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)

Idiopathic thrombocytopenic purpura (ITP) in the course of Hodgkin's disease is generally judged to be a paraneoplastic immune phenomenon. This concept finds support in the observation of a patient who developed simultaneously a recurrence of ITP and a protein anomaly in the form of an alpha-chain protein. Combined chemotherapy brought about remission of the Hodgkin's disease at the same time as normalisation of the platelet values and disappearance of the alpha-chain protein. There is no necessary correlation between tumour activity and ITP. But if ITP is observed, the most effective means would seem to be rigorous treatment of the Hodgkin's disease.
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PMID:[Idiopathic thrombocytopenic purpura in Hodgkin's disease--an early sign of a recurrence (author's transl)]. 56 41

The histology of 125 cases of primary gastrointestinal lymphomas arising in the stomach and small and large intestine has been reviewed. The material was gathered from the Bland-Sutton Institute of Pathology at the Middlesex Hospital and from the Westminster Hospital. Of the initial total of 143 cases diagnosed, 18 were rejected. Of the acceptable 125 cases, 51 lymphomas were arising in stomach, 53 in the small intestine and 21 in the large intestine including rectum. Excluding the four children in the series, ages ranged from 18 to 82 and were fairly evenly distributed across the decades. There was no significant sex difference in the Middlesex Hospital cases but in the Westminster Hospital series the male to female ratio was approximately 2.6 to 1. One significant finding to emerge from this histological survey, and which forms the basis of this communication, is the proportion of lymphomas considered to be predominantly of plasma cell type. These plasma cell tumours, or extramedullary plasmacytomas, accounted for 49 out of the 125 cases (39%) of gastrointestinal lymphomas. They were less common in stomach and most common in the intestine, the majority occurring in the ileocaecal region. Conversely, Hodgkin's disease, in contrast to some series, was not encountered. Of the non-Hodgkin's lymphomas, grade I tumours were uncommon and true histiocytic lymphomas were distinctly rare. The high incidence of plasma cell tumours were uncommon and true histiocytic lymphomas were distinctly rare. The high incidence of plasma cell tumours in our series is in keeping with the morphological findings of a previous study carried out in patients with alpha-chain disease and in a small series of primary gastrointestinal lymphomas.
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PMID:Primary lymphomas of the gastrointestinal tract. I. Plasma cell tumours. 61 34

Twenty-three monoclonal antibodies (MAbs) against the IL-2 receptor alpha-chain (CD25) were evaluated as ricin A-chain immunotoxins for the treatment of Hodgkin's disease. Primary screening used an indirect assay in which the cells were treated with the test antibody followed by a Fab' immunotoxin against mouse immunoglobulin. This screening identified 5 MAbs which inhibited protein synthesis in L540 Hodgkin cells by 50% at a concentration (IC50) of 6 x 10(-11) M or less: RFT5 gamma 1, RFT5 gamma 2a, B-B10, B-F2 and B-G3. These MAbs were then linked directly to deglycosylated ricin A-chain (dgA) and were confirmed to have potent and specific toxicity for L540 cells. The immunotoxins had the following potency order: RFT5 gamma 1 greater than RFT5 gamma 2a greater than B-B10 greater than B-F2 greater than B-G3. The most effective immunotoxin, RFT5 gamma 1.dgA, had an IC50 value of 7 x 10(-12) M, which is the same as that of whole ricin. In vivo, a single intravenous injection of 48 micrograms of RFT5 gamma 1.dgA, RFT5 gamma 2a.dgA, B-B10.dgA or B-F2 induced lasting complete remissions in 78, 66, 50 and 44%, respectively, of nude mice bearing subcutaneous solid L540 tumours of 0.7 cm diameter. Two tumours which regrew after B-B10.dgA treatment were re-established in tissue culture. Both had reduced sensitivity to B-B10.dgA in vitro but not to immunotoxins recognizing different antigens on Hodgkin cells. The MAbs that produced the most potent immunotoxins, RFT5 gamma 1, RFT5 gamma 2a and B-B10, had no significant cross-reactivity with normal human tissues outside the lymphoid system as judged from indirect immunoperoxidase staining of frozen sections. By contrast, B-F2 strongly stained normal human renal tubules.
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PMID:Immunotoxins constructed with anti-CD25 monoclonal antibodies and deglycosylated ricin A-chain have potent anti-tumour effects against human Hodgkin cells in vitro and solid Hodgkin tumours in mice. 191 43

A monoclonal antibody-secreting hybridoma cell line, VCD-1, was derived from the fusion of murine myeloma cells with splenocytes from a BALB/c mouse that had been immunised with chronic B-lymphocytic leukaemia cells. The cells came from a patient who had developed the leukaemia approximately 10 years after a course of radiotherapy for nodular sclerosing Hodgkin's disease. The antibody bound to a 30,000-dalton protein that was present in normal and malignant B cells, in monocytes, neutrophils, and interdigitating reticulum cells, and in malignant cells present in Hodgkin's disease lymph nodes. The reactive epitope was not accessible to antibody in viable intact cells; binding to peripheral blood cells could only be seen if the cells were fixed. The antibody recognises a determinant that probably resides on the alpha-chain of HLA class II molecules.
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PMID:A monoclonal antibody to an antigen present in cells from a patient with Hodgkin's disease. 331 34

