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)

We analyzed the series of 40 malignant lymphoproliferative diseases (MLD) in HIV positive patients, diagnosed between 1986 and 1993 in a University Hospital in Spain. Median age was 32 years. 52% of the patients belonged to the intravenous drug users risk group, and 30% were homosexual. 26 patients were diagnosed of a non-Hodgkin's lymphoma (NHL), 8 of Hodgkin's disease (HD) and 6 of a primary central nervous system lymphoma (PCL). The 6 patients with a PCL (median CD4 of 20 cells/mm3, 80% antecedent AIDS criteria) and 13 NHL with histology of immunoblastic, large cell, plasmablastic, and high grade lymphoma non-otherwise specified (median CD4 of 291, 58% with AIDS criteria) tended to appear in patients with a deteriorated clinical and immunological status due to the underlying HIV infection. However, the 14 small non-cleaved cell NHLs appeared in patients without a previous AIDS-defining condition (93% of the cases, p = 0.065 compared with other NHL histologies). Finally, 8 patients with HD had a low CD4 cell count (median 103 cells/mm3, p = 0.049 compared with median CD4 in NHL patients) without other previous AIDS criteria. In conclusion, The presenting characteristics of HIV positive patients with MLD allows to define four subgroups of patients with a high clinicopathological correlation.
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PMID:[Initial clinicopathological manifestations of malignant lymphoproliferative processes in patients with human immunodeficiency virus seropositivity. Study of 40 cases]. 806 Nov 35

Immunosuppressed individuals are at high risk for the development of hematologic malignancies. The typical lymphomas arising in organ transplant recipients are B-cell non-Hodgkin's lymphomas that contain Epstein-Barr virus (EBV) DNA sequences. We investigated the characteristics of posttransplant lymphomas that lacked expression of the usual markers associated with EBV transformation. We describe four large-cell lymphomas seen recently at our institution. Two of these four cases were CD4+, one was CD8+, and in one staining for CD4 and CD8 expression was not performed. One CD4+ lymphoma was a CD30+, EBV- large-cell lymphoma from a 65-year-old kidney transplant recipient, the second was an EBV+ large-cell lymphoma from a 25-year-old heart transplant patient. Two T-cell lymphomas were EBV+ and had clonal T-cell receptor beta gene rearrangements. The other two lymphomas expressed T-cell markers CD4 and CD43, and lacked expression of B-cell markers CD19, CD20, CD21, CD22, CD23, and surface Ig. Both CD4+ lymphomas were tumorigenic after their heterotransplantation into severe combined immunodeficient (SCID) mice. Cytogenetics, immunophenotyping, and genotyping of the secondary tumors from SCID mice showed their clonality and identity with the patients' primary tumors. Novel CD4+ lymphoma cell lines, LH521/4 and LK418/4, were established from tumors that had been passaged in SCID mice. An immunodeficient environment may facilitate the growth of these T-cell or biphenotypic lymphomas; the etiology of their genesis can include transformation with EBV and other, as yet unidentified mechanisms.
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PMID:Characterization of posttransplant lymphomas that express T-cell-associated markers: immunophenotypes, molecular genetics, cytogenetics, and heterotransplantation in severe combined immunodeficient mice. 810 Jul 21

Hematologic and immunologic recovery after treatment for different solid tumors was investigated in 11 children at cessation of therapy and at 1, 3, 6, 9, and 12 months after cessation of therapy by determining blood total leukocyte counts, leukocyte differentials, lymphocyte subsets, concentrations of serum immunoglobulins (Igs), and serum IgG subclasses. Lymphocyte subsets were analyzed from mononuclear cell fractions by flow cytometry and use of monoclonal antibodies CD3, CD20, CD4, CD8, CD4/Leu-8, and CD4/CD45RA. Peripheral blood total leukocyte, neutrophil, and B-cell counts recovered early, although defective B-cell function was seen in several patients. T-cell counts and thus total lymphocyte counts required a longer time to normalize even though inducer T-cell subsets (CD4+CD45RA+ and CD4+Leu-8-) were present in normal or high amounts. CD8+ T cells recovered earlier than CD4+ T cells. The lymphocyte, B-cell and T-cell counts of most patients normalized during the first 12 months after therapy. Recovery of total lymphocyte and T-cell counts was slow in patients with Hodgkin's disease or Burkitt's lymphoma and rapid in nephroblastoma. Radiotherapy seemed to prolong the recovery of study parameters, particularly T-cell recovery.
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PMID:Recovery of blood lymphocytes and serum immunoglobulins after treatment of solid tumors in children. 815 98

