Genomically amplified Akt3 activates DNA repair pathway and promotes glioma progression

Akt is a robust oncogene that plays key roles in the development and progression of many cancers, including glioma. We evaluated the differential propensities of the Akt isoforms toward progression in the well-characterized RCAS/Ntv-a mouse model of PDGFB-driven low grade glioma. A constitutively ac...
Ausführliche Beschreibung

Gespeichert in:
Autor*in:

David E. Cogdell [verfasserIn]

Olli Yli-Harja

Matti Nykter

Youting Sun

Xinhui Zhou

Kristen M. Turner

W. K. Alfred Yung

Brady Bernard

Gregory N. Fuller

Ping Ji

Kirsi J. Granberg

Wei Zhang

Limei Hu

Ilya Shmulevich

Format:

Artikel

Sprache:

Englisch

Erschienen:

2015

Rechteinformationen:

Nutzungsrecht: © COPYRIGHT 2015 National Academy of Sciences

Schlagwörter:

Signal Transduction - radiation effects

Gene Amplification - drug effects

Glioma - enzymology

Dacarbazine - therapeutic use

Brain Neoplasms - enzymology

Glioma - genetics

DNA Repair - drug effects

DNA Damage - genetics

Isoenzymes - chemistry

Drug Resistance, Neoplasm - drug effects

DNA Repair - radiation effects

Signal Transduction - drug effects

Signal Transduction - genetics

Radiation Tolerance - genetics

Proto-Oncogene Proteins c-akt - chemistry

Gene Amplification - radiation effects

Isoenzymes - metabolism

Brain Neoplasms - genetics

Dacarbazine - pharmacology

Proto-Oncogene Proteins c-akt - genetics

DNA Repair - genetics

Isoenzymes - genetics

Brain Neoplasms - pathology

Drug Resistance, Neoplasm - radiation effects

Glioma - pathology

Drug Resistance, Neoplasm - genetics

Proto-Oncogene Proteins c-akt - metabolism

Dacarbazine - analogs & derivatives

Deoxyribonucleic acid--DNA

Gene expression

Tumors

DNA repair

Gene amplification

Genomics

glioma

RCAS

tv-a mouse model

Biological Sciences

Akt

Übergeordnetes Werk:

Enthalten in: Proceedings of the National Academy of Sciences of the United States of America - Washington, DC : NAS, 1877, 112(2015), 11, Seite 3421-3426

Übergeordnetes Werk:

volume:112 ; year:2015 ; number:11 ; pages:3421-3426

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DOI / URN:

10.1073/pnas.1414573112

Katalog-ID:

OLC1970258969

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