@entity43 is the second leading cause of @entity5 in @entity1 worldwide. Despite optimal cytoreduction and adequate adjuvant therapies, initial @entity5 response is often followed by relapse suggesting the existence of a @entity5 niche. Targeted therapies have been evaluated in @entity43 to overcome resistant disease. Among them anti-angiogenic therapies inhibit new blood vessel growth, induce endothelial cell apoptosis, and block the incorporation of haematopoietic and endothelial progenitor cells into new blood vessels. Despite in vitro and in vivo successes, anti-vascular therapy with bevacizumab targeting @entity7 has limited efficacy in @entity43 . The precise molecular mechanisms underlying clinical resistance to anti- @entity7 therapies are not yet well understood. Among them, @entity5 and stromal heterogeneity might determine the treatment outcomes. The present study investigates whether @entity5 endothelium may contribute to treatment resistance to bevacizumab and promote a residual microscopic disease. Here we showed that @entity43 cells (OCC) activate @entity584 phosphorylation in endothelial cells inducing resistance to bevacizumab leading to an autocrine loop based on @entity540 secretion. Altogether our results point out the role of an activated endothelium in the resistance to bevacizumab and in the constitution of a niche for a @entity66 .

XXXX -activated endothelium constitute the niche for @entity66 and resistance to bevacizumab in @entity43 .

@entity43 :: ('MESH:D010051', 'Disease') :: ['ovarian cancer', 'Ovarian cancer'] @entity1 :: ('9606', 'Species') :: ['women'] @entity66 :: ('MESH:D004194', 'Disease') :: ['residual disease'] @entity7 :: ('7422', 'Gene') :: ['VEGF', 'VEGF-A'] @entity5 :: ('MESH:D009369', 'Disease') :: ['tumor', 'cancer-related death', 'abnormalities in the tumor'] @entity584 :: ('207', 'Gene') :: ['Akt'] @entity540 :: ('2247', 'Gene') :: ['FGF-2']
@entity584 :: (207,Gene) :: ['Akt']