We describe 4 cases of adult T-cell leukemia (ATL) with unusual morphology and aberrant immunophenotype. All patients were Japanese and born in the Nagasaki district, an area endemic for HTLV-I. Peripheral blood and/or bone marrow films revealed bizarre giant cells with and without large nucleoli; the cells were 5 to 6 times the diameter of erythrocytes, resembling Hodgkin's cells. Some peripheral blood cells were morphologically similar to prototypic ATL cells, while many other cells in the bone marrow showed unusual morphology. Furthermore, leukemic cells had aberrant immunophenotypes such as the CD8-positive type in patients 1 and 2, the CD4-.CD8- double-negative type in patient 3, and the CD5 antigen defect in patient 4. All patients had marked elevations of the serum calcium and LDH and organomegaly, while all had a short survival. Anti-HTLV-I antibodies and provirus DNA monoclonality were demonstrated in all patients. The results suggested that the unusual morphology and aberrant ATL cell immunophenotype may be indicative of a high grade malignant behaviour of ATL.
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PMID:Unusual morphological features of adult T-cell leukemia cells with aberrant immunophenotype. 816 29

A case report of a 28-year-old mother of two children with FUO is presented. Physical examination revealed an anemic and febrile woman, who lost 10 kg of weight during the past 3 months. Furthermore, two lymphatic nodes with diameters below 1 cm were detected at the neck and inguinal region. A search for origin of fever including evaluation of foci, malignancies and laboratory investigations was primarily unsuccessful. At day 7 after admission a pericardial murmur could be heard. Echocardiography revealed a pericardial effusion, which increased up to 4 cm during the following days, leading to hemodynamic impairment and asystole. Immediate CR was successful, pericardial effusion was aspirated. Looking for etiology of fever the presence of IgM-antibodies against toxoplasma gondii by an ELISA test was possible. Therefore, toxoplasmosis was diagnosed and a treatment-regimen comprising pyrimethamin and sulfadiazin was initiated. Because of the threat to life and very high titers of C-reactive protein, antibiotic therapy (imipenem) was given additionally. An immunologic impairment was excluded by normal ratio of CD4:CD8 of lymphocytes, normal HIV-test and a nonsuspicious Jamshidi-biopsy of the bone marrow. However, in week 9 after admission lymphatic node-tumors suddenly appeared at the neck and pulmonary hilus. After diagnostic exstirpation a malignant non-Hodgkin-lymphoma (T-cell-type) was diagnosed. It is concluded that in obscure pericardial effusion toxoplasmosis should be considered and that this manifestation may be a precursor of malignant non-Hodgkin-lymphoma.
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PMID:[Toxoplasmosis peri-myocarditis as initial manifestation of highly malignant non-Hodgkin's lymphoma]. 817 47

Acquired pure red cell aplasia (PRCA) has been associated with various lymphoproliferative conditions but its occurrence with Hodgkin's disease is rare. We report a case of PRCA occurring immediately following the completion of induction chemotherapy in a patient with Stage IIIB nodular sclerosing Hodgkin's disease. In vitro erythroid colony studies documented evidence for T cell mediated suppression of erythropoiesis and lack of a serum inhibitor. Addition of cyclosporin to the in vitro cultures stimulated erythroid colony growth. Following in vivo treatment with cyclosporin peripheral blood CD4/CD8 ratios returned to normal. However, serum erythropoietin levels were inappropriately low. Subsequent treatment with erythropoietin induced a reticulocytosis and transfusion independence. Since discontinuing the erythropoietin, the patient has been able to maintain a hemoglobin of 100 g/L. This case illustrates that red cell aplasia occurring in the setting of Hodgkin's disease may be due to T cell mediated suppression of erythropoiesis. A response to cyclosporin may be masked by inappropriately low erythropoietin levels.
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PMID:Pure red cell aplasia after chemotherapy for Hodgkin's lymphoma: in vitro evidence for T cell mediated suppression of erythropoiesis and response to sequential cyclosporin and erythropoietin. 818 75

