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an involvement of CD151 in regulation of ErbB2/ErbB3 heterodimerization and its impact on cell response to Herceptin, is reported.
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Our data support the combination of therapies targeting ERBB2/3 and mTORC1 signalling, together with fulvestrant, in patients who relapse on endocrine therapy and retain a functional ER.
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Despite both ligands binding to the EGFR, BTC biases the EGFR to dimerize with ErbB3 to regulate the biologic response.
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miR-125a-5p was downregulated in HBV-HCC tissues and cells. miR-125a-5p could inhibit the secretion of HBV proteins indirectly, but not inhibit HBV replication at the DNA level. Moreover, the upregulation of miR-125a-5p after HBV infection leads to an increased expression of one target, ErbB3, which might play important roles in chronic HBV infection and HCC development.
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ERBB3 and NGFR mark a distinct skeletal muscle progenitor cell in human development and pluripotent stem cells.
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High-throughput sequencing revealed a significant increase in HER3 mRNA and protein levels by the HER2 3'untranslated region (3'UTR). The HER2 3'UTR harboring a shared miR-125a/b response element induced miR-125a/b sequestration and thus resulted in HER3 mRNA derepression. Trastuzumab treatment upregulated HER3 via elevated HER2 mRNA expression, leading to trastuzumab resistance.
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Our results indicate that administration of U3-1402 alone or in combination with an EGFR-TKI may have potential as a novel therapy for EGFR-TKI-resistant EGFR-mutant non-small cell lung cancer (NSCLC)
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High HER3 expression is associated with progression of breast cancer.
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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.
