Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q06643 (non-Hodgkin's lymphoma)
 11,307 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Granulocyte macrophage colony-stimulating factor (GM-CSF) has been shown to inhibit the chemotaxis and enhance the oxidative burst response of human neutrophils in vitro. The present study describes the effect of recombinant GM-CSF on the neutrophil and monocyte function in patients with lymphoma undergoing GM-CSF treatment. Patients with either Hodgkin's or non-Hodgkin's lymphoma were treated with various dosages (2-16 micrograms kg-1 body weight per day for 5 days) of rhGM-CSF by intravenous or subcutaneous route. Prior to and on day 5 of rhGM-CSF treatment, neutrophil and monocyte chemotaxis and chemiluminescence responses to f-Met-Leu-Phe, zymosan activated serum (ZAS) and opsonized zymosan (OZ) were determined. It was observed that chemotactic response of neutrophils to f-Met-Leu-Phe and ZAS was reduced, whereas the chemiluminescence response of both cell types to f-Met-Leu-Phe and zymosan was enhanced by up to 43-fold. rhGM-CSF treatment did not affect degranulation of the neutrophils as measured by release of vitamin B12 binding protein. Degree of modulation of neutrophil and monocyte function by rhGM-CSF was independent of rhGM-CSF dosages administered. These data suggest that phagocytic defence system may be enhanced by GM-CSF treatment and that this cytokine may be a useful therapeutic adjunct in compromised patients.
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PMID:Modulation of neutrophil and monocyte function by recombinant human granulocyte macrophage colony-stimulating factor in patients with lymphoma. 190 35

Lactate dehydrogenase (LD) levels rose consistently during MACOP-B chemotherapy for intermediate and high-grade non-Hodgkin's lymphoma (NHL). Levels peaked at week nine and fell to normal within six weeks of completion of therapy. Isoenzyme patterns, studied prospectively in seven patients, showed a parallel rise in LD1 and LD2 suggesting a source other than tumour tissue for the rise in total LD. In the absence of evidence of myocardial or renal damage, haematopoietic tissue was the most likely source. With no evidence of haemolysis, normal serum levels of vitamin B12 and folate and normal red cell folate, dyserythropoiesis was considered to be the underlying mechanism. A rising mean corpuscular volume further reinforced this suggestion. Intensive use of methotrexate along with co-trimoxazole as prophylaxis against pneumoycystis carinii is considered the most likely cause of marrow dysfunction. Failure to recognise that rising LD levels during such therapy is treatment-related, rather than of tumour origin, may lead to inappropriate change or abandonment of therapy.
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PMID:Lactate dehydrogenase levels during MACOP-B chemotherapy for non-Hodgkin's lymphoma. 750 74

The role of dietary one-carbon determinants remains largely unexplored for non-Hodgkin's lymphoma (NHL). In a population-based case-control study of non-African-American adult (aged 20-74 years) women and men from four US Surveillance, Epidemiology, and End Results study centers (Detroit, Michigan; Iowa; Los Angeles, California; and Seattle, Washington; 1998-2000), the authors examined folate; vitamins B2, B6, and B12; methionine; and a one-carbon antagonist, alcohol, in 425 incident NHL cases and 359 controls who completed a detailed food frequency questionnaire. Adjusted odds ratios and 95% confidence intervals were estimated by using unconditional logistic regression. Higher intake of one-carbon determinants from food was associated with a lower risk of NHL, but that for only vitamin B6 (highest vs. lowest quartile: odds ratio = 0.57, 95% confidence interval: 0.34, 0.95; p trend = 0.01) and methionine (odds ratio = 0.49, 95% confidence interval: 0.31, 0.76; p trend = 0.002) reached statistical significance. Folate from food was inversely associated with diffuse subtype (odds ratio = 0.47, 95% confidence interval: 0.23, 0.94; p trend = 0.03). The authors found no association between total (food plus supplement) vitamins and NHL. Nonusers of alcohol had an elevated NHL risk compared with users, and alcohol did not modify other nutrient-NHL associations. Findings suggest that one-carbon nutrients, particularly vitamin B6 and methionine, may be protective against NHL.
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PMID:Dietary determinants of one-carbon metabolism and the risk of non-Hodgkin's lymphoma: NCI-SEER case-control study, 1998-2000. 1622 9