Expression of CD4 or CD8 on the cell surface is an important guide for discriminating the immunologic functions of T-cells. However, a minor T-cell subset lacking both CD4 and CD8 molecules but bearing the usual form of T-cell receptor (TCR)-alpha beta (CD4-CD8-TCR-alpha beta+ T-cells) has recently been found not only in mice but also in humans, and the clinical relevance of this newly defined subpopulation to human diseases is now of considerable interest. The authors present a patient in whom CD4-CD8-TCR-alpha beta+ T-cells showed monoclonal proliferation in the peripheral blood for more than 3 years, then disappeared spontaneously, followed by subsequent development of Hodgkin's disease. The pathologic roles of double-negative T-cell proliferation in this case are discussed from the viewpoint of premalignancy in lymphoproliferative diseases.
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PMID:Monoclonal proliferation of double-negative (CD4-CD8-) T-cells bearing T-cell receptor-alpha beta followed by subsequent development of Hodgkin's disease. 819 23

We measured the soluble (s) receptors CD23, CD8, CD4, interleukin-2 receptor (IL-2R, CD25), and transferrin receptor (TfR, CD71), in normal serum and in patients with chronic lymphocytic leukemia (CLL) and evaluated them in relation to clinical and biological parameters of the disease, as well as serum immunoglobulin E (IgE). Compared to 31 normal individuals, 42 CLL patients had increased levels of sCD23 (98.4 +/- 127.7 versus 0.9 +/- 0.3 U/ml, p < 0.001), sIL-2R (6080 +/- 7030 versus 1420 +/- 640 pg/ml, p < 0.001), sTfR (12,100 +/- 11,250 versus 5000 +/- 1050 ng/ml, p < 0.001), and sCD8 (510 +/- 191 versus 234 +/- 89 U/ml, p < 0.001), but normal sCD4 levels. Mean sCD23 levels remained normal in patients with non-Hodgkin's lymphoma (other than small lymphocytic), Hodgkin's disease, hairy cell leukemia, acute lymphoblastic leukemia (ALL), acute myelogenous leukemia (AML), chronic myelogenous leukemia (CML), multiple myeloma, or solid tumors. Advancing Rai clinical stage was associated with a progressive elevation of sCD23 (p < 0.001), while sCD8 (p < 0.05), sIL-2R (p < 0.001), and sTfR (p < 0.005) were highest in stage 2 patients. Discriminant analysis confirmed the value of soluble receptor determinations in the clinical evaluation of CLL patients. sCD23 correlated with sIL-2R (p < 0.001) and sTfR (p < 0.05) but not with sCD4 or sCD8, and displayed an inverse relationship with serum IgE (NS) and total gamma-globulin (p < 0.05). sIL-2R correlated with sCD23 (p < 0.001), sTfR (p < 0.001), sCD4 (p < 0.01), and sCD8 (p < 0.01). The lymphocyte count correlated with serum lactate dehydrogenase (LDH) (p < 0.05), sCD23 (p < 0.001) and sIL-2R (p < 0.01) but not sTfR, sCD8, or sCD4. Chemotherapy produced consistent reductions of sCD23 levels in two responding patients. We conclude that: (i) sCD23 is considerably elevated in CLL, correlates with the tumor mass and clinical stage, and could be helpful in monitoring these patients; and (ii) sIL-2R, sCD8, and sTfR levels are less specifically increased and could be influenced by other factors such as immune activation and erythropoiesis.
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PMID:Soluble CD23 and other receptors (CD4, CD8, CD25, CD71) in serum of patients with chronic lymphocytic leukemia. 825 2

