RapamycinFungusV1, Main, Exploration, bibRecord, 000977

The therapeutic potential of mTOR inhibitors in breast cancer.

Identifieur interne : 000977 ( Main/Exploration ); précédent : 000976; suivant : 000978

The therapeutic potential of mTOR inhibitors in breast cancer.

Auteurs : Linda S. Steelman [États-Unis] ; Alberto M. Martelli [Italie] ; Lucio Cocco [Italie] ; Massimo Libra [Italie] ; Ferdinando Nicoletti [Italie] ; Stephen L. Abrams [États-Unis] ; James A. Mccubrey [États-Unis]

Source :

British journal of clinical pharmacology [ 1365-2125 ] ; 2016.

RBID : pubmed:27059645

Descripteurs français

KwdFr :
- Complexe-1 cible mécanistique de la rapamycine (antagonistes et inhibiteurs), Femelle (MeSH), Humains (MeSH), Inhibiteurs de l'aromatase (usage thérapeutique), Inhibiteurs de protéines kinases (usage thérapeutique), Modèles biologiques (MeSH), Protocoles de polychimiothérapie antinéoplasique (usage thérapeutique), Transduction du signal (effets des médicaments et des substances chimiques), Tumeurs du sein (traitement médicamenteux).
MESH :
- antagonistes et inhibiteurs : Complexe-1 cible mécanistique de la rapamycine.
- effets des médicaments et des substances chimiques : Transduction du signal.
- traitement médicamenteux : Tumeurs du sein.
- usage thérapeutique : Inhibiteurs de l'aromatase, Inhibiteurs de protéines kinases, Protocoles de polychimiothérapie antinéoplasique.
- Femelle, Humains, Modèles biologiques.

English descriptors

KwdEn :
- Antineoplastic Combined Chemotherapy Protocols (therapeutic use), Aromatase Inhibitors (therapeutic use), Breast Neoplasms (drug therapy), Female (MeSH), Humans (MeSH), Mechanistic Target of Rapamycin Complex 1 (antagonists & inhibitors), Models, Biological (MeSH), Protein Kinase Inhibitors (therapeutic use), Signal Transduction (drug effects).
MESH :
- chemical , antagonists & inhibitors : Mechanistic Target of Rapamycin Complex 1.
- chemical , therapeutic use : Aromatase Inhibitors, Protein Kinase Inhibitors.
- drug effects : Signal Transduction.
- drug therapy : Breast Neoplasms.
- therapeutic use : Antineoplastic Combined Chemotherapy Protocols.
- Female, Humans, Models, Biological.

Abstract

Rapamycin and modified rapamycins (rapalogs) have been used to prevent allograft rejection after organ transplant for over 15 years. The mechanistic target of rapamycin (mTOR) has been determined to be a key component of the mTORC1 complex which consists of the serine/threonine kinase TOR and at least five other proteins which are involved in regulating its activity. Some of the best characterized substrates of mTORC1 are proteins which are key kinases involved in the regulation of cell growth (e.g., p70S6K) and protein translation (e.g., 4E-BP1). These proteins may in some cases serve as indicators to sensitivity to rapamycin-related therapies. Dysregulation of mTORC1 activity frequently occurs due to mutations at, or amplifications of, upstream growth factor receptors (e.g., human epidermal growth factor receptor-2, HER2) as well as kinases (e.g., PI3K) and phosphatases (e.g., PTEN) critical in the regulation of cell growth. More recently, it has been shown that certain rapalogs may enhance the effectiveness of hormonal-based therapies for breast cancer patients who have become resistant to endocrine therapy. The combined treatment of certain rapalogs (e.g., everolimus) and aromatase inhibitors (e.g., exemestane) has been approved by the United States Food and Drug Administration (US FDA) and other drug regulatory agencies to treat estrogen receptor positive (ER+) breast cancer patients who have become resistant to hormonal-based therapies and have progressed. This review will summarize recent basic and clinical research in the area and evaluate potential novel therapeutic approaches.

