Lymphangioleiomyomatosis: New Treatment Perspectives.
Identifieur interne : 000E79 ( Main/Exploration ); précédent : 000E78; suivant : 000E80Lymphangioleiomyomatosis: New Treatment Perspectives.
Auteurs : El Bieta Radzikowska [Pologne]Source :
- Lung [ 1432-1750 ] ; 2015.
Descripteurs français
- KwdFr :
- Animaux, Antagonistes des oestrogènes (usage thérapeutique), Autophagie (), Facteur de croissance endothéliale vasculaire de type D (antagonistes et inhibiteurs), Facteurs sexuels, Femelle, Humains, Immunothérapie, Inhibiteurs de l'hydroxyméthylglutaryl-CoA réductase (usage thérapeutique), Inhibiteurs de protéines kinases (usage thérapeutique), Kinase-2 cycline-dépendante (antagonistes et inhibiteurs), Lymphangioléiomyomatose (traitement médicamenteux), Metalloproteases (antagonistes et inhibiteurs), Sérine-thréonine kinases TOR (antagonistes et inhibiteurs).
- MESH :
- antagonistes et inhibiteurs : Facteur de croissance endothéliale vasculaire de type D, Kinase-2 cycline-dépendante, Metalloproteases, Sérine-thréonine kinases TOR.
- traitement médicamenteux : Lymphangioléiomyomatose.
- usage thérapeutique : Antagonistes des oestrogènes, Inhibiteurs de l'hydroxyméthylglutaryl-CoA réductase, Inhibiteurs de protéines kinases.
- Animaux, Autophagie, Facteurs sexuels, Femelle, Humains, Immunothérapie.
English descriptors
- KwdEn :
- Animals, Autophagy (drug effects), Cyclin-Dependent Kinase 2 (antagonists & inhibitors), Estrogen Antagonists (therapeutic use), Female, Humans, Hydroxymethylglutaryl-CoA Reductase Inhibitors (therapeutic use), Immunotherapy, Lymphangioleiomyomatosis (drug therapy), Metalloproteases (antagonists & inhibitors), Protein Kinase Inhibitors (therapeutic use), Sex Factors, TOR Serine-Threonine Kinases (antagonists & inhibitors), Vascular Endothelial Growth Factor D (antagonists & inhibitors).
- MESH :
- chemical , antagonists & inhibitors : Cyclin-Dependent Kinase 2, Metalloproteases, TOR Serine-Threonine Kinases, Vascular Endothelial Growth Factor D.
- drug effects : Autophagy.
- drug therapy : Lymphangioleiomyomatosis.
- chemical , therapeutic use : Estrogen Antagonists, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Protein Kinase Inhibitors.
- Animals, Female, Humans, Immunotherapy, Sex Factors.
Abstract
Lymphangioleiomyomatosis (LAM) is a rare multisystem disease, occurs in women, usually premenopausal, caused by the proliferation of neoplastic smooth muscle-derived cells. Mutations in the tuberous sclerosis complex genes, lead to the activation of mammalian target of rapamycin kinase (mTOR), results in proliferation of LAM cells, its increasing motility, and survival. Polycystic lung destruction, extensive involvement of lymphatic channels, chylothorax, chyloperitoneum, and renal angiomyolipomas can develop in LAM patients. The new, promising treatment strategies have been recently introduced due to discovery of the genetic and molecular mechanisms of LAM. Comprehension of the disease pathogenesis has resulted in the implementation of other therapeutic agents such as mTOR inhibitors, VEGF-D inhibitors, statins, interferon, chloroquine analogs, cyclin-dependent kinase inhibitors, matrix metalloproteinase inhibitors, aromatase inhibitors, and their combinations. The mTOR inhibitors appear to be the most important, and the efficacy of sirolimus in LAM treatment has been proved. The article discussed the new control studies with mTOR inhibitors, doxycycline, simvastatin, and combination of them in LAM patients.
DOI: 10.1007/s00408-015-9742-6
PubMed: 25980593
Affiliations:
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Le document en format XML
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<term>Antagonistes des oestrogènes (usage thérapeutique)</term>
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<term>Facteur de croissance endothéliale vasculaire de type D (antagonistes et inhibiteurs)</term>
<term>Facteurs sexuels</term>
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<term>Humains</term>
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<term>Inhibiteurs de protéines kinases (usage thérapeutique)</term>
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<term>Vascular Endothelial Growth Factor D</term>
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<term>Kinase-2 cycline-dépendante</term>
<term>Metalloproteases</term>
<term>Sérine-thréonine kinases TOR</term>
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<term>Sex Factors</term>
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<term>Autophagie</term>
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<front><div type="abstract" xml:lang="en">Lymphangioleiomyomatosis (LAM) is a rare multisystem disease, occurs in women, usually premenopausal, caused by the proliferation of neoplastic smooth muscle-derived cells. Mutations in the tuberous sclerosis complex genes, lead to the activation of mammalian target of rapamycin kinase (mTOR), results in proliferation of LAM cells, its increasing motility, and survival. Polycystic lung destruction, extensive involvement of lymphatic channels, chylothorax, chyloperitoneum, and renal angiomyolipomas can develop in LAM patients. The new, promising treatment strategies have been recently introduced due to discovery of the genetic and molecular mechanisms of LAM. Comprehension of the disease pathogenesis has resulted in the implementation of other therapeutic agents such as mTOR inhibitors, VEGF-D inhibitors, statins, interferon, chloroquine analogs, cyclin-dependent kinase inhibitors, matrix metalloproteinase inhibitors, aromatase inhibitors, and their combinations. The mTOR inhibitors appear to be the most important, and the efficacy of sirolimus in LAM treatment has been proved. The article discussed the new control studies with mTOR inhibitors, doxycycline, simvastatin, and combination of them in LAM patients. </div>
</front>
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