The data obtained on red cell hemolysates from 16 patients with Hodgkin's disease varying in age, sex, the disease stage and histology, time since the diagnosis served the basis for comparative evaluation of endogenic intraerythrocytic hemoglobin proteolysis and relevant products. The results show that Hodgkin's disease brings about a 10-15-fold increase in the quantity of accumulated hemoglobin alpha-chain fragments.
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PMID:[Changes in the intraerythrocytic proteolysis of human hemoglobin in lymphogranulomatosis]. 748 2

The erythrocyte lysate samples obtained from 10 healthy donors (aged of 23 +/- 12 years) and 16 patients with Hodgkin's disease (aged of 39 +/- 25 years) with the following histological types: 12 mixed cellularity and 4 nodular sclerosis, were studied. Patients with Hodgkin's disease (HD) were randomly selected before, during or after the completion of combined chemotherapy. A comparative analysis of peptide components of erythrocyte lysate samples of HD patients and healthy donors was carried out. The amino acid sequences of 4 peptides, corresponding to fragments 1-33, 1-32, 1-31 and 1-30 of human hemoglobin (Hb) alpha-chain were determined. Increase of the content of two fragments corresponding to 1-31 and 1-32 amino acid residues of alpha-globin were detected for HD patients. The link between the normal process of proteolytic degradation and those occurring during HD is proposed. The possibility of using the identified alterations recorded during HD diagnosis is discussed.
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PMID:Alteration of intraerythrocyte proteolytic degradation of hemoglobin during Hodgkin's disease. 881 85

CD30 ligand (CD30L) is a type-II membrane glycoprotein capable of transducing signals leading to either cell death or proliferation through its specific counterstructure CD30. Although several lines of evidence indicate that CD30L plays a key role as a paracrine- or autocrine-acting surface molecule in the deregulated cytokine cascade of Hodgkin's disease, little is known regarding its distribution and biologic significance in other human hematopoietic malignancies. By analyzing tumor cells from 181 patients with RNA studies and immunostaining by the anti-CD30L monoclonal antibody M80, we were able to show that human hematopoietic malignancies of different lineage and maturation stage display a frequent and broad expression of the ligand. CD30L mRNA and surface protein were detected in 60% of acute myeloid leukemias (AMLs), 54% of B-lineage acute lymphoblastic leukemias (ALLs), and in a consistent fraction (68%) of B-cell lymphoproliferative disorders. In this latter group, hairy cell leukemia and high-grade B-cell non-Hodgkin's lymphoma (B-NHL) expressed a higher surface density of CD30L as compared with B-cell chronic lymphocytic leukemia and low-grade B-NHL. Purified plasmacells from a fraction of multiple myeloma patients also displayed CD30L mRNA and protein. A more restricted expression of CD30L was found in T-cell tumors that was mainly confined to neoplasms with an activated peripheral T-cell phenotype, such as T-cell prolymphocytic leukemia, peripheral T-NHL, and adult T-cell leukemia/lymphoma. In contrast, none of the T-lineage ALLs analyzed expressed the ligand. In AML, a high cellular density of CD30L was detected in French-American-British M3, M4, and M5 phenotypes, which are directly associated with the presence on tumor cells of certain surface structures, including the p55 interleukin-2 receptor alpha-chain, the alpha(M) (CD11b) chain of beta2 integrins, and the intercellular adhesion molecule-1 (CD54). Analysis of normal hematopoietic cells evidenced that, in addition to circulating and tonsil B cells, a fraction of bone marrow myeloid precursors, erythroblasts, and subsets of megakaryocytes also express CD30L. Finally, we have shown that native CD30L expressed on primary leukemic cells is functionally active by triggering both mitogenic and antiproliferative signals on CD30+ target cells. As opposed to CD30L, only 10 of 181 primary tumors expressed CD30 mRNA or protein, rendering therefore unlikely a CD30-CD30L autocrine loop in human hematopoietic neoplasms. Taken together, our data indicate that CD30L is widely expressed from early to late stages of human hematopoiesis and suggest a regulatory role for this molecule in the interactions of normal and malignant hematopoietic cells with CD30+ immune effectors and/or microenvironmental accessory cells.
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PMID:CD30 ligand is frequently expressed in human hematopoietic malignancies of myeloid and lymphoid origin. 905 27

