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)

The activity of adenosine deaminase (ADA) and of purine nucleoside phosphorylase (PNP) was determined in the peripheral lymphocytes of patients with diseases associated with acquired partial dysfunction of the immune response. Increase ADA activity was found in patients with Waldenstrom's macroglobulinemia and in some patients with non-Hodgkin's lymphoma. Increased PNP activity was found in patients with non Hodgkin's lymphoma whereas decreased PNP activity was fund in patients with connective tissue disorders. The alternations found in ADA and PNP activities probably reflect changes in the lymphocyte subpopulations and do not seem to have an etiological role in the pathogenesis of the disturbed immune response.
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PMID:Activity of adenosine deaminase and of purine nucleoside phosphorylase in peripheral lymphocytes from patients with acquired immunological disorders. 677 94

The activity of adenosine deaminase (ADA) (EC3.5.4.4.) was determined in the blood plasma, erythrocytes, and lymphocytes of 23 patients with Hodgkin's disease and partly also in 99 control subjects. The enzyme activities were measured using adenosine as substrate and by analysis of ammonia. No correlation was found between the ADA activities in lymphocytes, erythrocytes, and blood plasma. The lymphocytes of the patients revealed lower ADA activities (U/g protein) than the lymphocytes of control subjects. The ADA activity is not reduced in plasma or erythrocytes. The lower activities of ADA in the lymphocytes of patients may be related to the impaired cell-mediated immunity of the Hodgkin's disease.
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PMID:[Adenosine deaminase activity in Hodgkin's disease (author's transl)]. 707 27

The importance of humoral immune defects and of the antibody deficiency syndrome, respectively, at adult age was examined on 69 patients. As immunological methods the estimation of the immunoglobulins G, A, M, D with Mancini's technique, of IgA-antibodies with Ouchterlony's technique, of T-lymphocytes with the sheep erythrocyte rosette test, of B-lymphocytes with direct immunofluorescence and mouse erythrocyte rosette test were used. The enzyme adenosine deaminase was determined in the plasma, the erythrocytes and the lymphocytes. 31 patients with primary antibody deficiency syndrome, of them 22 patients with selective IgA-deficiency could be diagnosed. 38 patients with secondary antibody deficiency syndrome came from groups of patients with lymphoproliferative diseases (non-Hodgkin-lymphoma and plasmocytoma), chronic dialysis and other haematological diseases. In 80% of the patients clinical symptoms of an immune defect could be proved. Chronically relapsing infections of the respiratory tract are in the first place. Familial accumulation, allergic reactions, antibodies against IgA, statistically significant accumulation of gastric and duodenal ulcers set off the anyway large group of patients with selective IgA-deficiency. An antibody deficiency syndrome with IgA-deficiency could be proved in 5 of 16 patients undergoing the dialysis programme, but clinically it is perhaps insignificant. Disturbances of the cell-mediated immune reaction occurred in a child with teleangiectatic ataxia and lymphoproliferative diseases. A deficiency of adenosine deaminase, which is of importance in combined immune defects syndrome at adult age, but it is to be proved in the plasmocytoma and the non-Hodgkin-lymphoma. The necessity of the knowledge of forms of the antibody deficiency syndrome at adult age results from the increasingly immunosuppressively acting therapeutic measures, correct and well-timed diagnosing as well as the necessity of aimed consultation of the physician in institutions specialised in immunology.
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PMID:[Humoral immune defects in adults]. 711 11

CD26 is identical to the cell surface ectoenzyme dipeptidyl peptidase IV (DPPIV). CD26/DPPIV is associated with T-cell activation and proliferation and also may function as an auxiliary adhesion factor. Although CD26/DPPIV has been previously studied on lymphoid populations and on leukemias/lymphomas of B- and T-cell phenotype, little is known about its expression and functional role in some specific types of lymphomas, such as CD30-positive anaplastic large cell (ALC) lymphomas and Hodgkin's disease (HD). A series of 81 lymphoma samples, including 23 cases of HD, 17 cases of CD30-positive ALC lymphomas, 41 cases of other non-Hodgkin's lymphomas (NHL), and a panel of HD- or ALC lymphoma-derived human cell lines were evaluated for CD26/DPPIV expression by enzyme histochemistry and immunohistochemistry on frozen sections and cell smears. CD26/DPPIV protein was expressed on neoplastic cells in 12 of 17 (71%) ALC lymphomas irrespective of their antigenic phenotype and in seven of 15 (47%) T-cell NHLs. In contrast, we did not detect CD26/DPPIV expression in tumor cells from 26 cases of B-cell NHL other than ALC lymphomas or in Reed Sternberg (RS) cells and variants of 21 of 23 HD cases. Accordingly, CD26/DPPIV expression was maintained on the CD30-positive ALC lymphoma cell line Karpas 299, but the molecule was not detected on HD-derived cell lines of B, T, or non-B non-T phenotype. These results may support a new potential tool for the phenotypic separation of ALC lymphomas from HD based on the differential expression of the CD26/DPPIV molecule. Moreover, given the demonstration that CD26/DPPIV is identical to the human adenosine deaminase (ADA) binding protein, it could be speculated that CD26/DPPIV also may function by interacting with ADA to regulate the growth of CD26/DPPIV expressing neoplastic cells in ALC lymphomas.
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PMID:CD26/dipeptidyl peptidase IV expression in human lymphomas is restricted to CD30-positive anaplastic large cell and a subset of T-cell non-Hodgkin's lymphomas. 800 32

