Regular ArticleThe HER-2/neu oncogene: prognostic factor, predictive factor and target for therapy☆
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2017, Molecular and Cellular ProteomicsGlycolytic activity in breast cancer using <sup>18</sup>F-FDG PET/CT as prognostic predictor: A molecular phenotype approach
2016, Revista Espanola de Medicina Nuclear e Imagen MolecularCitation Excerpt :No significant association was found about histopathologic lymph node involvement with OS and DFS, both in univariate and multivariate analysis (p = 0.342 and p = 0.342 for OS and p = 0.365 and p = 0.568 for DFS). In BC some groups of tumors display distinctive epidemiological phenotypes and molecular features with higher relapse rates and a poor prognosis, as basal or triple negative and HER-2 overexpression tumors.8–11 In the present work we decided to join both molecular phenotypes in the high-risk category and observed that this group of patients displayed a lower OS and DFS in 5 years comparing to the other groups (Table 5).
Lipid metabolism and cancer progression: The missing target in metastatic cancer treatment
2015, Journal of Applied BiomedicineCitation Excerpt :For instance, leptin affects the synthesis and/or function of estrogen receptor alpha (ERα), vascular endothelial growth factor (VEGF), and human epidermal growth factor receptor 2 (HER2) (Garofalo et al., 2006; Surmacz, 2007). HER2 is a tyrosine kinase that is amplified in 25–30% of breast tumors and it's over expression often correlates with a more aggressive, metastatic phenotype and worse prognosis (Ross and Fletcher, 1999; Yarden and Sliwkowski, 2001). In fact, data from clinical studies clearly revealed a correlation between presence of leptin and ObR (the overall association was about 93%) in both HER2-positive and HER2-negative subgroups in 59 breast cancer cases (Fiorio et al., 2008).
Transmembrane domain targeting peptide antagonizing ErbB2/Neu inhibits breast tumor growth and metastasis
2014, Cell ReportsCitation Excerpt :The ErbB family of tyrosine kinase receptors plays a key role in breast carcinogenesis through complex signaling networks made of multiple heterodimeric combinations of ErbB receptors (Eccles, 2011). Although having no identified ligand, ErbB2 is amplified and overexpressed in high-grade ductal carcinoma (Ross and Fletcher, 1999) and in high-grade inflammatory breast cancer (Charafe-Jauffret et al., 2004) thereby being largely involved in the induction and development of the malignant transformation (Freudenberg et al., 2009). Several studies revealed the importance of the dimeric status of ErbB2 triggering signaling cascades including the MAPK and PI3K/Akt pathways (Freudenberg et al., 2009).
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