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Akt as a therapeutic target in cancer

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Akt as a therapeutic target in cancer. / Steelman, Linda S; Stadelman, Kristin M; Chappell, William H; Horn, Stefan; Bäsecke, Jörg; Cervello, Melchiorre; Nicoletti, Ferdinando; Libra, Massimo; Stivala, Franca; Martelli, Alberto M; McCubrey, James A.

in: EXPERT OPIN THER TAR, Jahrgang 12, Nr. 9, 01.09.2008, S. 1139-65.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Steelman, LS, Stadelman, KM, Chappell, WH, Horn, S, Bäsecke, J, Cervello, M, Nicoletti, F, Libra, M, Stivala, F, Martelli, AM & McCubrey, JA 2008, 'Akt as a therapeutic target in cancer', EXPERT OPIN THER TAR, Jg. 12, Nr. 9, S. 1139-65. https://doi.org/10.1517/14728222.12.9.1139

APA

Steelman, L. S., Stadelman, K. M., Chappell, W. H., Horn, S., Bäsecke, J., Cervello, M., Nicoletti, F., Libra, M., Stivala, F., Martelli, A. M., & McCubrey, J. A. (2008). Akt as a therapeutic target in cancer. EXPERT OPIN THER TAR, 12(9), 1139-65. https://doi.org/10.1517/14728222.12.9.1139

Vancouver

Steelman LS, Stadelman KM, Chappell WH, Horn S, Bäsecke J, Cervello M et al. Akt as a therapeutic target in cancer. EXPERT OPIN THER TAR. 2008 Sep 1;12(9):1139-65. https://doi.org/10.1517/14728222.12.9.1139

Bibtex

@article{ebc9b39794b44c6fa9b4d54adf69e54a,
title = "Akt as a therapeutic target in cancer",
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.",
keywords = "Animals, Antineoplastic Agents, Humans, Mice, Neoplasms, Proto-Oncogene Proteins c-akt",
author = "Steelman, {Linda S} and Stadelman, {Kristin M} and Chappell, {William H} and Stefan Horn and J{\"o}rg B{\"a}secke and Melchiorre Cervello and Ferdinando Nicoletti and Massimo Libra and Franca Stivala and Martelli, {Alberto M} and McCubrey, {James A}",
year = "2008",
month = sep,
day = "1",
doi = "10.1517/14728222.12.9.1139",
language = "English",
volume = "12",
pages = "1139--65",
journal = "EXPERT OPIN THER TAR",
issn = "1472-8222",
publisher = "informa healthcare",
number = "9",

}

RIS

TY - JOUR

T1 - Akt as a therapeutic target in cancer

AU - Steelman, Linda S

AU - Stadelman, Kristin M

AU - Chappell, William H

AU - Horn, Stefan

AU - Bäsecke, Jörg

AU - Cervello, Melchiorre

AU - Nicoletti, Ferdinando

AU - Libra, Massimo

AU - Stivala, Franca

AU - Martelli, Alberto M

AU - McCubrey, James A

PY - 2008/9/1

Y1 - 2008/9/1

N2 - 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.

AB - 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.

KW - Animals

KW - Antineoplastic Agents

KW - Humans

KW - Mice

KW - Neoplasms

KW - Proto-Oncogene Proteins c-akt

U2 - 10.1517/14728222.12.9.1139

DO - 10.1517/14728222.12.9.1139

M3 - SCORING: Journal article

C2 - 18694380

VL - 12

SP - 1139

EP - 1165

JO - EXPERT OPIN THER TAR

JF - EXPERT OPIN THER TAR

SN - 1472-8222

IS - 9

ER -