RapamycinFungusV1, Main, Exploration, bibRecord, 000442

Therapeutic Targeting of mTOR in T-Cell Acute Lymphoblastic Leukemia: An Update.

Identifieur interne : 000442 ( Main/Exploration ); précédent : 000441; suivant : 000443

Therapeutic Targeting of mTOR in T-Cell Acute Lymphoblastic Leukemia: An Update.

Auteurs : Camilla Evangelisti [Italie] ; Francesca Chiarini [Italie] ; James A. Mccubrey [États-Unis] ; Alberto M. Martelli [Italie]

Source :

International journal of molecular sciences [ 1422-0067 ] ; 2018.

RBID : pubmed:29949919

Descripteurs français

KwdFr :
- Animaux (MeSH), Essais cliniques comme sujet (MeSH), Humains (MeSH), Leucémie-lymphome lymphoblastique à précurseurs T (anatomopathologie), Leucémie-lymphome lymphoblastique à précurseurs T (métabolisme), Leucémie-lymphome lymphoblastique à précurseurs T (traitement médicamenteux), Modèles biologiques (MeSH), Sérine-thréonine kinases TOR (antagonistes et inhibiteurs), Sérine-thréonine kinases TOR (composition chimique), Sérine-thréonine kinases TOR (métabolisme), Thérapie moléculaire ciblée (MeSH), Transduction du signal (MeSH).
MESH :
- anatomopathologie : Leucémie-lymphome lymphoblastique à précurseurs T.
- antagonistes et inhibiteurs : Sérine-thréonine kinases TOR.
- composition chimique : Sérine-thréonine kinases TOR.
- métabolisme : Leucémie-lymphome lymphoblastique à précurseurs T, Sérine-thréonine kinases TOR.
- traitement médicamenteux : Leucémie-lymphome lymphoblastique à précurseurs T.
- Animaux, Essais cliniques comme sujet, Humains, Modèles biologiques, Thérapie moléculaire ciblée, Transduction du signal.

English descriptors

KwdEn :
- Animals (MeSH), Clinical Trials as Topic (MeSH), Humans (MeSH), Models, Biological (MeSH), Molecular Targeted Therapy (MeSH), Precursor T-Cell Lymphoblastic Leukemia-Lymphoma (drug therapy), Precursor T-Cell Lymphoblastic Leukemia-Lymphoma (metabolism), Precursor T-Cell Lymphoblastic Leukemia-Lymphoma (pathology), Signal Transduction (MeSH), TOR Serine-Threonine Kinases (antagonists & inhibitors), TOR Serine-Threonine Kinases (chemistry), TOR Serine-Threonine Kinases (metabolism).
MESH :
- chemical , antagonists & inhibitors : TOR Serine-Threonine Kinases.
- chemical , chemistry : TOR Serine-Threonine Kinases.
- drug therapy : Precursor T-Cell Lymphoblastic Leukemia-Lymphoma.
- metabolism : Precursor T-Cell Lymphoblastic Leukemia-Lymphoma, TOR Serine-Threonine Kinases.
- pathology : Precursor T-Cell Lymphoblastic Leukemia-Lymphoma.
- Animals, Clinical Trials as Topic, Humans, Models, Biological, Molecular Targeted Therapy, Signal Transduction.

Abstract

T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive blood malignancy that arises from the clonal expansion of transformed T-cell precursors. Although T-ALL prognosis has significantly improved due to the development of intensive chemotherapeutic protocols, primary drug-resistant and relapsed patients still display a dismal outcome. In addition, lifelong irreversible late effects from conventional therapy are a growing problem for leukemia survivors. Therefore, novel targeted therapies are required to improve the prognosis of high-risk patients. The mechanistic target of rapamycin (mTOR) is the kinase subunit of two structurally and functionally distinct multiprotein complexes, which are referred to as mTOR complex 1 (mTORC1) and mTORC2. These two complexes regulate a variety of physiological cellular processes including protein, lipid, and nucleotide synthesis, as well as autophagy in response to external cues. However, mTOR activity is frequently deregulated in cancer, where it plays a key oncogenetic role driving tumor cell proliferation, survival, metabolic transformation, and metastatic potential. Promising preclinical studies using mTOR inhibitors have demonstrated efficacy in many human cancer types, including T-ALL. Here, we highlight our current knowledge of mTOR signaling and inhibitors in T-ALL, with an emphasis on emerging evidence of the superior efficacy of combinations consisting of mTOR inhibitors and either traditional or targeted therapeutics.

