expression of IL 2 and IL 2R was seen in 8 (16%) out of 56 patients examined. Therefore, a proliferation by autocrine mechanism does not seem to be a major course of ATLL progression.
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PMID:Pathoepidemiological features of adult T-cell lymphoma/leukemia in an endemic area: Kagoshima, Japan. 222 7

Morphological and immunological phenotyping was carried out on 20 cases of peripheral baboon T-cell non-Hodgkin's malignant lymphomas (NHL) observed in a Sukhumi monkey colony. Morphologically, the lymphomas were prolymphocytic, immunoblastic, or rarely lymphoblastic types. For immunophenotyping studies, the panel of 29 monoclonal antibodies (MAb) to human or mouse leukocytic antigens were used (18 CD clusters). Three polyclonal sera to human IgG and light chains kappa and lambda were also taken in experiments. The investigated NHLs and CD4+CD8- (12 cases) or CD4-CB8+ (5 cases) phenotypes. In some cases loss of pan T-cell antigens or unusual antigen expression--loss (one case) or coexpression (two cases) of T-subset antigens--or the presence of abnormal lymphoid antigens have been revealed. In most studies, baboon T-cell NHLs tumor cells belonged to activated T-cells because they expressed Ia-like antigens and IL2R at high levels. There was no correlation between the discovered immunophenotype and the morphological pattern of malignant lymphomas.
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PMID:[Non-Hodgkin's malignant lymphomas in primates (immunodiagnostic principles in T-cell lymphomas)]. 226 82

During the period 1972 till the end of 1987, 107 patients with the diagnosis of mycosis fungoides or cutaneous T-cell lymphoma were examined and treated in the Department of Dermatology, Marselisborg Hospital. This disease belongs to the group of non-Hodgkin T-cell lymphomata. The diagnosis is based on the occurrence of red, scaly plaques in the skin associated with itching or tumours in the skin and, simultaneously, of a pleomorphic infiltrate consisting of CD4-positive T-lymphocytes which show characteristically exocytoses in the epidermis with subsequent formation of Pautrier's microabscesses. The disease may progress with spread to the regional lymph nodes where lymphomata develop. Treatment is initially local with employment of chlormethin ("nitrogen mustard gas") and this treatment can maintain the patients in remission for prolonged periods. In cases with spread to lymph glands or in particularly aggressive forms with tumour formation in the skin, combined chemotherapy is administered (prednisone, cyclophosphamide, etretinate and bleomycin). Thirty-eight of the patients were in stage I in which a clinical suspicion of mycosis fungoides was present but where the histological changes were insufficient to confirm the diagnosis. IVa and ten in stage IVb. The age at the onset of the symptoms was from 59 to 64 years (median values) for the various stages. Stages I and II had approximately 80% five-year survival, while the stages with more extensive spread had approximately 50% survival. The etiology of the disease is unknown but, during recent years, certain evidence has been found suggesting that activation of a retrovirus in the epidermis may be a contributory factor.
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PMID:[Mycosis fungoides. A review of the clinical picture, treatment and course in 107 patients]. 234 94

Follicular dendritic cells (FDC) are located within follicles of secondary lymphoid tissue and in lymph nodes of patients with germinal center cell-derived non-Hodgkin lymphomas. Reliable antigenic phenotyping of FDC within tissue sections has been difficult due to simultaneous labeling of the surrounding germinal center cells. Using an enzyme cocktail to digest human tonsils and cervical lymph nodes with subsequent fractionation by albumin gradient centrifugation, cell isolates containing up to 20% FDC were obtained. This preparation allowed the determination of antigenic phenotype on individual FDC. Molecules expressed by FDC were detected by an isotype-specific immunocytochemical double-labeling procedure, i.e. a monoclonal antibody (mAb) specific for FDC (KiM4 or DRC1) in conjunction with a mAb reactive against an additional antigenic determinant. Nonspecific binding of mAb to immunoglobulin Fc receptors located on FDC membranes was avoided by incubation of cells with human IgG aggregates prior to immunostaining. The results revealed that isolated FDC from these lymphoid tissues express transferrin receptors, the intercellular adhesion molecule 1, class II antigens, the B cell antigens CD20 and CD21, and the myelomonocytic properties CD11b and CD14. Immunoglobulin mu or gamma heavy chains and the B cell antigens CD23 and CD24 are detected on 50% of an isolated FDC population. These FDC are negative for the T helper cell antigen CD4, the B cell cell antigens CD19 and CD22, the immunolobulin alpha and delta chains and the S-100 protein. FDC isolated from lymph nodes of patients with low-grade malignant non-Hodgkin lymphoma, identified by DRC1 or KiM4 mAb, presented the same antigenic profile as seen on FDC from nonmalignant tissue. This suggests that FDC from lymphoma tissue isolated in this manner have the same properties as those found in normal tissue.
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PMID:Antigenic phenotyping of human follicular dendritic cells isolated from nonmalignant and malignant lymphatic tissue. 235 15

