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)

Lactic acid dehydrogenase (LDH) is a glycolytic enzyme that may be elevated in the serum of patients with non-Hodgkin's lymphoma (NHL). In this investigation LDH was assayed in sera from 155 untreated patients with NHL. Serum LDH (S-LDH) was found to be significantly correlated both to the spread of the disease and to the histological grade of malignancy i.e. more advanced disease or more aggressive histopathology was associated with higher S-LDH values. A high pretreatment S-LDH level (greater than 8.0 mukat/l) in stages III and IV correlated significantly to a decreased survival time. The patients with a pretreatment level of less than 8.0 mukat/l had an actuarial 2-year survival of 80%, compared to 30% in the patients with levels greater than 8.0 mukat/l (P less than 0.001). In stages I and II all 6 patients with a high pretreatment level (greater than 8.0 mukat/l) relapsed during or a short time after radiotherapy. In a longitudinal study of 24 patients it was found that S-LDH reflected in the clinical course. In patients treated to partial or complete remission, S-LDH decreased and at relapse it rose again. It is concluded that S-LDH might be useful both as a prognostic marker and to monitor the course of the disease.
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PMID:Prognostic value of serum lactic dehydrogenase in non-Hodgkin's lymphoma. 686 8

K/BxN mice develop an inflammatory joint disease with many features characteristic of rheumatoid arthritis. In this model, the KRN transgenic T cells and nontransgenic B cells both recognize the glycolytic enzyme glucose-6-phosphate-isomerase (GPI) as an autoantigen. Here, we followed the anti-GPI B cell response that naturally arises in K/BxN mice. The anti-GPI B cell response was robust and arose at the same time as the development of serum anti-GPI autoantibody and joint inflammation. Surprisingly, although GPI was expressed systemically, the anti-GPI B cell response was focused to the lymph nodes (LN) draining the distal joints where arthritis was evident. In lymphotoxin-beta receptor-Ig-treated mice, which lack LNs, the development of arthritis was completely inhibited up to 5-6 weeks. At later times, some arthritis did develop, but at a significantly reduced level. Thus, in this spontaneous model of autoimmunity, the LNs draining the distal joints are essential for both the inhibition and amplification of the arthritogenic B cell response. These findings imply that the immune physiology of a joint is unique, resulting in a local immune response to a systemic autoantigen.
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PMID:Despite ubiquitous autoantigen expression, arthritogenic autoantibody response initiates in the local lymph node. 1239 19