The autophagy inhibitor chloroquine overcomes the innate resistance of wild-type EGFR non-small-cell lung cancer cells to erlotinib.
Identifieur interne : 001106 ( Main/Exploration ); précédent : 001105; suivant : 001107The autophagy inhibitor chloroquine overcomes the innate resistance of wild-type EGFR non-small-cell lung cancer cells to erlotinib.
Auteurs : Yiyu Zou [États-Unis] ; Yi-He Ling ; Juan Sironi ; Edward L. Schwartz ; Roman Perez-Soler ; Bilal PiperdiSource :
- Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer [ 1556-1380 ] ; 2013.
Descripteurs français
- KwdFr :
- Animaux, Antipaludiques (pharmacologie), Apoptose (), Autophagie (), Carcinome pulmonaire non à petites cellules (anatomopathologie), Carcinome pulmonaire non à petites cellules (traitement médicamenteux), Cellules cancéreuses en culture, Chlorhydrate d'erlotinib, Chloroquine (pharmacologie), Cycle cellulaire (), Cytométrie en flux, Humains, Inhibiteurs de protéines kinases (pharmacologie), Prolifération cellulaire (), Protocoles de polychimiothérapie antinéoplasique, Quinazolines (pharmacologie), Récepteurs ErbB (antagonistes et inhibiteurs), Résistance aux médicaments antinéoplasiques (), Souris, Souris nude, Technique de Western, Tests d'activité antitumorale sur modèle de xénogreffe, Tumeurs du poumon (anatomopathologie), Tumeurs du poumon (traitement médicamenteux).
- MESH :
- anatomopathologie : Carcinome pulmonaire non à petites cellules, Tumeurs du poumon.
- antagonistes et inhibiteurs : Récepteurs ErbB.
- pharmacologie : Antipaludiques, Chloroquine, Inhibiteurs de protéines kinases, Quinazolines.
- traitement médicamenteux : Carcinome pulmonaire non à petites cellules, Tumeurs du poumon.
- Animaux, Apoptose, Autophagie, Cellules cancéreuses en culture, Chlorhydrate d'erlotinib, Cycle cellulaire, Cytométrie en flux, Humains, Prolifération cellulaire, Protocoles de polychimiothérapie antinéoplasique, Résistance aux médicaments antinéoplasiques, Souris, Souris nude, Technique de Western, Tests d'activité antitumorale sur modèle de xénogreffe.
English descriptors
- KwdEn :
- Animals, Antimalarials (pharmacology), Antineoplastic Combined Chemotherapy Protocols, Apoptosis (drug effects), Autophagy (drug effects), Blotting, Western, Carcinoma, Non-Small-Cell Lung (drug therapy), Carcinoma, Non-Small-Cell Lung (pathology), Cell Cycle (drug effects), Cell Proliferation (drug effects), Chloroquine (pharmacology), Drug Resistance, Neoplasm (drug effects), ErbB Receptors (antagonists & inhibitors), Erlotinib Hydrochloride, Flow Cytometry, Humans, Lung Neoplasms (drug therapy), Lung Neoplasms (pathology), Mice, Mice, Nude, Protein Kinase Inhibitors (pharmacology), Quinazolines (pharmacology), Tumor Cells, Cultured, Xenograft Model Antitumor Assays.
- MESH :
- chemical , antagonists & inhibitors : ErbB Receptors.
- chemical , pharmacology : Antimalarials, Chloroquine, Protein Kinase Inhibitors, Quinazolines.
- drug effects : Apoptosis, Autophagy, Cell Cycle, Cell Proliferation, Drug Resistance, Neoplasm.
- drug therapy : Carcinoma, Non-Small-Cell Lung, Lung Neoplasms.
- pathology : Carcinoma, Non-Small-Cell Lung, Lung Neoplasms.
- Animals, Antineoplastic Combined Chemotherapy Protocols, Blotting, Western, Erlotinib Hydrochloride, Flow Cytometry, Humans, Mice, Mice, Nude, Tumor Cells, Cultured, Xenograft Model Antitumor Assays.
Abstract
The epidermal growth factor receptor (EGFR) inhibitor erlotinib is much less effective in non-small-cell lung cancer (NSCLC) tumors with wild-type EGFR, than in tumors with activating EGFR mutations. Autophagy is a tightly regulated lysosomal self-digestion process, which may alternatively promote cell survival or type II cell death. This study assessed the role of autophagy in erlotinib-mediated cytotoxicity.
