IndraLab
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"The STAT3 activating kinase, JAK2, is activated in GBM cell lines and combined inhibition of JAK2 and EGFR and EGFRvIII abolishes STAT3 activation and synergistically suppresses the growth of EGFR- and EGFRvIII expressing cell lines of breast cancer [XREF_BIBR] and epidermoid carcinoma [XREF_BIBR, XREF_BIBR], and GBM [XREF_BIBR]."
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"Interestingly, our results showed that KD of BCAP31 increased the recycling of EGFR to the membrane and the loss of resident EGFR in endocytic vesicles, decreasing overall membrane EGFR expression and autophosphorylation.Via observations of the interaction of BCAP31 with EGFR and its intracellular distribution, we found that although BCAP31 is mainly anchored to the ER, it co-localizes with EGFR throughout the whole endocardium system (Figure 5A-C)."
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"For example, a Bispecific T-cell Engager (BiTE) targeted to the epidermal growth factor receptor (EGFR) produced severe liver and kidney toxicities in non-human primates, in line with EGFR expression in these organs, and led to the termination of the animals (Klinger et al., 2016; Lutterbuese et al., 2010)."
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"The STAT3 activating kinase, JAK2, is activated in GBM cell lines and combined inhibition of JAK2 and EGFR and EGFRvIII abolishes STAT3 activation and synergistically suppresses the growth of EGFR- and EGFRvIII expressing cell lines of breast cancer [XREF_BIBR] and epidermoid carcinoma [XREF_BIBR, XREF_BIBR], and GBM [XREF_BIBR]."
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"The STAT3 activating kinase, JAK2, is activated in GBM cell lines and combined inhibition of JAK2 and EGFR and EGFRvIII abolishes STAT3 activation and synergistically suppresses the growth of EGFR- and EGFRvIII expressing cell lines of breast cancer [XREF_BIBR] and epidermoid carcinoma [XREF_BIBR, XREF_BIBR], and GBM [XREF_BIBR]."
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"44 The association between EGFR amplification, high Ki-67 labeling index, and low T1-Gad and PET (and also low T1-gad/T2) volume ratios is generally consistent with the notion that EGFR amplification leads to EGFR overexpression that promotes angiogenesis and aggressive tumor growth leading to glioma cell infiltration."
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"The STAT3 activating kinase, JAK2, is activated in GBM cell lines and combined inhibition of JAK2 and EGFR and EGFRvIII abolishes STAT3 activation and synergistically suppresses the growth of EGFR- and EGFRvIII expressing cell lines of breast cancer [XREF_BIBR] and epidermoid carcinoma [XREF_BIBR, XREF_BIBR], and GBM [XREF_BIBR]."
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"Moreover, it has been recently reported that treatment of EGFR overexpressing, ER negative breast cancer cells with SAHA could decrease the EGFR levels through destabilizing EGFR mRNA [XREF_BIBR], suggesting that combining anti-EGFR agents and HDACIs may provide a promising strategy for dual targeted therapy."
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"In addition, exploratory biomarker analyses, including the assessment of EGFR gene copy number by FISH, EGFR and p-AKT protein expression by IHC, EGFR, K-RAS and D-RAF mutational status, showed a trend towards a better survival outcome for gefitinib in patients with high EGFR-gene-copy number (HR 0.61 for high copy number and HR 1.16 for low copy number, P =.045), while patients with EGFR mutations obtained higher RR than wild-type patients (37.5% versus 2.6%) [XREF_BIBR]."
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"Response to EGFR targeted therapy and EGFR expression do not correlate well in colorectal cancer (even in the context of KRAS mutation) and confirmed reports of significant disease response has been observed in colorectal cancer patients whose tumors express little to no EGFR as detected by immunohistochemistry."
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"Normal hepatocytes express high levels of EGFR, EGFR activation contributes significantly to hepatocellular survival and proliferation during injury and regeneration, and also plays a fundamental role in the negative regulation of liver acute phase response triggered by inflammatory cytokines [XREF_BIBR]."
| PMC
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"The Egfr expression in the cells transfected with miR-sc8 inhibitor plus siRNA control was increased compared to that transfected with inhibitor control plus siRNA control, and the Egfr expression in the cells transfected with Egfr siRNA plus miR-sc8 inhibitor was similar to that transfected with inhibitor control plus siRNA control (XREF_FIG), suggesting that Egfr siRNA might attenuate miR-sc8 inhibitor induced increase in the Egfr expression to a certain degree."
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"However, re-expression of EGFR rescued EGFR expression in EGFR-KD and BCAP31-KD cells, but neither EGFR Y845 nor Y1068 sites showed autophosphorylation or downstream activation (Figure 4G), indicating that the role of BCAP31 in EGFR signalling is kinase-independent and Y845-dependent."