Akt as a therapeutic target in cancer.
Identifieur interne : 001654 ( Main/Exploration ); précédent : 001653; suivant : 001655Akt as a therapeutic target in cancer.
Auteurs : Linda S. Steelman [États-Unis] ; Kristin M. Stadelman ; William H. Chappell ; Stefan Horn ; Jörg B Secke ; Melchiorre Cervello ; Ferdinando Nicoletti ; Massimo Libra ; Franca Stivala ; Alberto M. Martelli ; James A. MccubreySource :
- Expert opinion on therapeutic targets [ 1744-7631 ] ; 2008.
Descripteurs français
- KwdFr :
- MESH :
- antagonistes et inhibiteurs : Protéines proto-oncogènes c-akt.
- pharmacologie : Antinéoplasiques.
- traitement médicamenteux : Tumeurs.
- Animaux, Humains, Souris.
English descriptors
- KwdEn :
- MESH :
- chemical , antagonists & inhibitors : Proto-Oncogene Proteins c-akt.
- chemical , pharmacology : Antineoplastic Agents.
- drug therapy : Neoplasms.
- Animals, Humans, Mice.
Abstract
BACKGROUND
The phosphatidylinositol 3-kinase (PI3K)/phosphatase and tensin homolog (PTEN)/v-akt murine thymoma viral oncogene homolog (Akt)/mammalian target of rapamycin (mTOR) pathway is central in the transmission of growth regulatory signals originating from cell surface receptors.
OBJECTIVE
This review discusses how mutations occur that result in elevated expression the PI3K/PTEN/Akt/mTOR pathway and lead to malignant transformation, and how effective targeting of this pathway may result in suppression of abnormal growth of cancer cells.
METHODS
We searched the literature for articles which dealt with altered expression of this pathway in various cancers including: hematopoietic, melanoma, non-small cell lung, pancreatic, endometrial and ovarian, breast, prostate and hepatocellular.
RESULTS/CONCLUSIONS
The PI3K/PTEN/Akt/mTOR pathway is frequently aberrantly regulated in various cancers and targeting this pathway with small molecule inhibitors and may result in novel, more effective anticancer therapies.
DOI: 10.1517/14728222.12.9.1139
PubMed: 18694380
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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<author><name sortKey="Steelman, Linda S" sort="Steelman, Linda S" uniqKey="Steelman L" first="Linda S" last="Steelman">Linda S. Steelman</name>
<affiliation wicri:level="2"><nlm:affiliation>Brody School of Medicine at East Carolina University, Department of Microbiology & Immunology, Greenville, NC 27858, USA.</nlm:affiliation>
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<wicri:regionArea>Brody School of Medicine at East Carolina University, Department of Microbiology & Immunology, Greenville, NC 27858</wicri:regionArea>
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<author><name sortKey="Stadelman, Kristin M" sort="Stadelman, Kristin M" uniqKey="Stadelman K" first="Kristin M" last="Stadelman">Kristin M. Stadelman</name>
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<author><name sortKey="Chappell, William H" sort="Chappell, William H" uniqKey="Chappell W" first="William H" last="Chappell">William H. Chappell</name>
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<author><name sortKey="Horn, Stefan" sort="Horn, Stefan" uniqKey="Horn S" first="Stefan" last="Horn">Stefan Horn</name>
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<author><name sortKey="B Secke, Jorg" sort="B Secke, Jorg" uniqKey="B Secke J" first="Jörg" last="B Secke">Jörg B Secke</name>
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<author><name sortKey="Cervello, Melchiorre" sort="Cervello, Melchiorre" uniqKey="Cervello M" first="Melchiorre" last="Cervello">Melchiorre Cervello</name>
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<author><name sortKey="Nicoletti, Ferdinando" sort="Nicoletti, Ferdinando" uniqKey="Nicoletti F" first="Ferdinando" last="Nicoletti">Ferdinando Nicoletti</name>
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<author><name sortKey="Libra, Massimo" sort="Libra, Massimo" uniqKey="Libra M" first="Massimo" last="Libra">Massimo Libra</name>
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<author><name sortKey="Stivala, Franca" sort="Stivala, Franca" uniqKey="Stivala F" first="Franca" last="Stivala">Franca Stivala</name>
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<affiliation wicri:level="2"><nlm:affiliation>Brody School of Medicine at East Carolina University, Department of Microbiology & Immunology, Greenville, NC 27858, USA.</nlm:affiliation>
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<author><name sortKey="Horn, Stefan" sort="Horn, Stefan" uniqKey="Horn S" first="Stefan" last="Horn">Stefan Horn</name>
