Optimizing treatments for lymphangioleiomyomatosis.
Identifieur interne : 001301 ( Main/Exploration ); précédent : 001300; suivant : 001302Optimizing treatments for lymphangioleiomyomatosis.
Auteurs : Angelo M. Taveira-Dasilva [États-Unis] ; Joel MossSource :
- Expert review of respiratory medicine [ 1747-6356 ] ; 2012.
Descripteurs français
- KwdFr :
- Animaux, Antinéoplasiques (), Antinéoplasiques (effets indésirables), Antinéoplasiques (usage thérapeutique), Conception de médicament, Femelle, Humains, Lymphangioléiomyomatose (), Lymphangioléiomyomatose (diagnostic), Lymphangioléiomyomatose (génétique), Lymphangioléiomyomatose (métabolisme), Mâle, Résistance aux médicaments antinéoplasiques, Résultat thérapeutique, Thérapie moléculaire ciblée, Transduction du signal ().
- MESH :
- diagnostic : Lymphangioléiomyomatose.
- effets indésirables : Antinéoplasiques.
- génétique : Lymphangioléiomyomatose.
- métabolisme : Lymphangioléiomyomatose.
- usage thérapeutique : Antinéoplasiques.
- Animaux, Antinéoplasiques, Conception de médicament, Femelle, Humains, Lymphangioléiomyomatose, Mâle, Résistance aux médicaments antinéoplasiques, Résultat thérapeutique, Thérapie moléculaire ciblée, Transduction du signal.
English descriptors
- KwdEn :
- Animals, Antineoplastic Agents (adverse effects), Antineoplastic Agents (chemistry), Antineoplastic Agents (therapeutic use), Drug Design, Drug Resistance, Neoplasm, Female, Humans, Lymphangioleiomyomatosis (diagnosis), Lymphangioleiomyomatosis (genetics), Lymphangioleiomyomatosis (metabolism), Lymphangioleiomyomatosis (therapy), Male, Molecular Targeted Therapy, Signal Transduction (drug effects), Treatment Outcome.
- MESH :
- chemical , adverse effects : Antineoplastic Agents.
- chemical , chemistry : Antineoplastic Agents.
- chemical , therapeutic use : Antineoplastic Agents.
- diagnosis : Lymphangioleiomyomatosis.
- drug effects : Signal Transduction.
- genetics : Lymphangioleiomyomatosis.
- metabolism : Lymphangioleiomyomatosis.
- therapy : Lymphangioleiomyomatosis.
- Animals, Drug Design, Drug Resistance, Neoplasm, Female, Humans, Male, Molecular Targeted Therapy, Treatment Outcome.
Abstract
Lymphangioleiomyomatosis (LAM), a multisystem disease predominantly affecting premenopausal women, is associated with cystic lung destruction and lymphatic and kidney tumors. LAM results from the proliferation of a neoplastic cell that has mutations in the tuberous sclerosis complex 1 or 2 genes, leading to activation of a critical regulatory protein, mammalian target of rapamycin. In this report, we discuss the molecular mechanisms regulating LAM cell growth and report the results of therapeutic trials employing new targeted agents. At present, inhibitors of mammalian target of rapamycin such as sirolimus appear to be the most promising therapeutic agents, although drug toxicity and development of resistance are potential problems. As the pathogenesis of LAM is being further recognized, other therapeutic agents such as matrix metalloproteinase inhibitors, statins, interferon, VEGF inhibitors, chloroquine analogs and cyclin-dependent kinase inhibitors, along with sirolimus or a combination of several of these agents, may offer the best hope for effective therapy.
