title: Epithelial growth factor receptor interacting agents.
abstract: The data reviewed here have further established the promise of anti-EGFR-targeted therapies. This statement is supported by the evidence of antitumor activity of the TK inhibitors ZD1839 and OSI-774 against several tumor types and by the ability of the monoclonal antibody IMC-C225 to reverse clinical chemotherapy resistance. These results are further supported by an emerging number of compounds, monoclonal antibodies, and TK inhibitors directed at the EGFR that are in clinical development (see Fig. 2, Table 1). Among the TK inhibitors, these compounds can be further categorized by their receptor specificity and reversibility of binding. In the case of anti-EGFR monoclonal antibodies, compounds in clinical development include chimeric, humanized, and bispecific antibodies. The fundamental observation is that these compounds have shown activity in several tumor types, including NSCL cancer, prostate carcinoma, colorectal carcinoma, ovarian carcinoma, renal cell carcinoma, and head and neck cancers. These findings observed with different agents and in different tumor types validate EGFR as a target for cancer therapy. The results of ongoing studies with these agents in diverse indications and tumor types may establish the role of these promising therapies to our current cancer treatments.
authors.affiliation: Medical Oncology Service, Hospital General Universitari Vall d'Hebron, Paseo Vall d'Hebron 119-129, 08035 Barcelona, Spain. baselga@hg.vhebron.es
authors.forename: Jose
authors.initials: J
authors.lastname: Baselga
authors.forename: Joan
authors.initials: J
authors.lastname: Albanell
mesh_terms: D000818:Animals; D000911:Antibodies, Monoclonal / Q000276:immunology / Q000494:pharmacology / Q000627:therapeutic use; D061067:Antibodies, Monoclonal, Humanized; D000970:Antineoplastic Agents / Q000493:pharmacokinetics / Q000494:pharmacology* / Q000627:therapeutic use; D002166:Camptothecin / Q000031:analogs & derivatives* / Q000627:therapeutic use; D000068818:Cetuximab; D002945:Cisplatin / Q000627:therapeutic use; D002986:Clinical Trials as Topic; D003131:Combined Modality Therapy; D015195:Drug Design; D004791:Enzyme Inhibitors / Q000494:pharmacology / Q000627:therapeutic use; D066246:ErbB Receptors / Q000037:antagonists & inhibitors* / Q000276:immunology; D000069347:Erlotinib Hydrochloride; D000077156:Gefitinib; D015972:Gene Expression Regulation, Neoplastic / Q000187:drug effects; D006801:Humans; D007116:Immunization, Passive; D000077146:Irinotecan; D020935:MAP Kinase Signaling System / Q000187:drug effects; D051379:Mice; D008819:Mice, Nude; D009363:Neoplasm Proteins / Q000037:antagonists & inhibitors / Q000276:immunology; D009369:Neoplasms / Q000628:therapy; D011799:Quinazolines / Q000494:pharmacology / Q000627:therapeutic use; D011993:Recombinant Fusion Proteins / Q000494:pharmacology / Q000627:therapeutic use; D023041:Xenograft Model Antitumor Assays
chemical_list: D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D000970:Antineoplastic Agents; D004791:Enzyme Inhibitors; D009363:Neoplasm Proteins; D011799:Quinazolines; D011993:Recombinant Fusion Proteins; D000077146:Irinotecan; D000069347:Erlotinib Hydrochloride; D066246:ErbB Receptors; D000068818:Cetuximab; D002945:Cisplatin; D000077156:Gefitinib; D002166:Camptothecin