Abstract
Hormonal dependence of breast cancer has been known for a long time, yet about half of breast cancers with estrogen receptor will not respond to antihormonal therapy. Now, we know that this resistance may be related to a dysfunction of the estrogen pathway, or that of growth factors and particularly the pathway of cell activation PI3K/Akt/mTOR. Prevention of these different mechanisms of resistance could involve combination therapies such as anti-estrogens (SERMs, aromatase inhibitors) with inhibitors of the activity of growth factors that are particularly temsirolimus and everolimus for the activation pathway cell PI3K/Akt/mTOR.
MeSH terms
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Antineoplastic Agents / therapeutic use*
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Breast Neoplasms / drug therapy*
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Breast Neoplasms / metabolism
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Drug Resistance, Neoplasm
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Everolimus
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Female
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Humans
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Neoplasm Proteins / antagonists & inhibitors*
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Neoplasm Proteins / metabolism
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Neoplasms, Hormone-Dependent / drug therapy*
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Phosphatidylinositol 3-Kinases / metabolism
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Protein Kinase Inhibitors / therapeutic use
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Proto-Oncogene Proteins c-akt / metabolism
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Sirolimus / analogs & derivatives*
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Sirolimus / therapeutic use
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TOR Serine-Threonine Kinases / antagonists & inhibitors*
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TOR Serine-Threonine Kinases / metabolism
Substances
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Antineoplastic Agents
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Neoplasm Proteins
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Protein Kinase Inhibitors
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temsirolimus
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Everolimus
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MTOR protein, human
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Proto-Oncogene Proteins c-akt
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TOR Serine-Threonine Kinases
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Sirolimus