Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0019829 (Hodgkin's disease)
 30,247 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present study was carried out to clarify the role of matrix metalloproteinase-2 and -9 (MMP-2 and MMP-9), tissue inhibitor of metalloproteinase-1 (TIMP-1), vascular endothelial growth factor (VEGF), and microvessel density (MVD) in the clinicopathologic behavior of childhood B-cell non-Hodgkin lymphoma (NHL). Paraffin-embedded biopsy specimens from 25 children with NHL were studied by immunohistochemically and the correlate the expression of these markers to clinicopathologic characteristics. Positive MMP-9 staining was associated with an increased prevalence of B-symptoms (p = .046). High microvessel density (MVD) showed a tendency toward an adverse outcome and it was correlated with clinical stage (p = .023). The event-free survival of high MVD patients was less than for those with low MVD, but the difference was not statistically significant (64.1% vs. 85.71% respectively, p = 0.15). The overall survival of high MVD patients was less than for those low with MVD and the difference was statistically significant (55.53% vs. 100% respectively, p = .039). Neither gelatinases nor VEGF correlated with age, sex, disease stage, the occurrence of bulky disease, or extranodal disease. The results showed that angiogenesis and angiogenic factors might have a role in development and clinical behavior of childhood NHL. Larger series of patients are needed to determine the prognostic value of angiogenesis in childhood non-Hodgkin lymphoma.
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PMID:Role of gelatinases (MMP-2 and MMP-9), TIMP-1, vascular endothelial growth factor (VEGF), and microvessel density on the clinicopathological behavior of childhood non-Hodgkin lymphoma. 1823 55

Tissue inhibitor of metalloproteinase-1 (TIMP1) is a survival factor of germinal center (GC) B cells, and its over-expression is correlated with aggressive B cell lymphomas and classical Hodgkin lymphomas. We previously demonstrated that TIMP1 down-regulates B-cell receptor and BCL6, and activates interleukins-6,-10 (ILs)/signal transducer and activator of transcription-3 (STAT3) signaling in GC B cells. The activation of ILs/STAT3 signaling can amplify CD44 function, and vice versa, and induce protein-tyrosine phosphatase SHP1 activity by a negative feedback mechanism. Here, we show that TIMP1 up-regulates cell surface CD44 (standard and variants 3 and 7-10) and induces the activity and nuclear localization of SHP1 in an Epstein Barr virus (EBV)-negative Burkitt lymphoma cell line, the neoplastic counterpart of GC centroblasts. These results suggest that TIMP1 functions as a differentiating and survival factor of GC B cells by modulating CD44 and SHP1 in the late centrocyte/post-GC stage, regardless of EBV infection.
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PMID:TIMP1 induces CD44 expression and the activation and nuclear translocation of SHP1 during the late centrocyte/post-germinal center B cell differentiation. 1850 33


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