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Year : 2016  |  Volume : 29  |  Issue : 2  |  Page : 379-382

Arginase-1 enzyme in B-cell non-Hodgkin lymphoma

Department of Clinical Pathology, Faculty of Medicine, Menoufia University, Menoufia, Egypt

Correspondence Address:
Hanem M Badwy
Department of Clinical Pathology, Faculty of Medicine, Menoufia University, Quesna, Menoufia, 32631
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/1110-2098.192422

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Objectives: Assessment of arginase-1 enzyme in B-cell non-Hodgkin lymphoma (NHL). Background: Arginase-1 enzyme is involved in the mechanism of immune suppression in NHL, which affects both the treatment outcome and the patient survival. Patients and methods: This study was carried out on 42 NHL patients attending the Oncology Department, Menoufia University Hospitals. Of the 42 NHL cases, 16 were relapsed or refractory (eight refractory: five cases relapsed within 1 year, two cases relapsed after 3 years, and one case after 4 years) and 26 were newly diagnosed cases. Follow-up for 24 months was carried out for the new cases. Sixteen of them achieved remission, two cases were relapsed (one case relapsed after 6 months and the other case relapsed after 9 months), whereas eight cases were lost to follow-up. Twenty age-matched and sex-matched individuals were selected as controls. A peripheral blood sample was drawn, and arginase-1 enzyme was analyzed by the enzyme-linked immunosorbent assay method. Results: The plasma level of arginase-1 enzyme was significantly increased in cases compared with controls. It was also increased in stages IV and III compared with stages I and II. Arginase-1 has the highest ratio in DLBCL compared with follicular lymphoma, which is higher than other indolent lymphomas. After patients were followed up for 2 years, the statistical data showed a highly significant difference in arginase-1 between patients with relapsed disease and patients with disease remission. Conclusion: The arginase-1 pathway is a main mechanism in the immune suppression in NHL as arginase-1 is increased in NHL patients. It is also increased in advanced stages of the disease and in a more aggressive pathology and in refractory and relapsed disease.

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