Journal
JOURNAL OF NEURO-ONCOLOGY
Volume 80, Issue 3, Pages 251-259Publisher
SPRINGER
DOI: 10.1007/s11060-006-9189-y
Keywords
angiogenesis; brain tumours; FGF1; S100A13; tumour grading; VEGF-A
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Funding
- NCRR NIH HHS [RR1555] Funding Source: Medline
- NHLBI NIH HHS [HL32348, HL35627] Funding Source: Medline
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S100 proteins are Ca2+-binding polypeptides involved in the tumourigenesis of several human neoplasms. S100A13 is a key regulator of the stress-dependent release of FGF1, the prototype of the FGF protein family involved in angiogenesis. Indeed, S100A13 is a copper binding protein able to enhance the export of FGF1 in response to stress in vitro and to induce the formation of a multiprotein aggregate responsible for FGF1 release. We investigated the expression of S100A13 in human astrocytic gliomas in relation to tumour grading and vascularization. A series of 26 astrocytic gliomas was studied to evaluate microvessel density and to assess FGF1, S100A13 and VEGF-A expression. FGF1 was equally expressed in the vast majority of tumours, whereas S100A13 and VEGF-A were significantly up-regulated in high-grade vascularized gliomas. Moreover, both S100A13 and VEGF-A expression significantly correlated with microvessel density and tumour grading. These data suggest that the up-regulation of S100A13 and VEGF-A expression correlates with the activation of angiogenesis in high-grade human astrocytic gliomas.
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