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  • HER2
  • The aim of this study was to determine whether human epidermal growth factor receptor 2 (HER2)/erbB-2, p-glycoprotein, or p53 expression correlated with histologic response to preoperative chemotherapy or event-free survival. (uni-bonn.de)
  • At the time of initial biopsy, 20 (42.6%) of 47 samples demonstrated high levels of HER2/erbB-2 expression. (uni-bonn.de)
  • Expression of HER2/erbB-2 correlated with a significantly worse histologic response (P =.03). (uni-bonn.de)
  • In patients presenting with nonmetastatic disease, expression of HER2/erbB-2 at the time of initial biopsy was associated with a significantly decreased event-free survival (47% v 79% at 5 years, P =.05). (uni-bonn.de)
  • The correlation of HER2/erbB-2 expression with histologic response to preoperative chemotherapy and event-free survival in this study suggests that HER2/erbB-2 should be evaluated prospectively as a prognostic indicator. (uni-bonn.de)
  • inhibitor
  • We show that initiation and progression of KRAS-driven lung tumors require input from ERBB family receptor tyrosine kinases (RTKs): Multiple ERBB RTKs are expressed and active from the earliest stages of KRAS-driven lung tumor development, and treatment with a multi-ERBB inhibitor suppresses formation of KRAS G12D -driven lung tumors. (sciencemag.org)
  • peptide
  • Synthetic peptide (the amino acid sequence is considered to be commercially sensitive) corresponding to Human ErbB 3 aa 1300 to the C-terminus (C terminal). (abcam.com)
  • RTKs
  • The ErbB family of receptor tyrosine kinases (RTKs) couples binding of extracellular growth factor ligands to intracellular signaling pathways regulating diverse biologic responses, including proliferation, differentiation, cell motility, and survival. (genome.jp)
  • vitro
  • Upon investigation of the expression of the neuregulin1/ErbB system in vitro , we explored the possibility to manipulate the system in order to increase the migration of Schwann cells, that play a fundamental role in the peripheral nerve regeneration. (hindawi.com)
  • To interfere with the neuregulin1/ErbB system, the soluble extracellular domain of the neuregulin1 receptor ErbB4 (ecto-ErbB4) was expressed in vitro in the neuregulin1 expressing cell line, and an unexpected increase in cell motility was observed. (hindawi.com)
  • genes
  • No obvious molecular interactions have been characterized between ERBB and HOX family genes. (aacrjournals.org)
  • Analysis focused on significant HOX and ERBB genes between non-malignant and malignant tumor samples determined using a bayesian T-test on intensities calculated using GCRMA. (aacrjournals.org)
  • Additionally, many ERBB genes were also correlated with HOX family genes. (aacrjournals.org)
  • ERBB4
  • These results indicate that ecto-ErbB4 could be used in vivo as a tool to manipulate the neuregulin1/ErbB system. (hindawi.com)
  • chemotherapy
  • RESULTS: Our data demonstrated that the levels of C-erbB-2, CXCR4 and ER-α in patients decreased after they received neo-adjuvant chemotherapy on full tissue sections and on TMAs. (biomedsearch.com)
  • The levels of C-erbB-2, CXCR4 and ER-α were also down-regulated after neo-adjuvant chemotherapy was administered, as detected by western blot. (biomedsearch.com)
  • In addition, the change expressions of C-erbB-2 and CXCR4 in specimens tended to be correlated with pathological change to neo-adjuvant chemotherapy on full tissue sections and on TMAs in a Pearson chi-square analysis. (biomedsearch.com)
  • diagnostic
  • The observed heterogeneity could hamper the exact diagnostic determination of the c‐erbB‐2 status in small biopsies and possibly influence the effectiveness of a potential c‐erbB‐2 targeting therapy. (hindawi.com)
  • evidence
  • Since the discovery that neuregulin-1 (NRG-1)/ErbB signaling is indispensable in cardiac development, evidence has shown that this system also plays a crucial role in the adult heart. (ahajournals.org)
  • Role
  • In vivo studies, however, did not uniformly reinforce a role for apoptosis in the development of cardiomyopathy induced by impaired NRG-1/ErbB signaling. (ahajournals.org)