DOI: 10.1097/JTO.0b013e31828c7210
PubMed: 23575415
Affiliations:
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Le document en format XML
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Schwartz</name></author><author><name sortKey="Perez Soler, Roman" sort="Perez Soler, Roman" uniqKey="Perez Soler R" first="Roman" last="Perez-Soler">Roman Perez-Soler</name></author><author><name sortKey="Piperdi, Bilal" sort="Piperdi, Bilal" uniqKey="Piperdi B" first="Bilal" last="Piperdi">Bilal Piperdi</name></author></analytic><series><title level="j">Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer</title><idno type="eISSN">1556-1380</idno><imprint><date when="2013" type="published">2013</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Antimalarials (pharmacology)</term><term>Antineoplastic Combined Chemotherapy Protocols</term><term>Apoptosis (drug effects)</term><term>Autophagy (drug effects)</term><term>Blotting, Western</term><term>Carcinoma, Non-Small-Cell Lung (drug therapy)</term><term>Carcinoma, Non-Small-Cell Lung (pathology)</term><term>Cell Cycle (drug effects)</term><term>Cell Proliferation (drug effects)</term><term>Chloroquine (pharmacology)</term><term>Drug Resistance, Neoplasm (drug effects)</term><term>ErbB Receptors (antagonists & inhibitors)</term><term>Erlotinib Hydrochloride</term><term>Flow Cytometry</term><term>Humans</term><term>Lung Neoplasms (drug therapy)</term><term>Lung Neoplasms (pathology)</term><term>Mice</term><term>Mice, Nude</term><term>Protein Kinase Inhibitors (pharmacology)</term><term>Quinazolines (pharmacology)</term><term>Tumor Cells, Cultured</term><term>Xenograft Model Antitumor Assays</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Antipaludiques (pharmacologie)</term><term>Apoptose ()</term><term>Autophagie ()</term><term>Carcinome pulmonaire non à petites cellules (anatomopathologie)</term><term>Carcinome pulmonaire non à petites cellules (traitement médicamenteux)</term><term>Cellules cancéreuses en culture</term><term>Chlorhydrate d'erlotinib</term><term>Chloroquine (pharmacologie)</term><term>Cycle cellulaire ()</term><term>Cytométrie en flux</term><term>Humains</term><term>Inhibiteurs de protéines kinases (pharmacologie)</term><term>Prolifération cellulaire ()</term><term>Protocoles de polychimiothérapie antinéoplasique</term><term>Quinazolines (pharmacologie)</term><term>Récepteurs ErbB (antagonistes et inhibiteurs)</term><term>Résistance aux médicaments antinéoplasiques ()</term><term>Souris</term><term>Souris nude</term><term>Technique de Western</term><term>Tests d'activité antitumorale sur modèle de xénogreffe</term><term>Tumeurs du poumon (anatomopathologie)</term><term>Tumeurs du poumon (traitement médicamenteux)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>ErbB Receptors</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" 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xml:lang="fr"><term>Antipaludiques</term><term>Chloroquine</term><term>Inhibiteurs de protéines kinases</term><term>Quinazolines</term></keywords><keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Carcinome pulmonaire non à petites cellules</term><term>Tumeurs du poumon</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Antineoplastic Combined Chemotherapy Protocols</term><term>Blotting, Western</term><term>Erlotinib Hydrochloride</term><term>Flow Cytometry</term><term>Humans</term><term>Mice</term><term>Mice, Nude</term><term>Tumor Cells, Cultured</term><term>Xenograft Model Antitumor Assays</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Apoptose</term><term>Autophagie</term><term>Cellules cancéreuses en culture</term><term>Chlorhydrate d'erlotinib</term><term>Cycle cellulaire</term><term>Cytométrie en flux</term><term>Humains</term><term>Prolifération cellulaire</term><term>Protocoles de polychimiothérapie antinéoplasique</term><term>Résistance aux médicaments antinéoplasiques</term><term>Souris</term><term>Souris nude</term><term>Technique de Western</term><term>Tests d'activité antitumorale sur modèle de xénogreffe</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The epidermal growth factor receptor (EGFR) inhibitor erlotinib is much less effective in non-small-cell lung cancer (NSCLC) tumors with wild-type EGFR, than in tumors with activating EGFR mutations. Autophagy is a tightly regulated lysosomal self-digestion process, which may alternatively promote cell survival or type II cell death. This study assessed the role of autophagy in erlotinib-mediated cytotoxicity.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>État de New York</li></region></list><tree><noCountry><name sortKey="Ling, Yi He" sort="Ling, Yi He" uniqKey="Ling Y" first="Yi-He" last="Ling">Yi-He Ling</name><name sortKey="Perez Soler, Roman" sort="Perez Soler, Roman" uniqKey="Perez Soler R" first="Roman" last="Perez-Soler">Roman Perez-Soler</name><name sortKey="Piperdi, Bilal" sort="Piperdi, Bilal" uniqKey="Piperdi B" first="Bilal" last="Piperdi">Bilal Piperdi</name><name sortKey="Schwartz, Edward L" sort="Schwartz, Edward L" uniqKey="Schwartz E" first="Edward L" last="Schwartz">Edward L. Schwartz</name><name sortKey="Sironi, Juan" sort="Sironi, Juan" uniqKey="Sironi J" first="Juan" last="Sironi">Juan Sironi</name></noCountry><country name="États-Unis"><region name="État de New York"><name sortKey="Zou, Yiyu" sort="Zou, Yiyu" uniqKey="Zou Y" first="Yiyu" last="Zou">Yiyu Zou</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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