The authors evaluated suppressed in vitro functions of peripheral blood lymphocytes (PBL) as a possible tool in the early diagnosis of human lymphoma. In 13 of 22 patients with recent onset of various types of nonleukemic lymphomas (Mb. Hodgkin and non-Hodgkin's lymphomas of B-cell and T-cell origin) the mitogen response of PBL against phytohemagglutinin (PHA) and concanavalin A (Con A), as measured by 3H-thymidine (3HTdR) uptake, was found to be significantly suppressed, whereas the response to pokeweed mitogen (PWM) was normal in 18 cases. In parallel, cytofluorimetric analysis was done with PBL after 72 hours in culture with and without PHA, using antibodies against the differentiation antigens: CD3, CD8, CD4, CD19, and CDw14 and the activation antigens: interleukin-2 (IL-2) receptor (IL-2R, CD25), human leukocyte antigen DR (HLA-DR), and transferrin receptor (TR). Compared with healthy controls and patients with other diseases, a significant reduction of the total T-cell blast response, i.e., the percentage of large T-cells bearing activation markers, was found in all lymphoma cases including those with a normal 3HTdR uptake. Furthermore, a pronounced inhibition in the expression of the activation markers Il-2R and TR, but not of HLA-DR, was detected on CD3+ cells in PHA-stimulated PBL of all lymphoma cases. Thus, polyclonal activation combined with activation antigens seems to give more accurate information about the functional defect(s) of PBL in an early state of lymphoma; these parameters may therefore be valuable diagnostically. The abnormal pattern in the expression of T-cell activation antigens after polyclonal stimulation may help in the understanding the cellular immune defects associated with lymphoma.
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PMID:Peripheral blood lymphocytes of nonleukemic lymphoma patients exhibit aberrant expression of T-cell activation markers after polyclonal stimulation in vitro. 238 99

UCHL1 is a murine monoclonal antibody that recognises a 180-185 kD determinant on CD4 (72%) and CD8 (36%) positive T cells. This antibody is effective in formalin fixed and paraffin embedded tissues, using the immunoperoxidase method. One hundred and forty three cases of malignant lymphoma were examined. Neoplastic cells in 100% of cases of Mycosis fungoides (n = 10), 83% of cases of peripheral T cell lymphoma (n = 25), and 78% of cases of (T-ALL) T acute lymphoblastic lymphoma (n = 9) were stained by this antibody. In addition, staining was seen in 100% of cases of malignant histiocytosis of the intestine (n = 13), a condition now thought to be a T cell lymphoma. Two cases of true histiocytic lymphoma were also positive. This antibody stained neither the neoplastic cells in a wide range of B cell lymphomas (n = 62) nor Reed-Sternberg cells in 16 cases of Hodgkin's disease. UCHL1 also stained neoplastic cells in four cases of granulocytic sarcoma. A panel of normal tissues was similarly studied. Staining was seen in normal T cells and mucosal intraepithelial lymphocytes, macrophages, mature myeloid cells, and endometrial stromal granulocytes. UCHL1 is a monoclonal antibody that identifies T cells in formalin fixed paraffin embedded tissues, and should prove useful for diagnosing T cell lymphomas, especially when only formalin fixed tissue is available for diagnosis.
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PMID:Monoclonal antibody (UCHL1) that recognises normal and neoplastic T cells in routinely fixed tissues. 242 19


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