2009
DOI: 10.1684/bdc.2009.0988
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Nouvelles molécules et thérapeutiques moléculaires ciblées dans les adénocarcinomes ovariens de stades avancés

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Cited by 5 publications
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“…A number of reports have reinforced the notion that inhibition of a single transduction pathway may be insufficient since activation of alternative signaling cascades may conceal efficacy, and that it would be more advantageous to target integrated cancer signals, for example, VEGFR- and EGFR-interdependent pathways [170] and heparin-binding epidermal growth factor-like growth factor (HB-EGF) [200, 201]. Remarkably also, the mammalian target of rapamycin (mTOR) is a central intracellular kinase that not only orchestrates proliferation, survival, and angiogenic pathways, but has also been linked to resistance to EGFR antagonists, and thus mTOR inhibition could be explored to interfere with tumor growth and expansion at multiple levels [4, 83, 84, 92, 159, 170, 202205]. Another multiple molecular targeting platform is provided by EGFR-induced EMT in EOC, possibly via mechanisms that incorporate estrogen signaling, E-cadherin downregulation and expression of matrix metalloproteinase-9 (MMP-9), and Snail transcription family members (SNAIL and SLUG) [79, 206, 207].…”
Section: Ovarian Cancer Biomarkers and Cellsignaling Pathwaysmentioning
confidence: 99%
“…A number of reports have reinforced the notion that inhibition of a single transduction pathway may be insufficient since activation of alternative signaling cascades may conceal efficacy, and that it would be more advantageous to target integrated cancer signals, for example, VEGFR- and EGFR-interdependent pathways [170] and heparin-binding epidermal growth factor-like growth factor (HB-EGF) [200, 201]. Remarkably also, the mammalian target of rapamycin (mTOR) is a central intracellular kinase that not only orchestrates proliferation, survival, and angiogenic pathways, but has also been linked to resistance to EGFR antagonists, and thus mTOR inhibition could be explored to interfere with tumor growth and expansion at multiple levels [4, 83, 84, 92, 159, 170, 202205]. Another multiple molecular targeting platform is provided by EGFR-induced EMT in EOC, possibly via mechanisms that incorporate estrogen signaling, E-cadherin downregulation and expression of matrix metalloproteinase-9 (MMP-9), and Snail transcription family members (SNAIL and SLUG) [79, 206, 207].…”
Section: Ovarian Cancer Biomarkers and Cellsignaling Pathwaysmentioning
confidence: 99%