Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0019829 (Hodgkin's disease)
 30,247 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

CD26/dipeptidyl peptidase IV is a cell surface antigen with multiple biological functions. Although its involvement in tumor biology has been suggested, the significance of its expression in malignant lymphoma has not been clarified in detail. This study examined the expression of CD26 and cell surface adenosine deaminase (ADA) in 42 cases of Hodgkin's lymphoma (HL) and T-cell lymphoma by immunohistochemistry on frozen sections. CD26 was expressed in three of 14 cases of HL, in four of eight cases of anaplastic large cell lymphoma (ALCL), in two of nine cases of peripheral T-cell lymphoma, in one of six cases of lymphoblastic lymphoma and in none of three cases of adult T-cell lymphoma/leukemia. Expression of cell surface ADA was fully correlated with the expression of CD26 and expression of CD26/ADA in ALCL and HL was also completely correlated with the expression of p80 and epithelial membrane antigen. Of 10 CD26-positive patients, seven had fever and elevated CRP at initial diagnosis and over a median follow-up of 61 months (range, 7 - 152 months) only three survived. This study suggested that CD26 is selectively expressed on ALK-positive, but not on ALK-negative, ALCL and HL. This is also the first report to demonstrate that ADA is coexpressed with CD26 on the cell surface of malignant neoplasms in vivo.
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PMID:CD26, together with cell surface adenosine deaminase, is selectively expressed on ALK-positive, but not on ALK-negative, anaplastic large cell lymphoma and Hodgkin's lymphoma. 1707 93

Hereditary adenosine deaminase deficiency results in failure of the lymphocyte development. This occurs because of the accumulation of deoxyadenine nucleotides in cells with high deoxycytidine kinase and low 5'-nucleotidase activity. 2-Chlorodeoxyadenosine (2-CdA) resists the action of adenosine deaminase and accumulates in cells with high deoxycytidine kinase and low 5'-nucleotidase activity. It is equally toxic to dividing and nondividing cells and may act by preventing repair of DNA single-strand breaks. In doses of 0.1 mg/kg/day given for seven days 2-CdA manifests low toxicity. It has been found to be effective in the treatment of patients with lymphoid neoplasms, including advanced cutaneous T-cell lymphomas, chronic lymphocytic leukemia, non-Hodgkin lymphomas, and hairy cell leukemia. In the latter disorder it appears to be as or more effective than the tight-binding adenosine deaminase inhibitor, deoxycoformycin, and is probably less toxic. 2-CdA also appears to be effective in controlling autoimmune hemolytic anemia and shows promise in the treatment of other autoimmune diseases.
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PMID:2-Chlorodeoxyadenosine (2-CdA): A Potent Chemotherapeutic and Immunosuppressive Nucleoside. 2746 4

Diffuse large B-cell lymphoma (DLBCL) is the most common type of non-Hodgkin lymphoma (NHL). DLBCL presents with pleural involvement at an advanced stage; however, primary pleural lymphomas without any other site of involvement are rare, and the possibility of misdiagnosis is high, particularly in developing countries, where tuberculosis or other severe pulmonary infections remain a major health concern. Furthermore, lymphoma and tuberculosis share a number of common clinical characteristics, such as fever, night sweats, feeling of satiety after a small meal, fatigue and unexplained weight loss, among others. We herein describe a case of misdiagnosis of primary pleural lymphoma as tuberculosis in a 49-year-old male patient who presented with pleural effusion and high adenosine deaminase (ADA) level in the pleural fluid. Anti-tuberculosis treatment was administered for 1 month, but the patient's condition deteriorated. A surgical biopsy was performed and was diagnostic of DLBCL. CHOP chemotherapy was administered with a significant delay due to the misdiagnosis, and it was not efficient, as rituximab was not added to the regimen. The therapeutic efficacy was monitored by computed tomography scans, which revealed that the lesion had shrunk slightly. The overall survival of the patient was ~1 year and he eventually succumbed to severe thoracic infection and pleural effusion. Suspicion should be raised when a patient presents with pleural effusion and extremely high ADA levels, as ADA activity of >250 U/L should raise the suspicion of empyema or lymphoma rather than tuberculosis.
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PMID:Misdiagnosis of primary pleural DLBCL as tuberculosis: A case report and literature review. 2973 55


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