Gliobastoma (GBM) is the most frequent brain tumor in adults. Despite progress in surgery, radiotherapy and chemotherapy, the
overall survival of patients with GBM remains extremely poor. The hallmark of GBM is local invasion of single tumor cells to adjacent
and distant brain structures that renders complete tumor resection impossible and leads to tumor recurrence and death of the
patient. In addition the particular GBM vasculatur has motivated us to study a number of angiogenesis actors. This is why we center
this research subject around the two following aspects: (1) Study of actors involved in GBM cell migration. In the literature, many
data support the implication of the IGF system in GBM pathogenesis. In addition, previous studies performed in our Department
showed that IGFs promote proliferation and migration of GBM cells. To improve the treatment, it is imperative to better understand the
molecular mechanisms involved in GBM pathogenesis, in order to develop new molecularly targeted therapies. The aim of this project
is to evaluate if the migration of the GBM cells in response to IGF-I might be due to tenascin-C secretion. Tenascin-C is a
component of the extracellular matrix that promotes the GBM cells migration. In a previous work, we showed that tenascin-C expression
is associated with a worse prognosis in grade II astrocytoma. The molecular mechanisms of these processes are still in study.(2) 
Study of actors involved in tumor angiogenesis. This project focuses on the study of isolated and coobined effects induced by
galectins-1 and 3 on angiogenesis. Our results show a synergistic effect of these two galectins on endothelial cell growth and tube
formation through activation of VEGFR1 and 2. We are now analyzing the signaling pathways that are potentially involved in these
effects. From a clinical point of view, we also analyze VEGF and VEGFR expression in endothelial cells in a large series of normal,
inflammatory and cancer tissue samples.