Autophagy in osteosarcoma.
Identifieur interne : 001035 ( Main/Exploration ); précédent : 001034; suivant : 001036Autophagy in osteosarcoma.
Auteurs : Janice Santiago O'Farrill [États-Unis] ; Nancy GordonSource :
- Advances in experimental medicine and biology [ 0065-2598 ] ; 2014.
Descripteurs français
- KwdFr :
- Animaux, Antinéoplasiques antimétabolites (pharmacologie), Autophagie (), Autophagie (génétique), Désoxycytidine (analogues et dérivés), Désoxycytidine (pharmacologie), Humains, Hydroxychloroquine (pharmacologie), Lignée cellulaire tumorale, Os et tissu osseux (), Os et tissu osseux (anatomopathologie), Os et tissu osseux (métabolisme), Ostéosarcome (génétique), Ostéosarcome (métabolisme), Ostéosarcome (secondaire), Ostéosarcome (traitement médicamenteux), Poumon (), Poumon (anatomopathologie), Poumon (métabolisme), Résistance aux médicaments antinéoplasiques (), Résistance aux médicaments antinéoplasiques (génétique), Souris, Spécificité d'espèce, Tumeurs du poumon (génétique), Tumeurs du poumon (métabolisme), Tumeurs du poumon (secondaire), Tumeurs du poumon (traitement médicamenteux), Tumeurs osseuses (anatomopathologie), Tumeurs osseuses (génétique), Tumeurs osseuses (métabolisme), Tumeurs osseuses (traitement médicamenteux).
- MESH :
- analogues et dérivés : Désoxycytidine.
- anatomopathologie : Os et tissu osseux, Poumon, Tumeurs osseuses.
- génétique : Autophagie, Ostéosarcome, Résistance aux médicaments antinéoplasiques, Tumeurs du poumon, Tumeurs osseuses.
- métabolisme : Os et tissu osseux, Ostéosarcome, Poumon, Tumeurs du poumon, Tumeurs osseuses.
- pharmacologie : Antinéoplasiques antimétabolites, Désoxycytidine, Hydroxychloroquine.
- secondaire : Ostéosarcome, Tumeurs du poumon.
- traitement médicamenteux : Ostéosarcome, Tumeurs du poumon, Tumeurs osseuses.
- Animaux, Autophagie, Humains, Lignée cellulaire tumorale, Os et tissu osseux, Poumon, Résistance aux médicaments antinéoplasiques, Souris, Spécificité d'espèce.
English descriptors
- KwdEn :
- Animals, Antimetabolites, Antineoplastic (pharmacology), Autophagy (drug effects), Autophagy (genetics), Bone Neoplasms (drug therapy), Bone Neoplasms (genetics), Bone Neoplasms (metabolism), Bone Neoplasms (pathology), Bone and Bones (drug effects), Bone and Bones (metabolism), Bone and Bones (pathology), Cell Line, Tumor, Deoxycytidine (analogs & derivatives), Deoxycytidine (pharmacology), Drug Resistance, Neoplasm (drug effects), Drug Resistance, Neoplasm (genetics), Humans, Hydroxychloroquine (pharmacology), Lung (drug effects), Lung (metabolism), Lung (pathology), Lung Neoplasms (drug therapy), Lung Neoplasms (genetics), Lung Neoplasms (metabolism), Lung Neoplasms (secondary), Mice, Osteosarcoma (drug therapy), Osteosarcoma (genetics), Osteosarcoma (metabolism), Osteosarcoma (secondary), Species Specificity.
- MESH :
- chemical , analogs & derivatives : Deoxycytidine.
- chemical , pharmacology : Antimetabolites, Antineoplastic, Deoxycytidine, Hydroxychloroquine.
- drug effects : Autophagy, Bone and Bones, Drug Resistance, Neoplasm, Lung.
- drug therapy : Bone Neoplasms, Lung Neoplasms, Osteosarcoma.