Pralatrexate, a 10-deazaaminopterin derivative, is being developed by Allos Therapeutics Inc for the potential treatment of malignancies. The folate analog inhibits dihydrofolate reductase and was developed to overcome the limitations of the folate analog methotrexate. Compared with methotrexate in preclinical studies, pralatrexate demonstrated superior intracellular transport via the reduced folate carrier, and increased accumulation within cells by enhanced polyglutamylation. Preclinical studies in vitro and in models of B-cell lymphomas, T-cell lymphomas and NSCLC indicated that pralatrexate exhibited antitumor activity that was superior to the activity of other antifolates. In phase I clinical trials, the DLT for pralatrexate was mucositis, which could be abrogated with folic acid and vitamin B12 supplementation. The administration of pralatrexate to patients with T-cell lymphomas and NSCLC resulted in significant tumor remissions. At the time of publication, pralatrexate was in phase II clinical trials for the treatment of peripheral T-cell lymphoma, a phase I/II trial in combination with gemcitabine for the treatment of non-Hodgkin's lymphoma, and a phase IIb trial in comparison with erlotinib in patients with NSCLC. Because of the limited therapies available for peripheral T-cell lymphoma, pralatrexate could have a secure niche for the treatment of this indication, if ongoing clinical trials and future phase III trials confirm the efficacy of the drug. In contrast, for pralatrexate to be incorporated into the accepted treatment options for NSCLC, the drug will need to prove clear superiority to established agents.
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PMID:Pralatrexate, a dihydrofolate reductase inhibitor for the potential treatment of several malignancies. 1860 May 98

Aggressive T-cell lymphomas represent a particularly poor-prognosis subgroup of lymphomas. This is especially true for patients with recurrent or refractory disease who typically have a limited response to salvage therapy and an extremely poor overall survival. There is thus a strong need to develop potentially active drugs for these malignancies. Pralatrexate is a novel antifolate designed to have high affinity for the reduced folate carrier type 1. Preclinical and clinical studies have demonstrated that pralatrexate has significant activity against T-cell lymphomas.The dose-limiting toxicity for pralatrexate is mucositis,which could be abrogated with folic acid and vitamin B12 supplementation. Pralatrexate is now being evaluated in phase II clinical trials for the treatment of peripheral T-cell lymphoma, and in a phase I/II trial in combination with gemcitabine for the treatment of non-Hodgkin's lymphoma. Because of the limited therapies available for aggressive T-cell lymphoma, pralatrexate could secure a niche for the treatment of this condition, provided on going clinical trials and future phase III trials confirm the efficacy of the drug.
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PMID:Pralatrexate, a new hope for aggressive T-cell lymphomas? 1938 Feb 98

Gluten-sensitive celiac disease (GSCD) belongs to systemic diseases one of manifestations of which may be various hematological disorders. Some patients with GSCD have blood changes, anemia in particular, which precede clinical symptoms of celiac disease. Anemia can arise as a result of disorders in iron, folic acid and/or vitamin B12 absorption. Celiac disease can be associated with thrombocytosis, thrombocytopenia, leucopenia, vein thrombosis, hyposplenism, immunoglobulin A deficiency. Patients with celiac disease have a high risk of lymphoma, especially of T-cell lymphoma associated with enteropathy, B-cell non-Hodgkin's lymphoma. Aglutenic diet, recovery of structure and function of the small intestine eliminate or attenuate hematological disorders associated with GSCD.
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PMID:[Hematological disorders in celiac disease]. 2189 56