Erlotinib-induced autophagy in epidermal growth factor receptor mutated non-small cell lung cancer.
Identifieur interne : 001115 ( Main/Exploration ); précédent : 001114; suivant : 001116Erlotinib-induced autophagy in epidermal growth factor receptor mutated non-small cell lung cancer.
Auteurs : Yuan-Yuan Li ; Sze-Kwan Lam ; Judith Choi-Wo Mak ; Chun-Yan Zheng ; James Chung-Man Ho [Hong Kong]Source :
- Lung cancer (Amsterdam, Netherlands) [ 1872-8332 ] ; 2013.
Descripteurs français
- KwdFr :
- Antinéoplasiques (pharmacologie), Antinéoplasiques (usage thérapeutique), Apoptose (), Apoptose (génétique), Autophagie (), Autophagie (génétique), Bécline-1, Carcinome pulmonaire non à petites cellules (génétique), Carcinome pulmonaire non à petites cellules (métabolisme), Chlorhydrate d'erlotinib, Humains, Inhibiteurs de protéines kinases (pharmacologie), Inhibiteurs de protéines kinases (usage thérapeutique), Lignée cellulaire tumorale, Mutation, Protéine-5 associée à l'autophagie, Protéines associées aux microtubules (génétique), Protéines membranaires (génétique), Protéines régulatrices de l'apoptose (génétique), Quinazolines (pharmacologie), Quinazolines (usage thérapeutique), Récepteurs ErbB (génétique), Résistance aux médicaments antinéoplasiques (génétique), Techniques de knock-down de gènes, Transduction du signal, Tumeurs du poumon (génétique), Tumeurs du poumon (métabolisme).
- MESH :
- génétique : Apoptose, Autophagie, Carcinome pulmonaire non à petites cellules, Protéines associées aux microtubules, Protéines membranaires, Protéines régulatrices de l'apoptose, Récepteurs ErbB, Résistance aux médicaments antinéoplasiques, Tumeurs du poumon.
- métabolisme : Carcinome pulmonaire non à petites cellules, Tumeurs du poumon.
- pharmacologie : Antinéoplasiques, Inhibiteurs de protéines kinases, Quinazolines.
- usage thérapeutique : Antinéoplasiques, Inhibiteurs de protéines kinases, Quinazolines.
- Apoptose, Autophagie, Bécline-1, Chlorhydrate d'erlotinib, Humains, Lignée cellulaire tumorale, Mutation, Protéine-5 associée à l'autophagie, Techniques de knock-down de gènes, Transduction du signal.
English descriptors
- KwdEn :
- Antineoplastic Agents (pharmacology), Antineoplastic Agents (therapeutic use), Apoptosis (drug effects), Apoptosis (genetics), Apoptosis Regulatory Proteins (genetics), Autophagy (drug effects), Autophagy (genetics), Autophagy-Related Protein 5, Beclin-1, Carcinoma, Non-Small-Cell Lung (genetics), Carcinoma, Non-Small-Cell Lung (metabolism), Cell Line, Tumor, Drug Resistance, Neoplasm (genetics), ErbB Receptors (genetics), Erlotinib Hydrochloride, Gene Knockdown Techniques, Humans, Lung Neoplasms (genetics), Lung Neoplasms (metabolism), Membrane Proteins (genetics), Microtubule-Associated Proteins (genetics), Mutation, Protein Kinase Inhibitors (pharmacology), Protein Kinase Inhibitors (therapeutic use), Quinazolines (pharmacology), Quinazolines (therapeutic use), Signal Transduction.
- MESH :
- chemical , genetics : Apoptosis Regulatory Proteins, ErbB Receptors, Membrane Proteins, Microtubule-Associated Proteins.
- chemical , pharmacology : Antineoplastic Agents, Protein Kinase Inhibitors, Quinazolines.
- chemical , therapeutic use : Antineoplastic Agents, Protein Kinase Inhibitors, Quinazolines.
- drug effects : Apoptosis, Autophagy.
- genetics : Apoptosis, Autophagy, Carcinoma, Non-Small-Cell Lung, Drug Resistance, Neoplasm, Lung Neoplasms.
- metabolism : Carcinoma, Non-Small-Cell Lung, Lung Neoplasms.
- chemical : Autophagy-Related Protein 5, Beclin-1, Cell Line, Tumor, Erlotinib Hydrochloride, Gene Knockdown Techniques, Humans, Mutation, Signal Transduction.
