NVP-BEZ235, a dual PI3K/mTOR inhibitor, prevents PI3K signaling and inhibits the growth of cancer cells with activating PI3K mutations.
By V. Serra, B. Markman, M. Scaltriti, P. J. Eichhorn, Vanesa Valero, M. Guzman, M. Botero, E. Llonch, F. Atzori, S. Di Cosimo and 5 more. Cancer Research, 2008
815 citations recorded by the source corpus.
Subfields: Genetics, Molecular Biology, Oncology
View Paper: https://www.semanticscholar.org/paper/8fa41e8f1268f9a83ce0307012255ef8f8f14f9b
How researchers see this paper
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In Genetics
- John Wongvipat
- Beth Levine
- C. Sawyers
- C. López‐Otín
- P. Bonaldo
- Carlos L. Arteaga
- D. Klionsky
- G. Hotamisligil
In Molecular Biology
- Beth Levine
- D. Klionsky
- V. Deretic
- Alec C. Kimmelman
- Guido Kroemer
- Eric H. Baehrecke
- Guillermo Mariño
- M. Jäättelä
In Oncology
- N. Hynes
- Carlos L. Arteaga
- J. Engelman
- Gwen Macdonald
- Jennifer Lippincott-Schwartz
- C. López‐Otín
- P. Bonaldo
- Beth Levine
Citations in the corpus
- The crucial role of protein phosphorylation in cell signaling and its use as targeted therapy (Review) (2017, neutral): “This drug also targets against PI3K in solid tumors (124,125), serine/threonine kinase BRAF to treat melanoma (126-128), the receptor tyrosine kinase EGFR for lung cancer (129,130), and serine/threonine kinase mTOR for the treatment of renal tumors (131).”
- Reciprocal feedback regulation of PI3K and androgen receptor signaling in PTEN-deficient prostate cancer. (2011, background): “Inhibition of thePI3KPathwayCausesGrowthArrest but Not Significant Tumor Regression in Pten-Negative Prostate Cancers We evaluated the therapeutic efficacy of PI3K pathway inhibition in mice with established prostate cancers caused by either conditional deletion of Pten (Pten PB-Cre, hereafter calle”
- Targeting the phosphoinositide 3-kinase (PI3K) pathway in cancer (2009, background): “Preclinical data show that BEZ235 has strong anti-proliferative activity against tumour xenografts that have abnormal PI3K signalling, including loss of PTEN function or gain-of-function PI3K mutation”
- Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition) (2012, neutral): “NVP-BEZ235 A dual inhibitor of PIK3CA/p110 and the MTOR catalytic site that activates autophagy.(1508,1509) 27.”
- Guidelines for the use and interpretation of assays for monitoring autophagy (2012, background): “NVP-BEZ235 A dual inhibitor of PIK3CD/p110 and the MTOR catalytic site that activates autophagy.(245,246)”
- ERBB receptors: From oncogene discovery to basic science to mechanism-based cancer therapeutics (2014, background): “Constitutive activation of PI3K, via overexpression of PIK3CA mutants, conferred resistance to the antibody in laboratory studies (Chakrabarty et al., 2010; Eichhorn et al., 2008; Serra et al., 2008).”
- ErbB receptors and signaling pathways in cancer. (2009, background): “By contrast, the introduction of a mutant p110a into trastuzumab sensitive ErbB2+ breast cancer cells also rendered them unresponsive to the antibody [56 ,57 ] and treatment of these tumor cells with a PI3K inhibitor overcame resistance [57 ] (Figure 2).”
- Ligand-independent HER2/HER3/PI3K complex is disrupted by trastuzumab and is effectively inhibited by the PI3K inhibitor GDC-0941. (2009, background): “However, the study did not demonstrate whether PI3K/mTOR inhibitor overcomes trastuzumab resistance in vivo (Serra et al., 2008).”