Abstract
Breast cancer is the most common cancer worldwide among women and the second most common cancer. Approximately 15-23% of breast cancers over-express human epidermal growth factor receptor2 (HER2), a 185-kDa transmembrane tyrosine kinase, which is mainly found at the cell surface of tumor cells. HER2-positive breast cancer, featuring amplification of HER2/neu and negative expression of ER and PR, has the three following characteristics: rapid tumor growth, lower survival rate, and better response to adjuvant therapies. Clinically, it is notable for its role in a pathogenesis that is associated with increased disease recurrence and acts as a worse prognosis. At the same time, it represents a good target for anti-cancer immunotherapy despite the prevalence of drug resistance. New treatments are a major topic of research, and a brighter future can be expected. This review discusses the role of HER2 in breast cancer, therapeutic modalities available and prognostic factors.
Highlights
Mechanism of human epidermal growth factor receptor2 (HER2) The HER2 oncogene is located on the long arm of chromosome 17 (17q12), consisting of EGFR (HER1/ ERBB1), HER3 (ERBB3), and HER4 (ERBB4) (Arcila et al, 2012; Kanthala et al, 2014; Kurata et al, 2014; Schroeder et al, 2014; Xu et al, 2014; Yan et al, 2014), it is a receptor tyrosine kinase (Morrison et al, 2014; Schroeder et al, 2014), once activated, by ways homodimerization or hetero-dimerization (Boulbes et al, 2014) will mediate signaling pathways including the phosphatidylinositol 3-kinase (PI3K) /protein kinase B (Akt) /mammalian target of rapamycin (mTOR) and mitogen-activated protein kinase (MAPK) pathways involved in cellular proliferation, differentiation, migration, and apoptosis (Bai et al, 2014; Dittrich et al, 2014; Lapin et al, 2014; Xu et al, 2014; Huang et al, 2015; Lanning et al, 2015).The HER2 mono-meric protein has three major regionsthe extracellular amino-terminal region comprised of four domains (domainsI-IV), the hydrophobic transmembrane domain, and thecarboxy-terminal kinase domain comprised of the jux-tamembrane domain, tyrosine kinase, and C-terminal tail with auto-phosphorylation sites
Even in the metastatic human epidermal growth factor receptor2 (HER2) breast cancer, trastuzumab is recommended in the first-line setting (Iqbal and Iqbal, 2014)
Nair et with phosphatidylinositol 3-kinase (PI3K)/Akt and Ras/MEK/ERK pathways (Huang et al (2014) proposed MYC amplification cooperated with al., 2015), simultaneous treatment targeting at mitogen-activated protein kinase (MAPK) Her2 drived a stem-like phenotype predicting diagnostic and BIM with gefitinib and calcitriol or EB1089 in and therapeutic consequences in breast cancer, only in the epidermal growth factor receptor (EGFR) and HER2 positive-breast cancer cells proved to context of Her2 activation did c-Myc drive the acquisition be significantly better to inhibit proliferation and induce of an aggressive stem-like phenotype (Nair et al, 2014)
Summary
Mechanism of HER2 The HER2 oncogene is located on the long arm of chromosome 17 (17q12), consisting of EGFR (HER1/ ERBB1), HER3 (ERBB3), and HER4 (ERBB4) (Arcila et al, 2012; Kanthala et al, 2014; Kurata et al, 2014; Schroeder et al, 2014; Xu et al, 2014; Yan et al, 2014), it is a receptor tyrosine kinase (Morrison et al, 2014; Schroeder et al, 2014), once activated, by ways homodimerization or hetero-dimerization (Boulbes et al, 2014) will mediate signaling pathways including the phosphatidylinositol 3-kinase (PI3K) /protein kinase B (Akt) /mammalian target of rapamycin (mTOR) and mitogen-activated protein kinase (MAPK) pathways involved in cellular proliferation, differentiation, migration, and apoptosis (Bai et al, 2014; Dittrich et al, 2014; Lapin et al, 2014; Xu et al, 2014; Huang et al, 2015; Lanning et al, 2015).The HER2 mono-meric protein has three major regionsthe extracellular amino-terminal region comprised of four domains (domainsI-IV), the hydrophobic transmembrane domain, and thecarboxy-terminal kinase domain comprised of the jux-tamembrane domain, tyrosine kinase, and C-terminal tail with auto-phosphorylation sites. A new member of the miRNAs come into being in the breast cancer filed, MiR-7 was proved to inhibit HER2D16 cell migration through a mechanism involving suppression of the miR-7 target gene EGFR and sensitize refractory HER2D16 expressing cells to trastuzumab (Huynh and Jones, 2014).
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