DOI: 10.1111/bcp.12958
PubMed: 27059645
PubMed Central: PMC5061784

Affiliations:

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

to stream Main, to step Corpus: 000A65
to stream Main, to step Curation: 000A65

Le document en format XML

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<term>Female (MeSH)</term>
<term>Humans (MeSH)</term>
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<term>Inhibiteurs de l'aromatase (usage thérapeutique)</term>
<term>Inhibiteurs de protéines kinases (usage thérapeutique)</term>
<term>Modèles biologiques (MeSH)</term>
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<front><div type="abstract" xml:lang="en">Rapamycin and modified rapamycins (rapalogs) have been used to prevent allograft rejection after organ transplant for over 15 years. The mechanistic target of rapamycin (mTOR) has been determined to be a key component of the mTORC1 complex which consists of the serine/threonine kinase TOR and at least five other proteins which are involved in regulating its activity. Some of the best characterized substrates of mTORC1 are proteins which are key kinases involved in the regulation of cell growth (e.g., p70S6K) and protein translation (e.g., 4E-BP1). These proteins may in some cases serve as indicators to sensitivity to rapamycin-related therapies. Dysregulation of mTORC1 activity frequently occurs due to mutations at, or amplifications of, upstream growth factor receptors (e.g., human epidermal growth factor receptor-2, HER2) as well as kinases (e.g., PI3K) and phosphatases (e.g., PTEN) critical in the regulation of cell growth. More recently, it has been shown that certain rapalogs may enhance the effectiveness of hormonal-based therapies for breast cancer patients who have become resistant to endocrine therapy. The combined treatment of certain rapalogs (e.g., everolimus) and aromatase inhibitors (e.g., exemestane) has been approved by the United States Food and Drug Administration (US FDA) and other drug regulatory agencies to treat estrogen receptor positive (ER+) breast cancer patients who have become resistant to hormonal-based therapies and have progressed. This review will summarize recent basic and clinical research in the area and evaluate potential novel therapeutic approaches.</div>
</front>
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<ArticleTitle>The therapeutic potential of mTOR inhibitors in breast cancer.</ArticleTitle>
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<Abstract><AbstractText>Rapamycin and modified rapamycins (rapalogs) have been used to prevent allograft rejection after organ transplant for over 15 years. The mechanistic target of rapamycin (mTOR) has been determined to be a key component of the mTORC1 complex which consists of the serine/threonine kinase TOR and at least five other proteins which are involved in regulating its activity. Some of the best characterized substrates of mTORC1 are proteins which are key kinases involved in the regulation of cell growth (e.g., p70S6K) and protein translation (e.g., 4E-BP1). These proteins may in some cases serve as indicators to sensitivity to rapamycin-related therapies. Dysregulation of mTORC1 activity frequently occurs due to mutations at, or amplifications of, upstream growth factor receptors (e.g., human epidermal growth factor receptor-2, HER2) as well as kinases (e.g., PI3K) and phosphatases (e.g., PTEN) critical in the regulation of cell growth. More recently, it has been shown that certain rapalogs may enhance the effectiveness of hormonal-based therapies for breast cancer patients who have become resistant to endocrine therapy. The combined treatment of certain rapalogs (e.g., everolimus) and aromatase inhibitors (e.g., exemestane) has been approved by the United States Food and Drug Administration (US FDA) and other drug regulatory agencies to treat estrogen receptor positive (ER+) breast cancer patients who have become resistant to hormonal-based therapies and have progressed. This review will summarize recent basic and clinical research in the area and evaluate potential novel therapeutic approaches.</AbstractText>
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<ForeName>Lucio</ForeName>
<Initials>L</Initials>
<AffiliationInfo><Affiliation>Dipartimento di Scienze Biomediche e Neuromotorie, Università di Bologna, Bologna, Italy.</Affiliation>
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<ForeName>Massimo</ForeName>
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<AffiliationInfo><Affiliation>Department of Biomedical and Biotechnological Sciences, Laboratory of Translational Oncology & Functional Genomics, Section of Pathology & Oncology, University of Catania, Catania, Italy.</Affiliation>
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<Initials>JA</Initials>
<AffiliationInfo><Affiliation>Department of Microbiology and Immunology, Brody School of Medicine at East Carolina University, Greenville, NC, USA. mccubreyj@ecu.edu.</Affiliation>
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<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
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The therapeutic potential of mTOR inhibitors in breast cancer.

The therapeutic potential of mTOR inhibitors in breast cancer.

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