Epstein-Barr virus (EBV) is associated with several human malignancies including Burkitt's lymphoma (BL), Hodgkin's disease (HD) and nasopharyngeal carcinoma. A variety of cytokines and receptors have been described to be activated by EBV. Here we show that the IL-2 receptor (IL-2R) alpha-chain, which is weakly expressed on normal resting lymphoid cells, is activated by EBV. Comparison of EBV-negative BL cell lines and their EBV convertants showed an enhanced CD25 expression in EBV-positive BL cells. Transient expression of the oncogenic virus protein latent membrane protein-1 (LMP1) in L428 Hodgkin's lymphoma cells and in Burkitt's lymphoma cells (BL2, BL41, BL30) cells leads to enhanced CD25 expression. Both C-terminal activating regions (CTARs) of LMP1 are involved in CD25 activation. Inhibition of LMP1-mediated NFkappaB enhancement by a constitutive repressive form of IkappaB-alpha resulted in decreased CD25 surface expression, indicating that NFkappaB is involved in CD25 gene regulation. Furthermore, LMP1-mediated CD25 activation was associated with enhanced levels of the soluble form of CD25 (sCD25) in L428 Hodgkin's lymphoma cells but not in BL cells. LMP1 associated enhanced expression of membrane CD25 and soluble CD25 may have immunomodulatory functions and could be involved in biology of EBV-associated diseases.
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PMID:Epstein-Barr virus latent membrane protein-1 activates CD25 expression in lymphoma cells involving the NFkappaB pathway. 1178 10

Adult T cell leukaemia (ATL) is an aggressive clonal malignancy of mature activated T cells, caused by the human T cell lymphotropic virus type I (HTLV-I) infection. ATL continues to have a very bad prognosis because of the intrinsic resistance of leukaemic cells to conventional or even high-dose chemotherapy and because of the associated severe immunosuppression. Even though conventional chemotherapy remains the standard treatment in acute and lymphomatous types of the disease, the benefit of this intensive approach is not well established in chronic and smouldering ATL. Combination chemotherapy regimens, in particular those designed for the treatment of aggressive non-Hodgkin's lymphomas or acute lymphoblastic leukaemia, have little effect in the treatment of ATL. Different combination regimens of conventional chemotherapy have been investigated in Japan, and recent results of intensive induction therapy showed a complete remission (CR) rate of about 40% in the aggressive forms of the disease. However, most of the patients relapsed and eventually died. Allogeneic bone marrow transplantation has been used in the treatment of a very small number of patients with ATL. High toxicity and transplant-related mortality were observed in these immunocompromised patients. New cytotoxic agents have also been used in pilot phase II studies in refractory or relapsed ATL patients, but significant results have only been observed with deoxycoformycin. Recently, promising results have been obtained with anti-Tac monoclonal antibodies directed against the alpha-chain of the interleukin-2 receptor (CD25), which is highly expressed on ATL cells but not on normal resting lymphocytes. Promising results were also reported in 2 phase II studies with combination therapy comprising the antiretroviral agent zidovudine and interferon-alpha (IFNalpha). In previously untreated patients with acute ATL, high and rapid (usually within 2 weeks) response rates were reported. In contrast, in lymphomatous ATL, both studies suggested a milder and slower effect of zidovudine and IFNalpha. In this case, this combination may be used as maintenance therapy after a CR or good partial response induced by polychemotherapy. Since cross resistance between chemotherapy and zidovudine and IFNalpha does not seem to occur, a combination with best induction polychemotherapy is warranted.
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PMID:Adult T cell leukaemia: a review of established and new treatments. 1802 Jun 14

PURPOSE: There is a need for new treatments for Hodgkin and T-cell lymphoma due to the development of drug resistance in a proportion of patients. This phase I study of radioimmunotherapy used CHT-25, a chimeric antibody to the alpha-chain of the interleukin-2 receptor, CD25, conjugated to iodine-131 ((131)I) in patients with refractory CD25-positive lymphomas. EXPERIMENTAL DESIGN: Fifteen patients were treated (Hodgkin lymphoma, 12; angioimmunoblastic T-cell lymphoma, 1; adult T-cell leukemia/lymphoma, 2). Tumor was monitored by computed tomography and in all but two patients by (18)F-fluorodeoxyglucose positron emission tomography. RESULTS: There were no grade 3 or 4 infusion reactions. At the maximum tolerated dose of 1,200 MBq/m(2), the major side effect was delayed myelotoxicity with the nadir for platelets at 38 days and for neutrophils at 53 days. One patient treated with 2,960 MBq/m(2) developed prolonged grade 4 neutropenia and thrombocytopenia and died of Pneumocystis jiroveci pneumonia. Nonhematologic toxicity was mild. Single photon emission computer tomography imaging showed tumor-specific uptake and retention of (131)I and no excessive retention in normal organs. Of nine patients receiving >/=1,200 MBq/m(2), six responded (three complete response and three partial response); one of six patients with administered radioactivity of </=740 MBq/m(2) had a complete response. CONCLUSIONS: CHT-25 is well tolerated with 1,200 MBq/m(2) administered radioactivity and shows clinical activity in patients who are refractory to conventional therapies. Phase II studies are justified to determine efficacy and toxicity in a broader range of clinical scenarios. (Clin Cancer Res 2009;15(24):7701-10).
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PMID:A Phase I Clinical Trial of CHT-25 a 131I-Labeled Chimeric Anti-CD25 Antibody Showing Efficacy in Patients with Refractory Lymphoma. 2000 55


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