The cell line AG-F was isolated from the marrow of a neuroblastoma patient undergoing myeloablative treatment and autologous bone marrow rescue. A year later, the patient developed a Hodgkin's type lymphoma. AG-F cell line demonstrated an unusual phenotype, lacking surface CD2 and CD3, but expressing high levels of CD4, CD5, CD7, CD29, and CD45RO. Markers associated with Hodgkin's lymphoma cells, CD15 and CD30, were also positive. AG-F cells grow in suspension in clusters of 50-200 cells, with a doubling time of 9 h. They can also grow in serum-free medium and form tumors in nude mice. AG-F cells have amplified N-myc and c-myc and high levels of the corresponding mRNA transcripts. Cytogenetic analysis revealed a DNA index by flow cytometry of near tetraploid cells and a karyotype of 85-87 chromosomes, with consistent abnormalities in chromosomes 1, 5, and 9. Gene rearrangement studies revealed rearrangement of the beta gene of the T-cell receptor. AG-F cells secrete high levels of IL-6, IL-8, IL-10, and GM-CSF. Cell adherence and formation of long processes could be induced by fibronectin and were enhanced by exposure to PMA. Cells exposed to phorbol myristate acetate (PMA) had increased expression of CD11a, CD11b, CD18, CD45RO, and HLA-DR, whereas expression of CD15 and CD30 was markedly decreased. Similarly, the level of c-myc and N-myc oncoproteins and the levels of the cytoskeletal proteins, actin, tubulin, and vimentin markedly decreased early after PMA-induced differentiation.
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PMID:Isolation and characterization of an early T-helper/inducer cell line with a unique pattern of surface phenotype, constitutive cytokine secretion and myc oncogene expression. 825 4

The recombination activating gene, RAG-1, which is supposed to encode a molecule regulating V(D)J recombination, has been isolated. In the current study, the distribution of RAG-1 expression in human neoplastic hematopoietic cells was compared with the phenotypic and genotypic status of differentiation. Thirty-one hematopoietic cell lines (16 B-lineage, 9 T-lineage, 2 Hodgkin's disease, and 4 nonlymphoid cell lines) were investigated for the expression of human RAG-1 using the reverse-transcriptase polymerase chain reaction (RT-PCR). RAG-1 was not expressed in nonlymphoid, Hodgkin's disease, or mature-stage lymphoid cell lines, but was present in some acute lymphoblastic leukemia (ALL)/lymphoblastic lymphoma (LBL) cell lines. The investigation was extended to 45 cases of fresh ALL/LBL cells. The patterns of RAG-1 expression found in the cell lines and fresh ALL/LBL cells were similar. In B-lineage cells, the product of RAG-1 RT-PCR was detected in CD19+ CD10- CD20- CD5- stage (stage II, Nadler's classification) and was at the highest level in CD19+ CD10+ CD20- CD5- stage (stage III), but was absent or limited in CD19+ CD10+ CD20-+ CD5- (stage IV) or CD19+ CD10+ (or CD10-) CD5+. In stage II, monoclonal gene rearrangements of only the immunoglobulin heavy chain (IgH) were found, whereas monoclonal gene rearrangements of both IgH and T-cell receptor (TCR)-beta chain were frequently noted in stages III and IV. The expression of CD20 or CD5 antigen apparently correlated with the decline of RAG-1 expression. In T-lineage cells, RAG-1 was highly expressed in CD3- CD4+ CD8+/CD3+ CD4+ CD8+ thymic stages, but was negative or only weakly expressed in the CD3- CD4- CD8- prothymic or early thymic stage, in which the TCR-beta gene was often germline, or the CD3+ CD4+ CD8- mature thymic stage. The relative levels of RAG-1 mRNA give an additional delineating frame to the schemes of lymphoid differentiation based on phenotypic and genotypic status. RAG-1 is exhibited by cells of the thymic stage capable of synthesizing TCR or expressing it on the cell surface. The weak or absent expression of RAG-1 in the prothymic or early thymic stage suggests that the contribution of RAG-1 to the gene rearrangement may differ quantitatively between TCR-delta/TCR-gamma and TCR-beta.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Human recombination activating gene-1 in leukemia/lymphoma cells: expression depends on stage of lymphoid differentiation defined by phenotype and genotype. 839 73


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