- genetics : Autophagy, Bone Neoplasms, Drug Resistance, Neoplasm, Lung Neoplasms, Osteosarcoma.
- metabolism : Bone Neoplasms, Bone and Bones, Lung, Lung Neoplasms, Osteosarcoma.
- pathology : Bone Neoplasms, Bone and Bones, Lung.
- secondary : Lung Neoplasms, Osteosarcoma.
- Animals, Cell Line, Tumor, Humans, Mice, Species Specificity.
Abstract
Osteosarcoma (OS) metastatic disease is resistant to conventional chemotherapy. Tumor resistance to chemotherapy has been one of the major areas of concern to clinicians and the topic of many laboratory investigators. Evaluation of mechanisms implicated in OS lung metastasis resistance to chemotherapy has been the focus of some of our most recent work. We have previously demonstrated the therapeutic efficacy of aerosol gemcitabine (GCB) in OS lung metastases. However, a subset of cells fails to respond to GCB treatment and persists as isolated lung metastases in vivo. Autophagy, a physiological mechanism that supports nutritional deprivation under stressful conditions, has been implicated in tumor resistance to chemotherapy. We demonstrated the induction of autophagy by GCB in LM7 metastatic human OS cells and K7M3 metastatic murine OS cells. Inhibition of autophagy resulted in increased sensitivity to GCB in LM7 cells. By contrast, inhibiting autophagy in K7M3 cells decreased GCB sensitivity. Defining the role autophagy plays in chemotherapy response in different tumor types has become of greater importance in order to identify the best suitable therapeutic approach. In this chapter, we summarize some of the most recent work related to autophagy in OS, identify some of the known mechanisms, and address the different roles autophagy plays in chemotherapy response.
DOI: 10.1007/978-3-319-04843-7_8
PubMed: 24924173
Affiliations:
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Le document en format XML
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effects)</term><term>Lung (metabolism)</term><term>Lung (pathology)</term><term>Lung Neoplasms (drug therapy)</term><term>Lung Neoplasms (genetics)</term><term>Lung Neoplasms (metabolism)</term><term>Lung Neoplasms (secondary)</term><term>Mice</term><term>Osteosarcoma (drug therapy)</term><term>Osteosarcoma (genetics)</term><term>Osteosarcoma (metabolism)</term><term>Osteosarcoma (secondary)</term><term>Species Specificity</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Antinéoplasiques antimétabolites (pharmacologie)</term><term>Autophagie ()</term><term>Autophagie (génétique)</term><term>Désoxycytidine (analogues et dérivés)</term><term>Désoxycytidine (pharmacologie)</term><term>Humains</term><term>Hydroxychloroquine (pharmacologie)</term><term>Lignée cellulaire tumorale</term><term>Os et tissu osseux ()</term><term>Os et tissu osseux (anatomopathologie)</term><term>Os et tissu osseux (métabolisme)</term><term>Ostéosarcome (génétique)</term><term>Ostéosarcome (métabolisme)</term><term>Ostéosarcome (secondaire)</term><term>Ostéosarcome (traitement médicamenteux)</term><term>Poumon ()</term><term>Poumon (anatomopathologie)</term><term>Poumon (métabolisme)</term><term>Résistance aux médicaments antinéoplasiques ()</term><term>Résistance aux médicaments antinéoplasiques (génétique)</term><term>Souris</term><term>Spécificité d'espèce</term><term>Tumeurs du poumon (génétique)</term><term>Tumeurs du poumon (métabolisme)</term><term>Tumeurs du poumon (secondaire)</term><term>Tumeurs du poumon (traitement médicamenteux)</term><term>Tumeurs osseuses (anatomopathologie)</term><term>Tumeurs osseuses (génétique)</term><term>Tumeurs osseuses (métabolisme)</term><term>Tumeurs osseuses (traitement médicamenteux)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analogs & derivatives" xml:lang="en"><term>Deoxycytidine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antimetabolites, Antineoplastic</term><term>Deoxycytidine</term><term>Hydroxychloroquine</term></keywords><keywords scheme="MESH" qualifier="analogues et dérivés" xml:lang="fr"><term>Désoxycytidine</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Os et tissu