IndraLab
Statements
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"In fact, HER-3 expression or signaling is associated with resistance to HER-2 inhibitors in HER-2-amplified breast cancers [ xref ], EGFR inhibitors in lung cancers [ xref ], pertuzumab in ovarian cancers [ xref ], antiestrogen therapies in ER-positive breast cancers [ xref – xref ], EGFR inhibitors in head and neck cancer [ xref ] and hormone therapies in prostate cancers [ xref ]."
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"This Minireview highlights selected developments in the application of protein biochips in these fields.
the protective role of ErbB4 in cancer to its ability to form benign heterodimers with the other ErbB receptors, thus decreasing the amount of oncogenic heterodimers of EGFR, ErbB2, and ErbB3 through a "buffering mechanism". [9] Gong et al. used a functional protein microarray to profile protein-protein and protein-DNA interactions on a global level for the plant Arabidopsis thaliana. [10] Starting from FAST nitrocellulose membrane slides, they constructed a microarray displaying 802 transcription factors (TFs) from Arabidopsis thaliana obtained by expression in yeast."
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"These findings support the need for more detailed investigation of HER2 and HER3, which can form heterodimers with the EGFR, as predictive biomarkers for the response to therapy and therapeutic targets for treatment with anti-EGFR antibodies and other forms of HER inhibitors, when used alone and or in combinations in mCRC [ xref , xref ]."
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"EGFR, HER2 and HER3 species were included in the model (HER4 was omitted as in the model by Schoeberl et al. , to reflect its undetectable levels in most cancer cell lines) and allowed to form EGFR–HER3, HER2–HER3, and HER3–HER3 dimers upon binding to the ligand NRG-1β (as NRG-1β is a HER3-specific ligand, it is not able to induce EGFR or HER2 homodimers). xref To represent HER3 catalytic activity, we implemented HER3 homodimerization and trans -autophosphorylation in our model, resulting in induction of PI3K–AKT signaling ( xref )."
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"Several studies have revealed aberrant expression or function of some ErbB receptors, mainly ErbB-2 dimers with ErbB-1 or ErbB-3, as a determinant of the pathogenesis of many malignancies, such as mesothelioma, epithelial ovarian carcinoma (EOC), or head and neck carcinoma [head and neck squamous cell (HNSCC)] ( xref – xref )."
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"We have also previously observed this for the formation of ERBB2:EGFR and ERBB2:ERBB3 heterodimers [ xref ], and here we have adapted this technique to screen for the formation of heterodimers between ERBB2 and a library of 46 full-length RTKs (Fig. xref ) (Additional file xref : Table S1)."
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"The upregulation of L1 cell adhesion molecule (L1CAM) enhances the activation of EGFR by interacting with EGFR, ERBB2, and ERBB3 and then increases resistance to cisplatin and proliferation of ICC cells through induction of its downstream signaling pathways including ERK and AKT [ xref , xref ]."
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"If we assume that the PPI interaction site of HER2 is similar to that of EGFR, we can propose that compound 21 binds to the pocket of HER2 PPI site in domain IV and thus inhibits protein-protein interactions of HER3-HER2 as well as EGFR-HER2, hence inhibiting the signaling for cell growth."
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"An experiment was performed to evaluate the effects of EGCG, a chief constituent of green tea on the HER3 RTK and on COX-2 expression in the SW837 human colon cancer cell line and results showed that treatment of SW837 colon cancer cells with 20 μ g/mL of EGCG caused decrease in the phosphorylated forms of EGFR, HER2, and HER3 within 6 hours of treatment [ xref ]."
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"Although ErbB3 is not a direct target of lapatinib, by inhibiting EGFR and ErbB2, lapatinib also has the potential to prevent the ErbB3 trans-phosphorylation that normally occurs when the kinase-deficient ErbB3 forms heterodimers with either EGFR or ErbB2 [ xref , xref , xref ]."
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"Our findings show that downmodulation of HER3 by EZN-3920 leads to the suppression of tumor growth in vitro and in vivo, suggesting that HER3 can be an effective target for the treatment of various cancers that have been activated by HER3 alone or where HER3 activation is associated with EGFR or HER2 expression."
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"HER2 forms heterodimers with HER3 and epidermal growth factor receptor, with each independently implicated as a key coreceptor that drives HER2 -amplified breast can-cer. xref , xref Data have indicated that HER3 is as critical as HER2 to maintaining cell proliferation in breast cancer cells, and a HER2 antibody that inhibits HER3 signaling by blocking ligand-induced heterodimerization can induce tumor regression with effects that are distinct from those of trastuzumab. xref These and other data xref have suggested that blocking HER3 in addition to HER2 may augment therapeutic efficacy by inhibition of HER2/HER3 signaling."
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"In contrast, high AIB1 expression in patients with human epidermal growth factor receptor (HER) 2- and HER3-overexpressing tumors or tumors expressing one or more of HER1, HER2, or HER3 (HER1-3 positive) was associated with an increased risk of relapse on tamoxifen [hazard ratio, 2.20; 95% confidence interval, 1.07-3.52 (P = 0.0416); hazard ratio, 2.42; 95% confidence interval, 1.32-4.43 (P = 0.0030), respectively]."
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"Finally, unlike trastuzumab which only disrupts ligand-independent ERBB2–ERBB3 signaling ( xref ) and has no effect on ERBB1, rhPEPD G278D disrupts both ligand-independent and ligand-stimulated ERBB2–ERBB3 and ERBB1–ERBB2 interaction and signaling, and downregulates both ERBB1 and ERBB2."
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"In view of these observations and the fact that multiple signaling pathways, including EGFRs and IGF-1R, are dysregulated in colorectal cancer, we examined the constitutive levels of total and the activated (tyrosine phosphorylation) forms of EGFR, HER-2, and HER-3 as well as the activation of IGF-1R in response to curcumin and/or resveratrol."
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"To determine whether and to what extent the signal transduction pathways activated by the receptor and non-receptor tyrosine kinases would be affected by curcumin and/or dasatinib, we examined the constitutive levels of activated (tyrosine phosphorylation) forms of EGFR, HER-2 and HER-3, IGF-1R as well as c-Src in HCT-116 (wt) cells following treatment with curcumin or dasatinib, or a combination of both for 48 h."
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"Retrospective data on a consecutive series with long term followup from the Charité Hospital in Berlin [ xref ] did detect correlations with outcome following radiotherapy and/or surgery but their data suggested that EGFR (HER1) overexpression was associated with a favourable outcome ( P = 0.006) Concomitant overexpression of HER2 or HER3, favourite heterodimeric binding partners for HER1 was interestingly highly significantly associated with a poor prognosis ( P = 0.006)."
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"The addition of EGF-type ligands to mouse fibroblasts which express fusion proteins in which the intracellular domain of the receptor chain is replaced by a fragment of the β-galactosidase reporter, revealed that ErbB2 can associate with the EGFR and ErbB3 upon stimulation, but does not spontaneously form homodimers."