Abstract
EGFR may be considered as an old target, which can be inhibited both by monoclonal antibodies and tyrosine kinase inhibitors. Those molecular targeted strategies are now approved in a wild range of tumors: colorectal cancer, lung cancer, pancreatic cancer and head and neck cancer. This paper proposes to describe the development of anti-EGFR drugs, highlighting several strategies points. Predicting biomarkers have been extensively studied for these agents, sustaining the hallmarks of the development of molecular targeting drugs.
MeSH terms
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Angiogenesis Inhibitors / therapeutic use
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Antibodies, Monoclonal / therapeutic use
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Antibodies, Monoclonal, Humanized / therapeutic use
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Antineoplastic Agents / therapeutic use*
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Bevacizumab
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Boronic Acids / therapeutic use
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Bortezomib
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Cetuximab
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Combined Modality Therapy / methods
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ErbB Receptors / antagonists & inhibitors*
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ErbB Receptors / genetics
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ErbB Receptors / physiology
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Erlotinib Hydrochloride
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Gefitinib
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Humans
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Mutation / genetics
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Neoplasm Proteins / antagonists & inhibitors*
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Neoplasm Proteins / physiology
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Neoplasms / drug therapy*
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Neoplasms / metabolism
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Panitumumab
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Prognosis
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Protein-Tyrosine Kinases / antagonists & inhibitors
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Proto-Oncogene Proteins / genetics
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Proto-Oncogene Proteins p21(ras)
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Pyrazines / therapeutic use
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Quinazolines / therapeutic use
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ras Proteins / genetics
Substances
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Angiogenesis Inhibitors
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Antibodies, Monoclonal
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Antibodies, Monoclonal, Humanized
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Antineoplastic Agents
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Boronic Acids
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KRAS protein, human
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Neoplasm Proteins
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Proto-Oncogene Proteins
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Pyrazines
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Quinazolines
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Bevacizumab
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Bortezomib
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Panitumumab
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Erlotinib Hydrochloride
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EGFR protein, human
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ErbB Receptors
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Protein-Tyrosine Kinases
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Proto-Oncogene Proteins p21(ras)
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ras Proteins
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Cetuximab
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Gefitinib