osseux</term><term>Poumon</term><term>Tumeurs osseuses</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Autophagy</term><term>Bone and Bones</term><term>Drug Resistance, Neoplasm</term><term>Lung</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Bone Neoplasms</term><term>Lung Neoplasms</term><term>Osteosarcoma</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Autophagy</term><term>Bone Neoplasms</term><term>Drug Resistance, Neoplasm</term><term>Lung Neoplasms</term><term>Osteosarcoma</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Autophagie</term><term>Ostéosarcome</term><term>Résistance aux médicaments antinéoplasiques</term><term>Tumeurs du poumon</term><term>Tumeurs osseuses</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Bone Neoplasms</term><term>Bone and Bones</term><term>Lung</term><term>Lung Neoplasms</term><term>Osteosarcoma</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Os et tissu osseux</term><term>Ostéosarcome</term><term>Poumon</term><term>Tumeurs du poumon</term><term>Tumeurs osseuses</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Bone Neoplasms</term><term>Bone and Bones</term><term>Lung</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Antinéoplasiques antimétabolites</term><term>Désoxycytidine</term><term>Hydroxychloroquine</term></keywords><keywords scheme="MESH" qualifier="secondaire" xml:lang="fr"><term>Ostéosarcome</term><term>Tumeurs du poumon</term></keywords><keywords scheme="MESH" qualifier="secondary" xml:lang="en"><term>Lung Neoplasms</term><term>Osteosarcoma</term></keywords><keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Ostéosarcome</term><term>Tumeurs du poumon</term><term>Tumeurs osseuses</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cell Line, Tumor</term><term>Humans</term><term>Mice</term><term>Species Specificity</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Autophagie</term><term>Humains</term><term>Lignée cellulaire tumorale</term><term>Os et tissu osseux</term><term>Poumon</term><term>Résistance aux médicaments antinéoplasiques</term><term>Souris</term><term>Spécificité d'espèce</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Osteosarcoma (OS) metastatic disease is resistant to conventional chemotherapy. Tumor resistance to chemotherapy has been one of the major areas of concern to clinicians and the topic of many laboratory investigators. Evaluation of mechanisms implicated in OS lung metastasis resistance to chemotherapy has been the focus of some of our most recent work. We have previously demonstrated the therapeutic efficacy of aerosol gemcitabine (GCB) in OS lung metastases. However, a subset of cells fails to respond to GCB treatment and persists as isolated lung metastases in vivo. Autophagy, a physiological mechanism that supports nutritional deprivation under stressful conditions, has been implicated in tumor resistance to chemotherapy. We demonstrated the induction of autophagy by GCB in LM7 metastatic human OS cells and K7M3 metastatic murine OS cells. Inhibition of autophagy resulted in increased sensitivity to GCB in LM7 cells. By contrast, inhibiting autophagy in K7M3 cells decreased GCB sensitivity. Defining the role autophagy plays in chemotherapy response in different tumor types has become of greater importance in order to identify the best suitable therapeutic approach. In this chapter, we summarize some of the most recent work related to autophagy in OS, identify some of the known mechanisms, and address the different roles autophagy plays in chemotherapy response. </div></front></TEI><affiliations><list><country><li>États-Unis</li></country></list><tree><noCountry><name sortKey="Gordon, Nancy" sort="Gordon, Nancy" uniqKey="Gordon N" first="Nancy" last="Gordon">Nancy Gordon</name></noCountry><country name="États-Unis"><noRegion><name sortKey="O Farrill, Janice Santiago" sort="O Farrill, Janice Santiago" uniqKey="O Farrill J" first="Janice Santiago" last="O'Farrill">Janice Santiago O'Farrill</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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