T-cell non-Hodgkin's lymphomas are a heterogeneous group of diseases that differ markedly in terms of their clinical behavior and prognosis. In recently developed classification systems, the sites of initial disease presentation assume a more prominent role in subgroup delineation. CD26, a structure with an integral role in human T-cell function that serves as the binding protein to adenosine deaminase, has been identified recently as a potential marker for certain aggressive T-cell lymphomas. To translate our knowledge of the basic biology of CD26/adenosine deaminase into clinical practice and to develop specific treatment for T-cell lymphomas based on CD26 expression, we, at M. D. Anderson Cancer Center, have initiated a phase II trial. This trial will evaluate the effect of pentostatin (Nipent), a potent adenosine deaminase inhibitor with known efficacy against T-cell malignancies, on relapsed/refractory T-cell lymphomas in relation to CD26 expression.
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PMID:CD26 in T-cell lymphomas: a potential clinical role? 1088 40

Pentostatin (2prime prime or minute-deoxycoformycin, dCF) is a product of the fermentation of Streptomyces antibioticus. It is a tight-binding inhibitor of adenosine deaminase (ADA), an enzyme essential in cellular metabolism of purines. Children with congenital absence of ADA suffer from atrophy of lymphoid tissues and severe combined immune deficiency (SCID) syndrome. It was speculated that pentostatin would be lymphocytotoxic, and this proved to be the case, promoting its investigation in lymphoid neoplasms. It was anticipated that pentostatin would be most active in neoplasms with high intracellular concentrations of ADA---e.g., acute lymphocytic leukemia (ALL), particularly its T cell variety. Although pentostatin proved to be active in ALL, large doses were required and toxic effects outweighted therapeutic benefits. By contrast, pentostatin proved to be exceptionally active in hairy cell leukemia (HCL), a B cell neoplasm with low intracellular concentrations of ADA. Pentostatin has since been shown to possess activity in chronic lymphocytic leukemia, prolymphocytic leukemia, cutaneous T cell lymphomas, adult T cell lymphoma-leukemia, and low-grade non-Hodgkin's lymphomas. It potentiates the activity of vidarabine against viruses and against the cells of acute myeloid leukemia. Pentostatin is inactive in melanoma and renal carcinoma, but has not been adequately evaluated in other solid tumors. The toxic effects of pentostatin include renal failure, central nervous system (CNS) depression, immunosuppression, keratoconjunctivitis, and opportunistic infections. In the absence of pre-existing bone marrow compromise, pentostatin produces only mild myelosuppression. Aside from its use as an antineoplastic agent, pentostatin has potential applications as an immunosuppresive drug, as an antiviral agent, as an antimalarial compound, and in the protection of cells of the CNS from damage induced by ischemia and anoxia.
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PMID:Pentostatin (2prime prime or minute-Deoxycoformycin): Clinical Pharmacology, Role In Cancer Chemotherapy, and Future Prospects. 1184 52

