Original ContributionExpression of Vascular Endothelial Growth Factor and HER2/neu in Stage II Colon Cancer and Correlation with Survival
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2014, Critical Reviews in Oncology/HematologyCitation Excerpt :Oncogenesis may result from destabilization of the equilibrium between proliferative and apoptotic signals, resulting in the overgrowth of cancer cells and the formation of solid tumors [11]. Many CRCs overexpress various growth factors and their respective receptors, including epidermal growth factor (EGF), transforming growth factor (TGF)-α, TGF-β1, platelet-derived growth factor (PDGF), human epidermal growth factor receptor-2 (HER2)/neu, VEGF, and fibroblast growth factor (FGF) [12–16]. Colorectal tumor growth and aggressiveness are modulated by genetic alterations in growth factors and their receptors via amplification and/or mutation in conjunction with multiple alterations in oncogenes and tumor suppressor genes.
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2011, Cancer LettersCitation Excerpt :New therapeutic strategies such as molecular-targeted agents are a high priority for patients with advanced stage disease [1]. A high percentage of CRCs overexpress a number of growth factors and their receptors, including the epidermal growth factor (EGF) receptor, EGF, transforming growth factor (TGF)-α, TGF-β1, platelet-derived growth factor (PDGF), HER2/neu, vascular endothelial growth factor (VEGF), fibroblast growth factor (FGF) 2, FGF1, FGF receptor (FGFR) 1, and FGFR2 [2–6]. Amplification and/or mutation of these growth factors and growth factor receptors influence CRC cell growth and cell behavior in an autocrine- and/or paracrine-dependent manner.
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