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Low HER3 expression is suggested to be a valuable prognostic biomarker to predict recurrence in HER2-amplified breast cancer.
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Results show that MEK inhibition promoted an ERK rebound during early phase treatment in head and neck squamous cell carcinoma (HNSCC) cells, which was due to feedback-induced, ligand-dependent activation of FGFR3 up-regulation.
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Results show that silencing HER3 increased the radiosensitivity of luminal A breast cancer cells in vitro and in vivo providing evidence for its role in breast cancer radiotherapy resistance.
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Study supports the involvement of EGFR, HER2 and HER3 in BCC aggressiveness of and in tumor differentiating towards different histological subtypes.
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HER2 and HER3 expression was detected in 22.2% and 86.1% of samples, respectively. The frequency of EGFR mutation was 45.7% and was not significantly different between stage 0 and IA1 (40.0% and 48.0%, respectively), suggesting that EGFR mutation does not correlate with cancer progression from stage 0 to IA1.
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ERBB3 mutations can be found in a wide variety of tumour types, and can be used to select treatment with HER family inhibitors.
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identified P2RX2, KCNQ5, ERBB3 and SOCS3 to be associated with the progression of age-related hearing impairment
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In this study, authors analyzed the immunoexpression of EGFR, HER2 (EGFR2) and HER3 (EGFR3) in 41 cases of serous borderline ovarian tumors and carcinomas, in relation to the degree of differentiation and tumor stage.
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Results demonstrate that 4-PBA promotes gastric cancer cells migration through upregulation of HER3/HER4 subsequent to increased levels of acetyl-histone and activation of ERK signaling.
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miR152 was found to be involved in the proliferation and metastasis of ovarian cancer cells through repression of ERBB3 expression.
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NRG1-dependent activation of HER3 induces primary resistance to trastuzumab in HER2-overexpressing breast cancer cells. HER3 monoclonal antibody combined with trastuzumab may serve as a treatment choice for patients with primary resistance to trastuzumab.
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This phase Ib study was designed to determine the MTD, safety, preliminary efficacy, and pharmacokinetics of the HER3 (ErbB3) mAb SAR256212 in combination with the oral PI3K inhibitor SAR245408 for patients with metastatic or locally advanced solid tumors.
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the present study suggests that HER2 has an important role in the regulation of the cancer stem-like cells phenotype in ALK translocated lung cancers that is mainly orchestrated by HER2/HER3 heterodimers.
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HER3 phosphorylation by EGFR depends on the ability of EGFR to homo-oligomerize.
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To determine additional resistance mechanisms to cetuximab treatment besides HER3 signaling.
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Study shows ErbB3 expression was markedly decreased in suicide completers compared to controls.
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EGFR expression is increased in oesophageal and gastric adenocarcinomas after neoadjuvant therapy and was significantly associated with a prolonged overall survival in univariable analysis.
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Using time-resolved-fluorescence energy transfer (TR-FRET), we demonstrated that in the presence of recombinant NRG1, binding of 9F7-F11 to HER3 is increased, whereas that of ligand-competing anti-HER3 antibodies (H4B-121, U3-1287, Ab#6, Mab205.10.2, and MOR09825) is decreased.
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This study uncovers a direct relationship between HPV infection and HER3 in head and neck squamous cell carcinomas and provides a rationale for the clinical evaluation of targeted HER3 therapy for the treatment of HPV(+) patients.
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Cetuximab treatment induced HER3 activation and HER2/HER3 dimerization in head and neck squamous cell carcinoma cell lines. Cetuximab induces HER3 expression and activation in HNSCC cell lines. Upregulation of HER3 by cetuximab is one mechanism underlying resistance to EGFR inhibition in HNSCC.
