RapamycinFungusV1, Main, Exploration, bibRecord, 001700

Rapamycin is efficacious against primary effusion lymphoma (PEL) cell lines in vivo by inhibiting autocrine signaling.

Identifieur interne : 001700 ( Main/Exploration ); précédent : 001699; suivant : 001701

Rapamycin is efficacious against primary effusion lymphoma (PEL) cell lines in vivo by inhibiting autocrine signaling.

Auteurs : Sang-Hoon Sin [États-Unis] ; Debasmita Roy ; Ling Wang ; Michelle R. Staudt ; Farnaz D. Fakhari ; Dhavalkumar D. Patel ; David Henry ; William J. Harrington ; Blossom A. Damania ; Dirk P. Dittmer

Source :

Blood [ 0006-4971 ] ; 2007.

RBID : pubmed:17082322

Descripteurs français

KwdFr :
- ARN messager (génétique), Animaux (MeSH), Communication autocrine (effets des médicaments et des substances chimiques), Cytokines (biosynthèse), Cytokines (génétique), Herpèsvirus humain de type 8 (effets des médicaments et des substances chimiques), Herpèsvirus humain de type 8 (génétique), Humains (MeSH), Lignée cellulaire tumorale (MeSH), Lymphomes (anatomopathologie), Lymphomes (métabolisme), Prolifération cellulaire (effets des médicaments et des substances chimiques), Sirolimus (pharmacologie), Souris (MeSH), Tests d'activité antitumorale sur modèle de xénogreffe (MeSH), Transcription génétique (génétique), Évolution de la maladie (MeSH).
MESH :
- anatomopathologie : Lymphomes.
- biosynthèse : Cytokines.
- effets des médicaments et des substances chimiques : Communication autocrine, Herpèsvirus humain de type 8, Prolifération cellulaire.
- génétique : ARN messager, Cytokines, Herpèsvirus humain de type 8, Transcription génétique.
- métabolisme : Lymphomes.
- pharmacologie : Sirolimus.
- Animaux, Humains, Lignée cellulaire tumorale, Souris, Tests d'activité antitumorale sur modèle de xénogreffe, Évolution de la maladie.

English descriptors

KwdEn :
- Animals (MeSH), Autocrine Communication (drug effects), Cell Line, Tumor (MeSH), Cell Proliferation (drug effects), Cytokines (biosynthesis), Cytokines (genetics), Disease Progression (MeSH), Herpesvirus 8, Human (drug effects), Herpesvirus 8, Human (genetics), Humans (MeSH), Lymphoma (metabolism), Lymphoma (pathology), Mice (MeSH), RNA, Messenger (genetics), Sirolimus (pharmacology), Transcription, Genetic (genetics), Xenograft Model Antitumor Assays (MeSH).
MESH :
- chemical , biosynthesis : Cytokines.
- drug effects : Autocrine Communication, Cell Proliferation, Herpesvirus 8, Human.
- chemical , genetics : Cytokines, Herpesvirus 8, Human, RNA, Messenger, Transcription, Genetic.
- metabolism : Lymphoma.
- pathology : Lymphoma.
- chemical , pharmacology : Sirolimus.
- Animals, Cell Line, Tumor, Disease Progression, Humans, Mice, Xenograft Model Antitumor Assays.

Abstract

The antitumor potency of the mTOR inhibitor rapamycin (sirolimus) is the subject of intense investigations. Primary effusion lymphoma (PEL) appears as an AIDS-defining lymphoma and like Kaposi sarcoma has been linked to Kaposi sarcoma-associated herpesvirus (KSHV). We find that (1) rapamycin is efficacious against PEL in culture and in a murine xenograft model; (2) mTOR, its activator Akt, and its target p70S6 kinase are phosphorylated in PEL; (3) rapamycin inhibits mTOR signaling as determined by S6 phosphorylation; (4) KSHV transcription is unaffected; (5) inhibition of IL-10 signaling correlates with drug sensitivity; and (6) addition of exogenous IL-10 or IL-6 can reverse the rapamycin growth arrest. This validates sirolimus as a new treatment option for PEL.