DOI: 10.1586/ers.12.26
PubMed: 22788941
Affiliations:
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Le document en format XML
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Taveira-Dasilva</name><affiliation wicri:level="2"><nlm:affiliation>Cardiovascular and Pulmonary Branch, Bldg. 10, Rm. 6D05, MSC 1590, NHLBI, NIH, Bethesda, MD 20892-1590, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Cardiovascular and Pulmonary Branch, Bldg. 10, Rm. 6D05, MSC 1590, NHLBI, NIH, Bethesda, MD 20892-1590</wicri:regionArea><placeName><region type="state">Maryland</region></placeName></affiliation></author><author><name sortKey="Moss, Joel" sort="Moss, Joel" uniqKey="Moss J" first="Joel" last="Moss">Joel Moss</name></author></analytic><series><title level="j">Expert review of respiratory medicine</title><idno type="eISSN">1747-6356</idno><imprint><date when="2012" type="published">2012</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Antineoplastic Agents (adverse effects)</term><term>Antineoplastic Agents (chemistry)</term><term>Antineoplastic Agents (therapeutic use)</term><term>Drug Design</term><term>Drug Resistance, Neoplasm</term><term>Female</term><term>Humans</term><term>Lymphangioleiomyomatosis (diagnosis)</term><term>Lymphangioleiomyomatosis (genetics)</term><term>Lymphangioleiomyomatosis (metabolism)</term><term>Lymphangioleiomyomatosis (therapy)</term><term>Male</term><term>Molecular Targeted Therapy</term><term>Signal Transduction (drug effects)</term><term>Treatment Outcome</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Antinéoplasiques ()</term><term>Antinéoplasiques (effets indésirables)</term><term>Antinéoplasiques (usage thérapeutique)</term><term>Conception de médicament</term><term>Femelle</term><term>Humains</term><term>Lymphangioléiomyomatose ()</term><term>Lymphangioléiomyomatose (diagnostic)</term><term>Lymphangioléiomyomatose (génétique)</term><term>Lymphangioléiomyomatose (métabolisme)</term><term>Mâle</term><term>Résistance aux médicaments antinéoplasiques</term><term>Résultat thérapeutique</term><term>Thérapie moléculaire ciblée</term><term>Transduction du signal ()</term></keywords><keywords scheme="MESH" type="chemical" qualifier="adverse effects" xml:lang="en"><term>Antineoplastic Agents</term></keywords><keywords scheme="MESH" type="chemical" qualifier="chemistry" xml:lang="en"><term>Antineoplastic Agents</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Antineoplastic Agents</term></keywords><keywords scheme="MESH" qualifier="diagnosis" xml:lang="en"><term>Lymphangioleiomyomatosis</term></keywords><keywords scheme="MESH" qualifier="diagnostic" xml:lang="fr"><term>Lymphangioléiomyomatose</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Signal Transduction</term></keywords><keywords scheme="MESH" qualifier="effets indésirables" xml:lang="fr"><term>Antinéoplasiques</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Lymphangioleiomyomatosis</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Lymphangioléiomyomatose</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Lymphangioleiomyomatosis</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Lymphangioléiomyomatose</term></keywords><keywords scheme="MESH" qualifier="therapy" xml:lang="en"><term>Lymphangioleiomyomatosis</term></keywords><keywords scheme="MESH" qualifier="usage thérapeutique" xml:lang="fr"><term>Antinéoplasiques</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Drug Design</term><term>Drug Resistance, Neoplasm</term><term>Female</term><term>Humans</term><term>Male</term><term>Molecular Targeted Therapy</term><term>Treatment Outcome</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Antinéoplasiques</term><term>Conception de médicament</term><term>Femelle</term><term>Humains</term><term>Lymphangioléiomyomatose</term><term>Mâle</term><term>Résistance aux médicaments antinéoplasiques</term><term>Résultat thérapeutique</term><term>Thérapie moléculaire ciblée</term><term>Transduction du signal</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Lymphangioleiomyomatosis (LAM), a multisystem disease predominantly affecting premenopausal women, is associated with cystic lung destruction and lymphatic and kidney tumors. LAM results from the proliferation of a neoplastic cell that has mutations in the tuberous sclerosis complex 1 or 2 genes, leading to activation of a critical regulatory protein, mammalian target of rapamycin. In this report, we discuss the molecular mechanisms regulating LAM cell growth and report the results of therapeutic trials employing new targeted agents. At present, inhibitors of mammalian target of rapamycin such as sirolimus appear to be the most promising therapeutic agents, although drug toxicity and development of resistance are potential problems. As the pathogenesis of LAM is being further recognized, other therapeutic agents such as matrix metalloproteinase inhibitors, statins, interferon, VEGF inhibitors, chloroquine analogs and cyclin-dependent kinase inhibitors, along with sirolimus or a combination of several of these agents, may offer the best hope for effective therapy.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Maryland</li></region></list><tree><noCountry><name sortKey="Moss, Joel" sort="Moss, Joel" uniqKey="Moss J" first="Joel" last="Moss">Joel Moss</name></noCountry><country name="États-Unis"><region name="Maryland"><name sortKey="Taveira Dasilva, Angelo M" sort="Taveira Dasilva, Angelo M" uniqKey="Taveira Dasilva A" first="Angelo M" last="Taveira-Dasilva">Angelo M. Taveira-Dasilva</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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