Vascular endothelial growth factor (VEGF) expression and survival in human epithelial ovarian carcinomas

A novel isoform of pro-interleukin-18 expressed in ovarian tumors is resistant to caspase-1 and -4 processing

“…Indeed tumor cells genetically engineered to express biologically active IL-15 (Meazza et al, 2000) or IL-18 (Osaki et al, 1999;Tatsumi et al, 2002) show a reduction in their tumorigenicity in experimental tumor models and induce immune reactions, in relationship to the induction of IFNg production (Coughlin et al, 1998;Meazza et al, 2000;Tatsumi et al, 2002). IFNg is not spontaneously secreted by ovarian tumors (Nash et al, 1998), which release several other cytokines involved in tumor progression or autocrine loops (Naylor et al, 1993;Wu et al, 1993;Hartenbach et al, 1997;Mesiano et al, 1998). In addition, IFNg has been shown to exert antitumor effects on ovarian cancer both in vitro (Kost et al, 1999) and in vivo (Windbichler et al, 2000), further suggesting that IFNg release from lymphoid cells triggered by biologically active IL-18 could inhibit ovarian tumor growth.…”

Expression of interleukin‐18 in human ovarian carcinoma and normal ovarian epithelium: Evidence for defective processing in tumor cells

“…In addition, mature IL-18 would also suppress tumor angiogenesis, which appears to be a relevant factor in ovarian carcinoma progression, through VEGF production. 42,43 In some ovarian tumors lack of mature IL-18 may be related to the downregulation of IL-18 or of ICE gene expression. Finally, our data indicate that the few ICE-and IL-18-positive ovarian carcinomas are also unable to process IL-18 adequately, thus suggesting the existence of additional mechanisms altering mature IL-18 production in some tumors.…”

HIF-1α, STAT3, CBP/p300 and Ref-1/APE are components of a transcriptional complex that regulates Src-dependent hypoxia-induced expression of VEGF in pancreatic and prostate carcinomas

“…Src activity often increases during tumor progression and may be predictive of poor prognosis (Talamonti et al, 1993;Summy and Gallick, 2003). By regulating both STAT3 activation and HIF-1a expression, increasing Src activity may augment the hypoxic response in VEGF expression, itself a prognostic marker in many tumors (Hartenbach et al, 1997;Niedergethmann et al, 2002;Nam et al, 2004;Uehara et al, 2004). In addition to enhancing angiogenesis, hypoxia-mediated activation of HIF-1a and STAT3 may also contribute to increased tumorigenic properties in pancreatic and prostrate carcinomas.…”