DOI: 10.1182/blood-2006-06-028092
PubMed: 17082322
PubMed Central: PMC1801055

Affiliations:

Links toward previous steps (curation, corpus...)

to stream Main, to step Corpus: 001750
to stream Main, to step Curation: 001750

Le document en format XML

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<term>Cytokines (biosynthesis)</term>
<term>Cytokines (genetics)</term>
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<term>Herpesvirus 8, Human (genetics)</term>
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<term>Sirolimus (pharmacology)</term>
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<term>Xenograft Model Antitumor Assays (MeSH)</term>
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<term>Cytokines (biosynthèse)</term>
<term>Cytokines (génétique)</term>
<term>Herpèsvirus humain de type 8 (effets des médicaments et des substances chimiques)</term>
<term>Herpèsvirus humain de type 8 (génétique)</term>
<term>Humains (MeSH)</term>
<term>Lignée cellulaire tumorale (MeSH)</term>
<term>Lymphomes (anatomopathologie)</term>
<term>Lymphomes (métabolisme)</term>
<term>Prolifération cellulaire (effets des médicaments et des substances chimiques)</term>
<term>Sirolimus (pharmacologie)</term>
<term>Souris (MeSH)</term>
<term>Tests d'activité antitumorale sur modèle de xénogreffe (MeSH)</term>
<term>Transcription génétique (génétique)</term>
<term>Évolution de la maladie (MeSH)</term>
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<term>Prolifération cellulaire</term>
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<term>Cell Line, Tumor</term>
<term>Disease Progression</term>
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<term>Mice</term>
<term>Xenograft Model Antitumor Assays</term>
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<term>Humains</term>
<term>Lignée cellulaire tumorale</term>
<term>Souris</term>
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<front><div type="abstract" xml:lang="en">The antitumor potency of the mTOR inhibitor rapamycin (sirolimus) is the subject of intense investigations. Primary effusion lymphoma (PEL) appears as an AIDS-defining lymphoma and like Kaposi sarcoma has been linked to Kaposi sarcoma-associated herpesvirus (KSHV). We find that (1) rapamycin is efficacious against PEL in culture and in a murine xenograft model; (2) mTOR, its activator Akt, and its target p70S6 kinase are phosphorylated in PEL; (3) rapamycin inhibits mTOR signaling as determined by S6 phosphorylation; (4) KSHV transcription is unaffected; (5) inhibition of IL-10 signaling correlates with drug sensitivity; and (6) addition of exogenous IL-10 or IL-6 can reverse the rapamycin growth arrest. This validates sirolimus as a new treatment option for PEL.</div>
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<Abstract><AbstractText>The antitumor potency of the mTOR inhibitor rapamycin (sirolimus) is the subject of intense investigations. Primary effusion lymphoma (PEL) appears as an AIDS-defining lymphoma and like Kaposi sarcoma has been linked to Kaposi sarcoma-associated herpesvirus (KSHV). We find that (1) rapamycin is efficacious against PEL in culture and in a murine xenograft model; (2) mTOR, its activator Akt, and its target p70S6 kinase are phosphorylated in PEL; (3) rapamycin inhibits mTOR signaling as determined by S6 phosphorylation; (4) KSHV transcription is unaffected; (5) inhibition of IL-10 signaling correlates with drug sensitivity; and (6) addition of exogenous IL-10 or IL-6 can reverse the rapamycin growth arrest. This validates sirolimus as a new treatment option for PEL.</AbstractText>
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   |texte=   Rapamycin is efficacious against primary effusion lymphoma (PEL) cell lines in vivo by inhibiting autocrine signaling.
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	Serveur d'exploration sur la rapamycine et les champignons
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Rapamycin is efficacious against primary effusion lymphoma (PEL) cell lines in vivo by inhibiting autocrine signaling.

Rapamycin is efficacious against primary effusion lymphoma (PEL) cell lines in vivo by inhibiting autocrine signaling.

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