The combinatorial activation of the PI3K and Ras/MAPK pathways is sufficient for aggressive tumor formation, while individual pathway activation supports cell persistence.

Thompson, Keyata N; Whipple, Rebecca A; Yoon, Jennifer R; Lipsky, Michael; Charpentier, Monica S; Boggs, Amanda E; Chakrabarti, Kristi R; Bhandary, Lekhana; Hessler, Lindsay K; Martin, Stuart S; Vitolo, Michele I

Thompson, Keyata N; Whipple, Rebecca A; Yoon, Jennifer R; Lipsky, Michael; Charpentier, Monica S; Boggs, Amanda E; Chakrabarti, Kristi R; Bhandary, Lekhana; Hessler, Lindsay K; Martin, Stuart S; Vitolo, Michele I.

Afiliação

Thompson KN; University of Maryland School of Medicine, Marlene and Stewart Greenebaum National Cancer Institute Cancer Center, University of Maryland School of Medicine, Baltimore, MD, USA.
Whipple RA; University of Maryland School of Medicine, Marlene and Stewart Greenebaum National Cancer Institute Cancer Center, University of Maryland School of Medicine, Baltimore, MD, USA.
Yoon JR; University of Maryland School of Medicine, Marlene and Stewart Greenebaum National Cancer Institute Cancer Center, University of Maryland School of Medicine, Baltimore, MD, USA.
Lipsky M; Department of Pathology, University of Maryland School of Medicine, Baltimore, MD, USA.
Charpentier MS; University of Maryland School of Medicine, Marlene and Stewart Greenebaum National Cancer Institute Cancer Center, University of Maryland School of Medicine, Baltimore, MD, USA.
Boggs AE; Graduate Program in Molecular Medicine, University of Maryland School of Medicine, Baltimore, MD, USA.
Chakrabarti KR; University of Maryland School of Medicine, Marlene and Stewart Greenebaum National Cancer Institute Cancer Center, University of Maryland School of Medicine, Baltimore, MD, USA.
Bhandary L; Graduate Program in Molecular Medicine, University of Maryland School of Medicine, Baltimore, MD, USA.
Hessler LK; Department of Pathology and Laboratory Medicine, Perelman School of Medicine, Univesity of Pennsylvainia, Philadelphia, PA, USA.
Martin SS; University of Maryland School of Medicine, Marlene and Stewart Greenebaum National Cancer Institute Cancer Center, University of Maryland School of Medicine, Baltimore, MD, USA.
Vitolo MI; Graduate Program in Molecular Medicine, University of Maryland School of Medicine, Baltimore, MD, USA.

Oncotarget ; 6(34): 35231-46, 2015 Nov 03.

Article em En | MEDLINE | ID: mdl-26497685

Assuntos

Neoplasias da Mama/metabolismo; Quinases de Proteína Quinase Ativadas por Mitógeno/metabolismo; Fosfatidilinositol 3-Quinases/metabolismo; Proteínas Proto-Oncogênicas c-akt/metabolismo; Proteínas ras/metabolismo; Animais; Apoptose/fisiologia; Neoplasias da Mama/enzimologia; Neoplasias da Mama/genética; Neoplasias da Mama/patologia; Linhagem Celular Tumoral; Proliferação de Células/fisiologia; Ativação Enzimática; Feminino; Humanos; Sistema de Sinalização das MAP Quinases; Camundongos; Quinases de Proteína Quinase Ativadas por Mitógeno/genética; Fosfatidilinositol 3-Quinases/genética; Proteínas Proto-Oncogênicas c-akt/genética; Proteínas ras/genética

Palavras-chave

MAPK; PI3K; PTEN; breast cancer; dormancy

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Texto completo: 1 Base de dados: MEDLINE Assunto principal: Neoplasias da Mama / Proteínas ras / Fosfatidilinositol 3-Quinases / Quinases de Proteína Quinase Ativadas por Mitógeno / Proteínas Proto-Oncogênicas c-akt Limite: Animals / Female / Humans Idioma: En Ano de publicação: 2015 Tipo de documento: Article

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