EGFR antagonists in cancer treatment.
By Fortunato Ciardiello, G. Tortora. New England Journal of Medicine, 2008
2,077 citations recorded by the source corpus.
Subfields: Oncology, Pulmonary and Respiratory Medicine
View Paper: https://www.semanticscholar.org/paper/60e1c3d02c029fa23f608271f9bfe404572eb501
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In Oncology
In Pulmonary and Respiratory Medicine
Citations in the corpus
- Activating and resistance mutations of EGFR in non-small-cell lung cancer: role in clinical response to EGFR tyrosine kinase inhibitors (2009, neutral): “(Ciardello and Tortora, 2008) Improper activation of EGFR TK results in increased malignant cell survival, proliferation, invasion and metastasis.”
- Differential Macrophage Programming in the Tumor Microenvironment (2012, neutral): “Monoclonal antibodies and small molecular inhibitors targeting the VEGF and EGF pathways are already approved for treatment of various carcinomas alone or in combination, although none were designed specifically to target TAM function and their clinical efficacy has been mixed [121, 122].”
- Cell-free nucleic acids as biomarkers in cancer patients (2011, background): “EGFR mutations that occur in a specific subset of patients with lung cancer”
- Epidermal Growth Factor Receptor Cell Proliferation Signaling Pathways (2017, background): “TKIs are ATP mimetics that bind to the receptor’s kinase pocket, which excludes ATP and prevents signal transduction [374].”
- Amplification of the MET receptor drives resistance to anti-EGFR therapies in colorectal cancer (2013, neutral): “Among these, inhibitors of receptor tyrosine kinases (antibodies or small molecules) have shown marked clinical activity (1).”
- Targeting the cancer kinome through polypharmacology (2010, neutral): “…improved by identifying markers for patients that are more likely to respond to kinase inhibitor therapy — such as EGFR mutations in lung cancer 18 , ERBB2 overexpression in breast cancer 19 , and wild-type KRAS in lung and colorectal cancer 20,21 — but even among these sub-groups, relapse is…”
- PI3K/AKT/mTOR signaling transduction pathway and targeted therapies in cancer (2023, background): “RTKs are often induced following treatment with specific inhibitors, and as a result, they promote the activation of the PAM and Ras/MEK/ERK signalling cascades [163, 337].”