Abstract
Erlotinib is a commonly used tyrosine kinase inhibitor (TKI) in non-small cell lung cancer (NSCLC). Autophagy is a catabolic process in response to stress and deprivation of nutrients. This study aims to investigate whether autophagy confers acquired resistance to erlotinib treatment in NSCLC.
DOI: 10.1016/j.lungcan.2013.05.012
PubMed: 23769318
Affiliations:
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Le document en format XML
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<term>Apoptosis (drug effects)</term>
<term>Apoptosis (genetics)</term>
<term>Apoptosis Regulatory Proteins (genetics)</term>
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<term>Autophagy (genetics)</term>
<term>Autophagy-Related Protein 5</term>
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<term>Cell Line, Tumor</term>
<term>Drug Resistance, Neoplasm (genetics)</term>
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<term>Erlotinib Hydrochloride</term>
<term>Gene Knockdown Techniques</term>
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<term>Lung Neoplasms (genetics)</term>
<term>Lung Neoplasms (metabolism)</term>
<term>Membrane Proteins (genetics)</term>
<term>Microtubule-Associated Proteins (genetics)</term>
<term>Mutation</term>
<term>Protein Kinase Inhibitors (pharmacology)</term>
<term>Protein Kinase Inhibitors (therapeutic use)</term>
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<term>Quinazolines (therapeutic use)</term>
<term>Signal Transduction</term>
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<term>Antinéoplasiques (usage thérapeutique)</term>
<term>Apoptose ()</term>
<term>Apoptose (génétique)</term>
<term>Autophagie ()</term>
<term>Autophagie (génétique)</term>
<term>Bécline-1</term>
<term>Carcinome pulmonaire non à petites cellules (génétique)</term>
<term>Carcinome pulmonaire non à petites cellules (métabolisme)</term>
<term>Chlorhydrate d'erlotinib</term>
<term>Humains</term>
<term>Inhibiteurs de protéines kinases (pharmacologie)</term>
<term>Inhibiteurs de protéines kinases (usage thérapeutique)</term>
<term>Lignée cellulaire tumorale</term>
<term>Mutation</term>
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<term>Protéines régulatrices de l'apoptose (génétique)</term>
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<term>Techniques de knock-down de gènes</term>
<term>Transduction du signal</term>
<term>Tumeurs du poumon (génétique)</term>
<term>Tumeurs du poumon (métabolisme)</term>
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<term>ErbB Receptors</term>
<term>Membrane Proteins</term>
<term>Microtubule-Associated Proteins</term>
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<term>Protein Kinase Inhibitors</term>
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<term>Carcinoma, Non-Small-Cell Lung</term>
<term>Drug Resistance, Neoplasm</term>
<term>Lung Neoplasms</term>
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<term>Protéines régulatrices de l'apoptose</term>
<term>Récepteurs ErbB</term>
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<term>Tumeurs du poumon</term>
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<term>Inhibiteurs de protéines kinases</term>
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<front><div type="abstract" xml:lang="en">Erlotinib is a commonly used tyrosine kinase inhibitor (TKI) in non-small cell lung cancer (NSCLC). Autophagy is a catabolic process in response to stress and deprivation of nutrients. This study aims to investigate whether autophagy confers acquired resistance to erlotinib treatment in NSCLC.</div>
</front>
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<affiliations><list><country><li>Hong Kong</li>
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<tree><noCountry><name sortKey="Lam, Sze Kwan" sort="Lam, Sze Kwan" uniqKey="Lam S" first="Sze-Kwan" last="Lam">Sze-Kwan Lam</name>
<name sortKey="Li, Yuan Yuan" sort="Li, Yuan Yuan" uniqKey="Li Y" first="Yuan-Yuan" last="Li">Yuan-Yuan Li</name>
<name sortKey="Mak, Judith Choi Wo" sort="Mak, Judith Choi Wo" uniqKey="Mak J" first="Judith Choi-Wo" last="Mak">Judith Choi-Wo Mak</name>
<name sortKey="Zheng, Chun Yan" sort="Zheng, Chun Yan" uniqKey="Zheng C" first="Chun-Yan" last="Zheng">Chun-Yan Zheng</name>
</noCountry>
<country name="Hong Kong"><noRegion><name sortKey="Ho, James Chung Man" sort="Ho, James Chung Man" uniqKey="Ho J" first="James Chung-Man" last="Ho">James Chung-Man Ho</name>
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