The epidermal growth factor receptor/Erb-B/HER family in normal and malignant breast biology

Eccles, Suzanne A.

doi:10.1387/ijdb.113396se

Cited by 158 publications

(135 citation statements)

References 56 publications

(63 reference statements)

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“…1B). Next, we investigated EGFR signaling because it is often dysregulated in breast cancer and is commonly upstream of Ras and ERK (40). We found that treatment of MCF-10A cells with increasing concentrations of the specific EGFR kinase inhibitor AG1478, subsequent to up-regulation of CD147, resulted in attenuated p-ERK (Fig.…”

Section: Up-regulation Of Cd147 Induces Activation Of Egfr-ras-erk Simentioning

confidence: 99%

CD147, CD44, and the Epidermal Growth Factor Receptor (EGFR) Signaling Pathway Cooperate to Regulate Breast Epithelial Cell Invasiveness

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Tolliver

Bratoeva

et al. 2013

Journal of Biological Chemistry

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Background: CD147 induces invadopodia activity and invasiveness in breast epithelial cells. Results: CD147 forms complexes with CD44 and EGFR in lipid raftlike membrane domains and induces hyaluronan-CD44-dependent EGFR-Ras-ERK signaling that promotes invadopodia activity and invasiveness. Conclusion: CD147 induces signaling complexes critical to invasiveness in breast epithelial cells. Significance: CD147 is a potential therapeutic target and disease marker in breast cancer.

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Section: Up-regulation Of Cd147 Induces Activation Of Egfr-ras-erk Simentioning

confidence: 99%

CD147, CD44, and the Epidermal Growth Factor Receptor (EGFR) Signaling Pathway Cooperate to Regulate Breast Epithelial Cell Invasiveness

Grass

Tolliver

Bratoeva

et al. 2013

Journal of Biological Chemistry

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“…Overexpression of HER2 (ERBB2), a member of the epidermal growth factor receptor family, is one of the best described mechanisms of AE-resistance. 4,5,16 Near to 30% of breast cancers show HER2 alterations which are associated with poor prognosis. Furthermore, EGFR and IGFR are also known to be involved in AE-resistance and all the pathways, such as PI3K/AKT and MAPK/ERK, acting downstream from theses membrane receptors are responsible for the phosphorylation of ERα and its coregulators.…”

Section: Transcriptional Mechanisms In Ae-resistancementioning

confidence: 99%

Endocrine resistance in breast cancer: From cellular signaling pathways to epigenetic mechanisms

Bianco

Gévry²

2012

Transcription

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“…Since HER2 has no specific ligand, its antibodies usually inhibit tumor cells by blocking dimerization and activation of the receptor and mediating killing effect of immune system. 2,3 …”

Section: Introductionmentioning

confidence: 99%

Structural and functional characterization of MBS301, an afucosylated bispecific anti-HER2 antibody

Huang

Liu

et al. 2018

mAbs

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MBS301, a glyco-engineered bispecific anti-human epidermal growth factor receptor 2 (HER2) antibody with a typical IgG1 monoclonal antibody structure, was developed through dual-cell expression and in vitro assembling process. MBS301 consists of two half antibodies engineered from trastuzumab and pertuzumab, respectively. Integrity and purity profiles of MB301 indicated that the heterodimerization of the two half antibodies was successful. The high and similar melting temperatures (Tm1,72.0°C and Tm2, 84.8°C) of MBS301 compared with those of its parental monoclonal antibodies trastuzumab and pertuzumab (in-house made T-mab and P-mab, respectively) revealed its structural compactness. With computer-modeling experiments and Biacore binding and competition kinetics studies, the binding stoichiometry between MBS301 and HER2-ECD was determined to be 1:1 and the two arms of MBS301 were shown to bind to domains II and IV of HER2-ECD antigen simultaneously. MBS301 displayed synergistic bioactivities as the combination of T-mab and P-mab in vitro in multiple cancer cell lines and in vivo in xenograft mouse model studies, and showed more effective activity than T-mab or P-mab used individually. Moreover, fucose-knockout dramatically increased MBS301’s binding affinity to low affinity FcγRIIIa allotype 158F (KD = 2.35 × 10−7M) to near the high affinity level of allotype V158 (KD = 1.17 × 10−7M). This resulted in far more effective ADCC activity of MBS301 than the combination of T-mab and P-mab in killing HER2-positive cancer cells. Hence, a novel fully afucosylated anti-HER2 bispecific antibody with improved antitumor activities was generated and shown to have the potential to be used for treating HER2-positive but trastuzumab-resistant solid tumors.

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The epidermal growth factor receptor/Erb-B/HER family in normal and malignant breast biology

Cited by 158 publications

References 56 publications

CD147, CD44, and the Epidermal Growth Factor Receptor (EGFR) Signaling Pathway Cooperate to Regulate Breast Epithelial Cell Invasiveness

CD147, CD44, and the Epidermal Growth Factor Receptor (EGFR) Signaling Pathway Cooperate to Regulate Breast Epithelial Cell Invasiveness

Endocrine resistance in breast cancer: From cellular signaling pathways to epigenetic mechanisms

Structural and functional characterization of MBS301, an afucosylated bispecific anti-HER2 antibody

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