Pentostatin (2'-deoxycoformycin, dCF) is a purine nucleoside analog and a product of the fermentation of Streptomyces antibioticus. It is a tight-binding inhibitor of adenosine deaminase (ADA), an enzyme essential in the cellular metabolism of purines. Children with congenital absence of ADA suffer from atrophy of lymphoid tissues and severe combined immune deficiency (SCID) syndrome. It was hypothesized that pentostatin would be lymphocytotoxic and this proved to be true; this finding prompted its investigation in lymphoid neoplasms. It was anticipated that pentostatin would be most active in neoplasms with high intracellular concentrations of ADA, e.g. acute lymphocytic leukemia (ALL), particularly of the T-cell variety. Although pentostatin proved to be active in ALL, large doses were required and major toxic effects outweighed therapeutic benefits. By contrast, pentostatin proved to be exceptionally active in hairy cell leukemia (HCL), a B-cell neoplasm with low intracellular concentrations of ADA. Pentostatin has since been shown to possess activity in chronic lymphocytic leukemia, prolymphocytic leukemia, cutaneous T-cell lymphomas, adult T-cell lymphoma-leukemia, and low grade non-Hodgkin's lymphomas. It potentiates the activity of vidarabine against viruses and against the cells of acute myeloid leukemia. Pentostatin is inactive in melanoma and renal carcinoma, but has not been adequately evaluated in other solid tumors. The toxic effects of pentostatin include renal failure, central nervous system (CNS) depression, immunosuppresion, keratoconjunctivitis, and opportunistic infections. In the absence of pre-existing bone marrow compromise, pentostatin produces only mild myelosuppression. Aside from its use as an antineoplastic agent, pentostatin has potential applications as an immunosuppressive drug, as an antiviral agent, as an antimalarial compound, and in the protection of cells of the CNS from damage induced by ischemia and anoxia. Clinical studies with pentostatin are ongoing, and its roles in the management of neoplastic and non-neoplastic diseases have yet to be fully defined.
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PMID:Deoxycoformycin (pentostatin): clinical pharmacology, role in the chemotherapy of cancer, and use in other diseases. 1465 Dec 24

Cladribine is a purine analogue that is resistant to degradation by adenosine deaminase. We describe the efficacy of cladribine monotherapy in 8 patients with relapsed or refractory indolent non-Hodgkin lymphoma. The median age of the patients was 57 years. All patients were given 1-3 courses of cladribine monotherapy at 0.09 mg/kg/day continuous infusion for 7 days. Although all patients had been treated with rituximab and CHOP-like regimens, the response rate was excellent (85.7%). Thus we consider that cladribine is the first treatment of choice in the patients with relapsed or refractory indolent lymphoma.
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PMID:[Cladribine monotherapy for patients with relapsed or refractory indolent non-Hodgkin lymphoma]. 1535 18

Abdominal tuberculosis is still a medical problem in developing countries. The clinical presentation of tuberculous (TB) peritonitis may be similar to that of peritoneal carcinomatosis. Therefore, its diagnosis is rather difficult only with laboratory investigations. Ascitic fluid adenosine deaminase (ADA) activity has been proposed as a useful diagnostic test in tuberculous peritonitis, as many studies reported high ADA levels in TB peritonitis. On the other hand, ADA activity is usually lower in peritoneal carcinomatosis and malignant ascites. This study described a patient with non-Hodgkin lymphoma with elevated (67 U L(-1)) ADA levels and clinical signs mimicking peritoneal tuberculosis. On admission, this study focused on the high value of ADA in ascites and strongly suspected TP. Although anti-tuberculous agents were initiated, his general condition did not improve. Finally, laparoscopic peritoneal biopsy was performed and non-Hodgkin lymphoma diagnosed. In the light of these findings, ADA level may not reflect TB peritonitis in the absence of histopathological examination. Therefore, non-Hodgkin lymphoma should be kept in mind in the differential diagnosis in patients with high ascitic fluid ADA levels and in non-responders to anti-tuberculosis treatment.
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PMID:Non-Hodgkin lymphoma with high adenosine deaminase levels mimicking peritoneal tuberculosis: an unusual presentation. 1639 83

Pentostatin has been shown to be active in a variety of B- and T-cell malignancies. The drug is a tight inhibitor of adenosine deaminase, a key degradative enzyme of purine metabolism present in all human tissues, with the highest levels found in the lymphoid system. Early clinical trials indicated that this agent was highly active in acute lymphoblastic leukemias with high intracellular adenosine deaminase levels. Relatively high doses of the drug were needed, which was associated with severe adverse events. Through the efforts of a few investigators, better tolerated, low-dose regimens have been shown to be extremely active in lymphoproliferative diseases with very low intracellular adenosine deaminase levels such as hairy cell leukemia, B- and T-cell chronic leukemias, T-cell cutaneous lymphomas and low-grade non-Hodgkin lymphomas. Clinical as well as experimental data have indicated that this drug induces lymphocyte-specific cytotoxicity, and myelosuppressive adverse events have been minimal. Although all the purine analogs have shown similar activity, the advantage of pentostatin is the relatively specific cytotoxicity against lymphocytes, which permits treatment even in patients with severe cytopenias. Although no direct comparisons of the purine analogs have been performed, pentostatin may be preferred due to this property.
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PMID:Pentostatin and purine analogs for indolent lymphoid malignancies. 1656 86


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