Roles of the Raf/MEK/ERK and PI3K/PTEN/Akt/mtor pathways in controlling growth and sensitivity to therapy-implications for cancer and aging

6533b828fe1ef96bd1287be8

RESEARCH PRODUCT

Roles of the Raf/MEK/ERK and PI3K/PTEN/Akt/mtor pathways in controlling growth and sensitivity to therapy-implications for cancer and aging

Stephen L. Abrams William H. Chappell Jacquelyn M. Long Paolo Fagone Agostino Tafuri Piotr Laidler Lucio Cocco Giuseppe Montalto Alberto M. Martelli Marco Donia Melchiorre Cervello Camilla Evangelisti Michele Milella Jörg Bäsecke Massimo Libra Sanja Mijatović C. Ruth Kempf James A. Mccubrey Maria Clorinda Mazzarino Franca Stivala Ferdinando Nicoletti Linda S. Steelman Danijela Maksimović-ivanić Antonio Bonati Graziella Malaponte

subject

Male MAPK/ERK pathway Aging MAP Kinase Signaling System Cancer aging RAF MEK mTOR Apoptosis Review Biology PI3K Models Biological Apoptosis; Cancer; Kinases; MEK; MTOR; PI3K; Protein phosphorylation; RAF; Signal transduction Mice Phosphatidylinositol 3-Kinases 03 medical and health sciences 0302 clinical medicine Cancer stem cell Neoplasms cancer Animals Humans PTEN Protein kinase B Cellular Senescence PI3K/AKT/mTOR pathway Cell Proliferation 030304 developmental biology 0303 health sciences Kinase TOR Serine-Threonine Kinases apoptosis PTEN Phosphohydrolase Raf Cell Biology MEK protein phosphorylation 3. Good health Cell biology Crosstalk (biology)kinases 030220 oncology & carcinogenesis Mutation mTOR Cancer research biology.protein Female raf Kinases Proto-Oncogene Proteins c-akt Cell aging signal transduction

description

Dysregulated signaling through the Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR pathways is often the result of genetic alterations in critical components in these pathways or upstream activators. Unrestricted cellular proliferation and decreased sensitivity to apoptotic-inducing agents are typically associated with activation of these pro-survival pathways. This review discusses the functions these pathways have in normal and neoplastic tissue growth and how they contribute to resistance to apoptotic stimuli. Crosstalk and commonly identified mutations that occur within these pathways that contribute to abnormal activation and cancer growth will also be addressed. Finally the recently described roles of these pathways in cancer stem cells, cellular senescence and aging will be evaluated. Controlling the expression of these pathways could ameliorate human health.

year	journal	country	edition	language
2011-01-01

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