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)

Alternating non-cross-resistant chemotherapy has been induced for the treatment of non-Hodgkin's lymphoma (NHL) with the aim of cure, even in advanced cases. We formulated a new high dose regimen, CAMBO-VIP, which was a weekly treatment. They were administered during alternate weeks for a total period of 12 weeks. We obtained high response rate and prolonged disease-free survival with this regimen. We noticed the elevation of serum LDH level in some patients at or shortly after the completion of CAMBO-VIP treatment. LDH elevation was not associated with liver function abnormality in terms of elevation of GOT or total bilirubin. All of these patients were in complete or partial response with no evidence of tumor progression. An LDH isozyme study which was done at the time of LDH elevation showed elevation of both LDH1 and LDH2. Interestingly serum haptoglobin was undetectable in all 6 patients measured at the time of LDH elevation. Reticulocytosis and leukoerythroblastosis in peripheral blood were also observed in all of these patients. These abnormalities including LDH elevation returned to normal within a rather short period, usually within 1 to 3 weeks. From these observations, it is most likely that these abnormalities were due to excessive blood cell destruction, which was observed in association with rapid recovery from myelosuppression.
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PMID:[Increased blood cell destruction during vigorous regeneration of bone marrow after CAMBO-VIP chemotherapy for non-Hodgkin's lymphoma]. 751 Nov 81

Based on the possibility of tumor necrosis factor (TNF)-alpha to perform multiple and opposite biologic effects, we simultaneously investigated in vitro its effects on intracellular lactate dehydrogenase (LDH)-H and LDH-M isoenzyme activity and morphological characteristics following induction of apoptosis in peripheral blood mononuclear cells (PBMC) of non-Hodgkin's lymphoma patients (NHL) prior to and after the end of applied chemotherapy. TNF-alpha showed a significant increase ( p<0.05) of LDH-H and LDH-M activity in sonified PBMC of healthy controls after 18 h cultures accompanied with an increase of apoptotic index (AI) from 2.3 to 16.2%. Contrary to this, in PBMC of NHL patients prior to therapy TNF-alpha induced a significant decrease ( p<0.05) of LDH-H isotype activity. In patients after administration of chemotherapy, TNF-alpha in a dose of 100 U/ml induced a significant increase ( p<0.05) of LDH-M isotype activity, but not of LDH-H. In the PBMC of NHL patients prior to chemotherapy, TNF-alpha in vitro induced an increase of AI from 2.8 up to 6.8%, while in PBMC of NHL patients after applied chemotherapy AI changed from 7.2 to 14.4%. However, there was no significant difference in the increase of apoptosis in PBMC of NHL patients with high-grade malignancy and high rate response among patients who received first-line therapy, high-dose therapy, or third-line therapy regimens after in vitro TNF-alpha treatment. These results indicated different susceptibilities of PBMC of NHL to TNF-alpha when effects were analyzed by determination of intracellular LDH isotype profile and induction of apoptosis prior to and after administration of therapy in comparison to effects on healthy controls PBMC.
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PMID:TNF-alpha induces changes in LDH isotype profile following triggering of apoptosis in PBL of non-Hodgkin's lymphomas. 1458 59