Specific apoptosis induction by the dual PI3K/mTor inhibitor NVP-BEZ235 in HER2 amplified and PIK3CA mutant breast cancer cells
出版年份 2009 全文链接
标题
Specific apoptosis induction by the dual PI3K/mTor inhibitor NVP-BEZ235 in HER2 amplified and PIK3CA mutant breast cancer cells
作者
关键词
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出版物
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 106, Issue 52, Pages 22299-22304
出版商
Proceedings of the National Academy of Sciences
发表日期
2009-12-11
DOI
10.1073/pnas.0905152106
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注意:仅列出部分参考文献,下载原文获取全部文献信息。- Single-vector inducible lentiviral RNAi system for oncology target validation
- (2011) Dmitri Wiederschain et al. CELL CYCLE
- Activity of a novel, dual PI3-kinase/mTor inhibitor NVP-BEZ235 against primary human pancreatic cancers grown as orthotopic xenografts
- (2009) P Cao et al. BRITISH JOURNAL OF CANCER
- Ligand-Independent HER2/HER3/PI3K Complex Is Disrupted by Trastuzumab and Is Effectively Inhibited by the PI3K Inhibitor GDC-0941
- (2009) Teemu T. Junttila et al. CANCER CELL
- PI3K Pathway Activation Mediates Resistance to MEK Inhibitors in KRAS Mutant Cancers
- (2009) S. Wee et al. CANCER RESEARCH
- Suppression of HER2/HER3-Mediated Growth of Breast Cancer Cells with Combinations of GDC-0941 PI3K Inhibitor, Trastuzumab, and Pertuzumab
- (2009) E. Yao et al. CLINICAL CANCER RESEARCH
- mTOR Inhibitor RAD001 (Everolimus) Has Antiangiogenic/Vascular Properties Distinct from a VEGFR Tyrosine Kinase Inhibitor
- (2009) H. A. Lane et al. CLINICAL CANCER RESEARCH
- In vivo Antitumor Activity of MEK and Phosphatidylinositol 3-Kinase Inhibitors in Basal-Like Breast Cancer Models
- (2009) K. P. Hoeflich et al. CLINICAL CANCER RESEARCH
- Increased AKT S473 phosphorylation after mTORC1 inhibition is rictor dependent and does not predict tumor cell response to PI3K/mTOR inhibition
- (2009) M. Breuleux et al. MOLECULAR CANCER THERAPEUTICS
- Active-Site Inhibitors of mTOR Target Rapamycin-Resistant Outputs of mTORC1 and mTORC2
- (2009) Morris E Feldman et al. PLOS BIOLOGY
- Effects of the Dual Phosphatidylinositol 3-Kinase/Mammalian Target of Rapamycin Inhibitor NVP-BEZ235 on the Tumor Vasculature: Implications for Clinical Imaging
- (2008) C. R. Schnell et al. CANCER RESEARCH
- NVP-BEZ235, a Dual PI3K/mTOR Inhibitor, Prevents PI3K Signaling and Inhibits the Growth of Cancer Cells with Activating PI3K Mutations
- (2008) V. Serra et al. CANCER RESEARCH
- Genetic Predictors of MEK Dependence in Non-Small Cell Lung Cancer
- (2008) C. A. Pratilas et al. CANCER RESEARCH
- A Central Role for HER3 in HER2-Amplified Breast Cancer: Implications for Targeted Therapy
- (2008) S. T. Lee-Hoeflich et al. CANCER RESEARCH
- Chk1 Suppresses a Caspase-2 Apoptotic Response to DNA Damage that Bypasses p53, Bcl-2, and Caspase-3
- (2008) Samuel Sidi et al. CELL
- The enigma of caspase-2: the laymen's view
- (2008) G Krumschnabel et al. CELL DEATH AND DIFFERENTIATION
- Phosphatase and tensin homologue deleted on chromosome 10: Extending its PTENtacles
- (2008) Bangyan L. Stiles INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY
- Identification and characterization of NVP-BEZ235, a new orally available dual phosphatidylinositol 3-kinase/mammalian target of rapamycin inhibitor with potent in vivo antitumor activity
- (2008) S.-M. Maira et al. MOLECULAR CANCER THERAPEUTICS
- Effective use of PI3K and MEK inhibitors to treat mutant Kras G12D and PIK3CA H1047R murine lung cancers
- (2008) Jeffrey A Engelman et al. NATURE MEDICINE
- Class I PI3K in oncogenic cellular transformation
- (2008) L Zhao et al. ONCOGENE
- Drug discovery approaches targeting the PI3K/Akt pathway in cancer
- (2008) C Garcia-Echeverria et al. ONCOGENE
- PI3K pathway alterations in cancer: variations on a theme
- (2008) T L Yuan et al. ONCOGENE
- Breast Tumor Cells with PI3K Mutation or HER2 Amplification Are Selectively Addicted to Akt Signaling
- (2008) Qing-Bai She et al. PLoS One
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