Alterations in Polyamine Metabolism in Patients With Lymphangioleiomyomatosis and Tuberous Sclerosis Complex 2-Deficient Cells.
Identifieur interne : 000A98 ( Main/Exploration ); précédent : 000A97; suivant : 000A99Alterations in Polyamine Metabolism in Patients With Lymphangioleiomyomatosis and Tuberous Sclerosis Complex 2-Deficient Cells.
Auteurs : Yan Tang [États-Unis] ; Souheil El-Chemaly [États-Unis] ; Angelo Taveira-Dasilva [États-Unis] ; Hilary J. Goldberg [États-Unis] ; Shefali Bagwe [États-Unis] ; Ivan O. Rosas [États-Unis] ; Joel Moss [États-Unis] ; Carmen Priolo [États-Unis] ; Elizabeth P. Henske [États-Unis]Source :
- Chest [ 1931-3543 ] ; 2019.
Abstract
Lymphangioleiomyomatosis (LAM), a destructive lung disease that affects primarily women, is caused by loss-of-function mutations in TSC1 or TSC2, leading to hyperactivation of mechanistic/mammalian target of rapamycin complex 1 (mTORC1). Rapamycin (sirolimus) treatment suppresses mTORC1 but also induces autophagy, which promotes the survival of TSC2-deficient cells. Based on the hypothesis that simultaneous inhibition of mTORC1 and autophagy would limit the availability of critical nutrients and inhibit LAM cells, we conducted a phase 1 clinical trial of sirolimus and hydroxychloroquine for LAM. Here, we report the analyses of plasma metabolomic profiles from the clinical trial.
DOI: 10.1016/j.chest.2019.05.038
PubMed: 31299246
Affiliations:
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Electronic address: Carmen_priolo@dfci.harvard.edu.</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Massachusetts</region></placeName><wicri:cityArea>Pulmonary and Critical Care Medicine Division, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston</wicri:cityArea></affiliation></author><author><name sortKey="Henske, Elizabeth P" sort="Henske, Elizabeth P" uniqKey="Henske E" first="Elizabeth P" last="Henske">Elizabeth P. Henske</name><affiliation wicri:level="2"><nlm:affiliation>Pulmonary and Critical Care Medicine Division, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Massachusetts</region></placeName><wicri:cityArea>Pulmonary and Critical Care Medicine Division, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston</wicri:cityArea></affiliation></author></analytic><series><title level="j">Chest</title><idno type="eISSN">1931-3543</idno><imprint><date when="2019" type="published">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Lymphangioleiomyomatosis (LAM), a destructive lung disease that affects primarily women, is caused by loss-of-function mutations in TSC1 or TSC2, leading to hyperactivation of mechanistic/mammalian target of rapamycin complex 1 (mTORC1). Rapamycin (sirolimus) treatment suppresses mTORC1 but also induces autophagy, which promotes the survival of TSC2-deficient cells. Based on the hypothesis that simultaneous inhibition of mTORC1 and autophagy would limit the availability of critical nutrients and inhibit LAM cells, we conducted a phase 1 clinical trial of sirolimus and hydroxychloroquine for LAM. Here, we report the analyses of plasma metabolomic profiles from the clinical trial.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Maryland</li><li>Massachusetts</li></region></list><tree><country name="États-Unis"><region name="Massachusetts"><name sortKey="Tang, Yan" sort="Tang, Yan" uniqKey="Tang Y" first="Yan" last="Tang">Yan Tang</name></region><name sortKey="Bagwe, Shefali" sort="Bagwe, Shefali" uniqKey="Bagwe S" first="Shefali" last="Bagwe">Shefali Bagwe</name><name sortKey="El Chemaly, Souheil" sort="El Chemaly, Souheil" uniqKey="El Chemaly S" first="Souheil" last="El-Chemaly">Souheil El-Chemaly</name><name sortKey="Goldberg, Hilary J" sort="Goldberg, Hilary J" uniqKey="Goldberg H" first="Hilary J" last="Goldberg">Hilary J. Goldberg</name><name sortKey="Henske, Elizabeth P" sort="Henske, Elizabeth P" uniqKey="Henske E" first="Elizabeth P" last="Henske">Elizabeth P. Henske</name><name sortKey="Moss, Joel" sort="Moss, Joel" uniqKey="Moss J" first="Joel" last="Moss">Joel Moss</name><name sortKey="Priolo, Carmen" sort="Priolo, Carmen" uniqKey="Priolo C" first="Carmen" last="Priolo">Carmen Priolo</name><name sortKey="Rosas, Ivan O" sort="Rosas, Ivan O" uniqKey="Rosas I" first="Ivan O" last="Rosas">Ivan O. Rosas</name><name sortKey="Taveira Dasilva, Angelo" sort="Taveira Dasilva, Angelo" uniqKey="Taveira Dasilva A" first="Angelo" last="Taveira-Dasilva">Angelo Taveira-Dasilva</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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