Original articleHuman ovarian tumors of epithelial origin express PDGF in vitro and in vivo
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2009, Molecular TherapyCitation Excerpt :The present model showed that even the combination of antiangiogenic and antilymphangiogenic therapy was insufficient to induce tumor reggression, even though tumor vasculature was reduced throughout the tumor after the gene delivery. It is plausible that the ability of the tumors to escape the treatment is because of the upregulation of other angiogenic factors such as PDGF-B (platelet-derived growth factor),24 Ang-1 or Ang-2 (ref. 25). Although antiangiogenic agents alone are unlikely to eradicate tumors completely, similar strategies have been applied in ovarian cancer clinical trials using antihuman VEGF monoclonal antibody bevacizumab,26 soluble hybrid decoy receptor VEGF-Trap,27 tyrosine kinase inhibitor AZD 2171 (ref. 28), recombinant human IL-12 (ref. 29) and thalidomide.30
Expression, mutational analysis and in vitro response of imatinib mesylate and nilotinib target genes in ovarian granulosa cell tumors
2008, Gynecologic OncologyCitation Excerpt :These findings led us to explore the expression of tyrosine kinase genes where products are known to respond to imatinib and to characterize the response of the COV434 and KGN cell lines to imatinib. Several studies have examined the expression of the tyrosine kinase receptors c-kit, PDGFR-α, PDGFR-β and c-Abl in ovarian cancers [19–21] but expression profiles in GCT have not been previously reported. All four genes c-Abl, c-kit, PDGFR-α, and PDGFR-β were found to be expressed in the GCT and in the normal ovary samples.
Phase II trial of imatinib mesylate in patients with recurrent platinum- and taxane-resistant epithelial ovarian and primary peritoneal cancers
2006, Gynecologic OncologyCitation Excerpt :Imatinib has had a dramatic impact on the clinical management of select malignancies and is approved for the first-line treatment of adult patients with newly diagnosed Philadelphia chromosome-positive chronic myelogenous leukemia at all stages and patients with c-Kit-expressing metastatic or unresectable malignant gastrointestinal stromal tumors [2,4]. Preclinical studies of ovarian cancer indicate that c-Kit and PDGFR may have a role in ovarian tumorigenesis [5–14]. In one study, Northern blot analysis revealed c-Kit mRNA expression in two of four ovarian carcinoma samples [14].