ERBB Receptors and Cancer: The Complexity of Targeted Inhibitors

By N. Hynes, H. Lane. Nature Reviews. Cancer, 2005

1,812 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/061b3915441528f214e1387345836f6e8d22b650

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Citations in the corpus

A molecularly annotated platform of patient-derived xenografts ("xenopatients") identifies HER2 as an effective therapeutic target in cetuximab-resistant colorectal cancer. (2011, background): “Overexpression of receptor tyrosine kinases (RTK) other than EGFR has been shown to obviate the need for activated EGFR signaling and be responsible for resistance to anti-EGFR therapies in various tumor settings (37).”
WHSC1L1-mediated EGFR mono-methylation enhances the cytoplasmic and nuclear oncogenic activity of EGFR in head and neck cancer (2017, neutral): “In the nucleus, it interacts with E2F1, RNA helicase A, DNA-dependent protein kinase (DNA-PK), signal transducer and activator of transcription 3 (STAT3), STAT5 and proliferating cell nuclear antigen (PCNA) 18,19 .”
A central role for HER3 in HER2-amplified breast cancer: implications for targeted therapy. (2008, background): “Activation of the ErbB/HER network is tightly regulated throughout development and in the adult (6, 23).”
Efficient selection of DARPins with sub-nanomolar affinities using SRP phage display. (2008, background): “Antibodies to ErbB1 (EGFR) and the other members of the ErbB receptor family, notably ErbB2 (HER2), are being developed as anti-tumor therapeutics.(26) Here, we describe the selection of DARPin binders against ErbB1, ErbB2 and ErbB4.”
The epidermal growth factor receptor family: Biology driving targeted therapeutics (2008, background): “Understanding the complexities in the targeted therapy of ErbB proteins is critical to develop highly effective treatments for cancers driven by this oncogenic family of receptors [190].”
Mechanisms of cutaneous toxicities to EGFR inhibitors (2006, background): “jpg" NDATA ITEM> ]> Agents that target the epidermal growth factor receptor ( EGFR ) have emerged as a robust therapy against various malignancie”
Structures of lung cancer-derived EGFR mutants and inhibitor complexes: mechanism of activation and insights into differential inhibitor sensitivity. (2007, background): “Overexpression or mutational activation of the EGFR is implicated in the development and progression of numerous human malignancies, and C a number of small-molecule tyrosine kinase inhibitors (TKIs) have been developed to target the ATP-binding cleft of the EGFR (Hynes and Lane, 2005).”
Mechanism of activation and inhibition of the HER4/ErbB4 kinase. (2008, background): “Each ErbB receptor is essential for normal animal development (Olayioye et al., 2000), and abnormal expression and activation of ErbBs is associated with many human cancers (Hynes and Lane, 2005).”
Protein lysine methyltransferase SMYD3 is involved in tumorigenesis through regulation of HER2 homodimerization (2017, background): “A HER2- specific ligand(s) has not been identified [8], but HER2 protein is known to make a homodimer or a heterodimer with a member of other EGFR proteins, and then drive autophosphorylation in C- terminal tyrosine residues, followed by activation of its downstream pathways [1, 9].”
Inorganic Nanoparticles in Cancer Therapy (2010, positive): “It is also in different phases of clinical trials for many other malignancies (74,75).”
Matrix Metalloproteinases: Regulators of the Tumor Microenvironment (2010, background): “Malfunction of this system by genetic mutations of the molecules involved is frequently observed in breast cancer and other malignant diseases (Hynes and Lane, 2005).”