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By contrast to the conventional cytotoxic chemotherapy that damages all dividing cells, both cancer and non-cancer cells, targeted therapies refer to cancer drugs that are directed specifically to molecular targets that govern specific and crucial process for the development and the growth of the tumour cells. Therefore, their objective is to improve the efficacy and to limit the toxicity of the cancer therapies. Among the targeted cancer therapies, those targeting the epidermal growth factor receptor (EGFR) have shown clinical interesting efficacy in terms of response rate, survival without progression and overall survival in several cancers including head and neck squamous cell carcinoma, lung, pancreas and colorectal cancers. Two classes of drugs are widely used nowadays for cancer therapy; these therapies are on the one hand, the EGFR tyrosine kinase inhibitors (Erlotinib and Gefitinib) and on the other hand, the monoclonal antibodies against EGFR (Cetuximab and Panitumumab). Interestingly, these two classes of molecules differ not only in their molecular targets but also in their pharmacodynamics and pharmacokinetic properties, their route of administration and the dose used for therapy. Despite their clinical efficacy, resistance to these molecules has been reported. This inter-individual variability in efficacy and toxicity is due to resistance of the tumour cells through oncogenic somatic mutations (EGFR, KRAS, MET, PIK3CA et BRAF) and/or caused by variability in the pharmacodynamics and pharmacokinetic parameters of these molecules through polymorphic mutations (CYP3A4/5, CYP2D6, FCGR3A eFCGRT). Therefore, the identification of biomarkers though pharmacogenetics and pharmacogenomics approaches is of clinical significance; it should allow a better prediction of the therapeutic responses in terms of efficacy and toxicity. Finally, these biomarkers could be integrated in clinical practice to optimize the use of these drugs in a personalized treatment of cancer patients. Contrairement à la chimiothérapie cytotoxique conventionnelle qui s'attaque à toutes les cellules capables de se diviser, cancéreuses ou non, les thérapies ciblées font référence à un panel d'agents anticancéreux dirigés spécifiquement contre des cibles moléculaires qui gouvernent des processus spécifiques et cruciaux au développement et à la croissance de la cellule tumorale. Ainsi, leur objectif est d'augmenter l'efficacité tout en limitant la toxicité de la thérapie anticancéreuse. Parmi ces thérapies cancéreuses ciblées, les thérapies ciblant le récepteur à l'EGF (« Epidermal Growth Factor ») ont montré une efficacité clinique intéressante en terme de taux de réponse, de survie sans progression de la maladie et de survie globale dans de nombreux cancers ; notamment dans les cancers des poumons, colorectaux, des voies aérodigestives supérieures et du pancréas. Deux classes de molécules sont aujourd'hui largement utilisées dans le traitement de ces cancers : d'une part, les inhibiteurs de tyrosine kinase du récepteur à l'EGF (Erlotinib et Géfitinib) et d'autre part, les anticorps monoclonaux dirigés contre le récepteur à l'EGF (Cétuximab et Panitumumab). De manière intéressante, ces deux classes de molécules diffèrent non seulement au niveau de leurs cibles moléculaires, mais aussi au niveau de leurs propriétés pharmacodynamiques et pharmacocinétiques, leur voie d'administration et leur posologie. Malgré une efficacité prouvée de ces médicaments, des cas de résistance sont rapportés. Cette variabilité interindividuelle d'efficacité de ces médicaments peut être due à des mécanismes de résistance propres de la cellule tumorale via des mutations somatiques oncogéniques (EGFR, KRAS, MET, PIK3CA et BRAF) et/ou à des variations dans les paramètres pharmacodynamiques et pharmacocinétiques et de ces molécules causées par des variants de gènes (CYP3A4/5, CYP2D6, FCGR3A et FCGRn. Ainsi, l'identification de biomarqueurs par des approches de pharmacogénétique et de pharrnacogénomique est d'une importance clinique; ils permettraient une meilleure prédiction des réponses thérapeutiques en termes d'efficacité et de toxicité. Enfin, ces biomarqueurs pourraient être intégrés en pratique clinique afin d'optimiser l'utilisation de ces médicaments dans le traitement personnalisé des patients atteints de cancer.

Pharmacokinetics --- Pharmacogenetics --- Antineoplastic Agents --- Receptor, Epidermal Growth Factor

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Radiation Tolerance --- Receptor, Epidermal Growth Factor --- Genetic Therapy --- Neoplasms --- Cytoprotection --- physiology --- radiotherapy

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Ovarian Neoplasms --- Receptor, Epidermal Growth Factor --- Tumor Suppressor Protein p53 --- enzymology --- metabolism --- biosynthesis

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Cancer invasiveness --- Cancer --- Epidermal growth factor --- Epidermal growth factor --- Tumors --- Disease Progression --- Neoplasms --- Receptor, Epidermal Growth Factor --- Receptor Protein-Tyrosine Kinases --- Signal Transduction --- Immunotherapy --- Receptors --- Growth --- drug therapy

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The epidermal growth factor (EGF) receptor and its downstream signal transduction networks have been implicated in the ontology and maintenance of tumor tissues, which has motivated the discovery and development of molecularly targeted anti-EGFR therapies. Edited by John Haley and William J. Gullick, EGFR Signaling Networks in Cancer Therapy, is separated into two sections. The first of which probes the molecular pathways and the intersection of signaling networks which are frequently deregulated in human cancers, with a view to describing EGF receptor in a tumor tissue specific context. Meanwhile, the second section illustrates the many ways in which EGF receptor contribute to abnormal survival and migration signaling in cancer cells and to epithelial to mesenchymal transition and metastasis. The book also describes the mitogenic, survival, adhesive and migratory pathways within a framework of interacting subsystems that contribute to the activity and physiological regulation of the receptor in normal and neoplastic tissues. Even though there is still much to learn, this volume explores this fascinating system with compelling information.

Medicine & Public Health. --- Oncology. --- Cancer Research. --- Medicine. --- Médecine --- Cancérologie --- Cancer --Chemotherapy. --- Cancer --Treatment. --- Cancer --- Receptors, Gastrointestinal Hormone --- Receptor Protein-Tyrosine Kinases --- Cell Physiological Processes --- Diseases --- Receptors, Growth Factor --- Biochemical Processes --- Receptors, Cell Surface --- Cell Physiological Phenomena --- Biochemical Phenomena --- Receptors, Peptide --- Protein-Tyrosine Kinases --- Chemical Processes --- Chemical Phenomena --- Membrane Proteins --- Phenomena and Processes --- Protein Kinases --- Phosphotransferases (Alcohol Group Acceptor) --- Proteins --- Amino Acids, Peptides, and Proteins --- Phosphotransferases --- Chemicals and Drugs --- Transferases --- Enzymes --- Enzymes and Coenzymes --- Receptor, Epidermal Growth Factor --- Signal Transduction --- Neoplasms --- Medicine --- Health & Biological Sciences --- Oncology --- Treatment --- Chemotherapy --- Chemotherapy. --- Treatment. --- Cancer therapy --- Cancer treatment --- Therapy --- Cancer research. --- Tumors --- Cancer research --- Clinical sciences --- Medical profession --- Human biology --- Life sciences --- Medical sciences --- Pathology --- Physicians --- Antineoplastic agents