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

(1 --> 3)- beta - D -Glucan ( beta -glucan), a fungal cell wall component existing in plasma was measured by the kinetic turbidimetric limulus test. Here 3 reported cases have proven the clinical usefulness of plasma beta -glucan. Case 1: A 46-year-old female with non-Hodgkin's lymphoma was admitted for severe hepatitis type B in June 1997. During hospitalization, the fever rose with no response to antibiotics and with a negative blood culture. Although the plasma beta -glucan concentration was high, the patient was administered with antimycotics (fluconazole; FLCZ) and she showed some signs of improvement. Case 2: A 52-year-old male with jaundice was hospitalized in November 1997. The third day following the operation on the pancreas head carcinoma, the body temperature rose higher with a negative blood culture. The fourth day, the plasma beta -glucan concentration was positive with negative endotoxin. As some improvements were obserbed from taking FLCZ, he was discharged in January 1998. Case 3: A 19-year-old male with epilepsy was hospitalized for ARDS in August 1997. A butterfly-like shadow was observed in the chest roentgenogram (suspected malignant lymphoma). The high titer of beta -glucan has continued and endotoxin was detected. The symptoms showed some signs of improvement and the titer of beta -glucan reduced with FLCZ. Although a high level of beta -glucan still remained, the patient was discharged, but has to under go regular follow-up examinations. The measurment of beta -glucan proved very useful not only as a diagnosis for the screening of deep mycosis but also as monitoring for therapies.
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PMID:[The Clinical Significance of Plasma] 1003 84

Effective prophylaxis against fungal infection is important in neutropenic patients with hematologic malignancies, but the best method remains unclear. We investigated the effectiveness of fungal prophylaxis with amphotericin B or fluconazole. We reviewed the data on fungal isolates, plasma (1-->3)-beta-D glucan (beta-D glucan) levels, febrile periods (the number of days with an axillary temperature > 38 degrees C), and the duration of an axillary temperature > 38 degrees C when the neutrophil count was < 500/microliter. Of the 124 patients studied, 57 had acute myelogenous leukemia, 19 had acute lymphoblastic leukemia, 18 had non-Hodgkin's lymphoma, six had chronic myeloid leukemia, three had adult T-cell leukemia, and five had chronic lymphocytic leukemia. There were no significant differences in clinical characteristics between the 70 patients treated with amphotericin B and the 54 patients given fluconazole. There was a significant decrease of fungal isolates (chi 2-test, p < 0.001), the plasma beta-D glucan level (Wilcoxon test, p = 0.0001), and the febrile period (t-test, p < 0.05) in the patients given fluconazole compared with those given amphotericin B. In neutropenic patients with hematologic malignancies, prophylaxis with fluconazole significantly decreased fungal isolation and other indicators of fungal infection when compared with amphotericin B. Fluconazole may therefore be more effective for fungal prophylaxis in these patients.
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PMID:Fluconazole versus amphotericin B for the prevention of fungal infection in neutropenic patients with hematologic malignancy. 1044 77

By activating complement, antitumor monoclonal antibodies coat tumor cells with iC3b. beta-glucans, naturally occurring glucose polymers, bind to the lectin domain of the leukocyte receptor CR3, prime it for binding to iC3b, and trigger cytotoxicity of iC3b-coated tumor cells. We studied the combination of the complement-activating antibody rituximab with barley-derived (1-->3),(1-->4)-beta-D-glucan (BG) against CD-20 positive lymphoma xenografts in SCID mice. Growth of established subcutaneous non-Hodgkin's lymphoma (NHL) (Daudi and EBV-derived B-NHL) or Hodgkin's disease (Hs445 and RPMI6666) was significantly suppressed in mice treated with a combination of intravenous rituximab and oral BG, when compared to mice treated with rituximab or BG alone. Survival of mice with disseminated lymphoma was significantly increased in the combination group as compared to other treatment groups. No clinical toxicity was observed. The therapeutic efficacy and lack of toxicity of this combination supports further investigation into its clinical utility.
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PMID:Rituximab therapy of lymphoma is enhanced by orally administered (1-->3),(1-->4)-D-beta-glucan. 1586 94

Rituximab, a genetically engineered chimeric monoclonal antibody specifically binding to CD20, was the first antibody approved by the U.S. Food and Drug Administration for the treatment of cancer. Rituximab significantly improves treatment outcome in relapsed or refractory, low-grade or follicular B-cell non-Hodgkin's lymphoma (NHL). However, there are also some challenges for us to overcome: why approximately 50% of patients are unresponsive to rituximab in spite of the expression of CD20, and why some responsive patients develop resistance to further treatment. Although the antitumor mechanisms of rituximab are not completely understood, several distinct antitumor activities of rituximab have been suspected, including complement-dependent cytotoxicity (CDC), antibody-dependent cellular cytotoxicity (ADCC), apoptosis, and direct growth arrest. To counteract resistance to rituximab therapy, several strategies have been developed to: (a) augment the CDC effect by increasing CD20 expression, heteroconjugating rituximab to cobra venom factor and C3b, and inhibiting membrane complement regulatory protein, especially CD59, function; (b) enhance the ADCC effect through some immunomodulatory cytokines and CR3-binding beta-glucan; and (c) reduce the apoptotic threshold or induce apoptotic signaling on the tumor. Extensive studies indicate that rituximab combined with these approaches is more effective than a single rituximab approach. Herein, the mechanism of action of and resistance to rituximab therapy in B-cell NHL, in particular, the involvement of the complement system, are extensively reviewed.
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PMID:The role of complement in the mechanism of action of rituximab for B-cell lymphoma: implications for therapy. 1877 37