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<author><name sortKey="B Secke, Jorg" sort="B Secke, Jorg" uniqKey="B Secke J" first="Jörg" last="B Secke">Jörg B Secke</name>
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<author><name sortKey="Cervello, Melchiorre" sort="Cervello, Melchiorre" uniqKey="Cervello M" first="Melchiorre" last="Cervello">Melchiorre Cervello</name>
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<author><name sortKey="Nicoletti, Ferdinando" sort="Nicoletti, Ferdinando" uniqKey="Nicoletti F" first="Ferdinando" last="Nicoletti">Ferdinando Nicoletti</name>
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<author><name sortKey="Libra, Massimo" sort="Libra, Massimo" uniqKey="Libra M" first="Massimo" last="Libra">Massimo Libra</name>
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<author><name sortKey="Stivala, Franca" sort="Stivala, Franca" uniqKey="Stivala F" first="Franca" last="Stivala">Franca Stivala</name>
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<author><name sortKey="Martelli, Alberto M" sort="Martelli, Alberto M" uniqKey="Martelli A" first="Alberto M" last="Martelli">Alberto M. Martelli</name>
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<series><title level="j">Expert opinion on therapeutic targets</title>
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<term>Antineoplastic Agents (pharmacology)</term>
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<term>Mice (MeSH)</term>
<term>Neoplasms (drug therapy)</term>
<term>Proto-Oncogene Proteins c-akt (antagonists & inhibitors)</term>
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<keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term>
<term>Antinéoplasiques (pharmacologie)</term>
<term>Humains (MeSH)</term>
<term>Protéines proto-oncogènes c-akt (antagonistes et inhibiteurs)</term>
<term>Souris (MeSH)</term>
<term>Tumeurs (traitement médicamenteux)</term>
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<keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Proto-Oncogene Proteins c-akt</term>
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<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antineoplastic Agents</term>
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<keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Protéines proto-oncogènes c-akt</term>
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<keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Neoplasms</term>
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<term>Humans</term>
<term>Mice</term>
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<front><div type="abstract" xml:lang="en"><p><b>BACKGROUND</b>
</p>
<p>The phosphatidylinositol 3-kinase (PI3K)/phosphatase and tensin homolog (PTEN)/v-akt murine thymoma viral oncogene homolog (Akt)/mammalian target of rapamycin (mTOR) pathway is central in the transmission of growth regulatory signals originating from cell surface receptors.</p>
</div>
<div type="abstract" xml:lang="en"><p><b>OBJECTIVE</b>
</p>
<p>This review discusses how mutations occur that result in elevated expression the PI3K/PTEN/Akt/mTOR pathway and lead to malignant transformation, and how effective targeting of this pathway may result in suppression of abnormal growth of cancer cells.</p>
</div>
<div type="abstract" xml:lang="en"><p><b>METHODS</b>
</p>
<p>We searched the literature for articles which dealt with altered expression of this pathway in various cancers including: hematopoietic, melanoma, non-small cell lung, pancreatic, endometrial and ovarian, breast, prostate and hepatocellular.</p>
</div>
<div type="abstract" xml:lang="en"><p><b>RESULTS/CONCLUSIONS</b>
</p>
<p>The PI3K/PTEN/Akt/mTOR pathway is frequently aberrantly regulated in various cancers and targeting this pathway with small molecule inhibitors and may result in novel, more effective anticancer therapies.</p>
</div>
</front>
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<AbstractText Label="OBJECTIVE" NlmCategory="OBJECTIVE">This review discusses how mutations occur that result in elevated expression the PI3K/PTEN/Akt/mTOR pathway and lead to malignant transformation, and how effective targeting of this pathway may result in suppression of abnormal growth of cancer cells.</AbstractText>
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<country name="États-Unis"><region name="Caroline du Nord"><name sortKey="Steelman, Linda S" sort="Steelman, Linda S" uniqKey="Steelman L" first="Linda S" last="Steelman">Linda S. Steelman</name>
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