DOI: 10.3390/ijms19071878
PubMed: 29949919
PubMed Central: PMC6073309

Affiliations:

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

to stream Main, to step Corpus: 000517
to stream Main, to step Curation: 000517

Le document en format XML

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<term>Leucémie-lymphome lymphoblastique à précurseurs T (métabolisme)</term>
<term>Leucémie-lymphome lymphoblastique à précurseurs T (traitement médicamenteux)</term>
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<term>Sérine-thréonine kinases TOR (composition chimique)</term>
<term>Sérine-thréonine kinases TOR (métabolisme)</term>
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<keywords scheme="MESH" qualifier="composition chimique" xml:lang="fr"><term>Sérine-thréonine kinases TOR</term>
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<front><div type="abstract" xml:lang="en">T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive blood malignancy that arises from the clonal expansion of transformed T-cell precursors. Although T-ALL prognosis has significantly improved due to the development of intensive chemotherapeutic protocols, primary drug-resistant and relapsed patients still display a dismal outcome. In addition, lifelong irreversible late effects from conventional therapy are a growing problem for leukemia survivors. Therefore, novel targeted therapies are required to improve the prognosis of high-risk patients. The mechanistic target of rapamycin (mTOR) is the kinase subunit of two structurally and functionally distinct multiprotein complexes, which are referred to as mTOR complex 1 (mTORC1) and mTORC2. These two complexes regulate a variety of physiological cellular processes including protein, lipid, and nucleotide synthesis, as well as autophagy in response to external cues. However, mTOR activity is frequently deregulated in cancer, where it plays a key oncogenetic role driving tumor cell proliferation, survival, metabolic transformation, and metastatic potential. Promising preclinical studies using mTOR inhibitors have demonstrated efficacy in many human cancer types, including T-ALL. Here, we highlight our current knowledge of mTOR signaling and inhibitors in T-ALL, with an emphasis on emerging evidence of the superior efficacy of combinations consisting of mTOR inhibitors and either traditional or targeted therapeutics.</div>
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<Abstract><AbstractText>T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive blood malignancy that arises from the clonal expansion of transformed T-cell precursors. Although T-ALL prognosis has significantly improved due to the development of intensive chemotherapeutic protocols, primary drug-resistant and relapsed patients still display a dismal outcome. In addition, lifelong irreversible late effects from conventional therapy are a growing problem for leukemia survivors. Therefore, novel targeted therapies are required to improve the prognosis of high-risk patients. The mechanistic target of rapamycin (mTOR) is the kinase subunit of two structurally and functionally distinct multiprotein complexes, which are referred to as mTOR complex 1 (mTORC1) and mTORC2. These two complexes regulate a variety of physiological cellular processes including protein, lipid, and nucleotide synthesis, as well as autophagy in response to external cues. However, mTOR activity is frequently deregulated in cancer, where it plays a key oncogenetic role driving tumor cell proliferation, survival, metabolic transformation, and metastatic potential. Promising preclinical studies using mTOR inhibitors have demonstrated efficacy in many human cancer types, including T-ALL. Here, we highlight our current knowledge of mTOR signaling and inhibitors in T-ALL, with an emphasis on emerging evidence of the superior efficacy of combinations consisting of mTOR inhibitors and either traditional or targeted therapeutics.</AbstractText>
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Therapeutic Targeting of mTOR in T-Cell Acute Lymphoblastic Leukemia: An Update.

Therapeutic Targeting of mTOR in T-Cell Acute Lymphoblastic Leukemia: An Update.

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