Exploring IKKβ as an anti-angiogenic therapeutic target in KRAS-induced lung cancer (2016)
- Autor:
- Autor USP: BASSÈRES, DANIELA SANCHEZ - IQ
- Unidade: IQ
- Subjects: NEOPLASIAS PULMONARES; MUTAÇÃO
- Language: Inglês
- Imprenta:
- Publisher: Sociedade Brasileira de Biologia Celular (SBBC)
- Publisher place: São Paulo
- Date published: 2016
- Source:
- Título: Resumos
- Conference titles: Congresso da Sociedade Brasileira de Biologia Celular
-
ABNT
BASSÈRES, Daniela Sanchez. Exploring IKKβ as an anti-angiogenic therapeutic target in KRAS-induced lung cancer. 2016, Anais.. São Paulo: Sociedade Brasileira de Biologia Celular (SBBC), 2016. . Acesso em: 13 nov. 2024. -
APA
Bassères, D. S. (2016). Exploring IKKβ as an anti-angiogenic therapeutic target in KRAS-induced lung cancer. In Resumos. São Paulo: Sociedade Brasileira de Biologia Celular (SBBC). -
NLM
Bassères DS. Exploring IKKβ as an anti-angiogenic therapeutic target in KRAS-induced lung cancer. Resumos. 2016 ;[citado 2024 nov. 13 ] -
Vancouver
Bassères DS. Exploring IKKβ as an anti-angiogenic therapeutic target in KRAS-induced lung cancer. Resumos. 2016 ;[citado 2024 nov. 13 ] - Aurora kinases: potential therapeutic targets in K-Ras-induced lung cancer
- Targeted BMI1 inhibition impairs tumor growth in lung adenocarcinomas with low CEBP alpha expression
- Exploring IKKβ kinase as a therapeutic target for KRAS-driven lung tumor initiating cells
- Exploring IKKβ as an anti-metastatic therapeutic target in KRAS-induced lung cancer
- Targeting Aurora A kinase activity in lung cancer initiating cells driven by oncogenic KRAS
- IKKβ inhibition suppresses sphere formation and self renewal of lung cancer initiating cells
- Aurora kinase targeting in lung cancer reduces KRAS-induced transformation
- IKKβ kinase promotes stemness, migration, and invasion in KRAS-driven lung adenocarcinoma cells
- Identification of a targetable KRAS-mutant epithelial population in non-small cell lung cancer
- Tumor microenvironment landscapes supporting EGFR-mutant NSCLC are modulated at the single-cell interaction level by unesbulin treatment
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