|1.||Workman, Paul: 7 articles (01/2014 - 06/2007)|
|2.||Clarke, Paul A: 7 articles (01/2014 - 06/2007)|
|3.||Fan, Qi-Wen: 5 articles (01/2012 - 05/2006)|
|4.||Weiss, William A: 5 articles (01/2012 - 05/2006)|
|5.||Shokat, Kevan M: 5 articles (01/2010 - 05/2006)|
|6.||Fulda, Simone: 4 articles (04/2015 - 05/2011)|
|7.||Valenti, Melanie: 4 articles (08/2013 - 06/2007)|
|8.||Raynaud, Florence I: 4 articles (07/2010 - 06/2007)|
|9.||Knight, Zachary A: 4 articles (10/2008 - 05/2006)|
|10.||Leach, Martin O: 3 articles (01/2014 - 07/2010)|
01/01/2011 - "Using bimodal optical imaging, we show that when different regimens of systemic PI-103 delivery are combined with NSC-derived S-TRAIL, a significant reduction in tumor volumes is observed compared with PI-103 treatment alone. "
01/01/2011 - "We show that PI-103 inhibits proliferation and invasion, causes G(0)-G(1) arrest in cell cycle, and results in significant attenuation of orthotopic tumor growth in vivo. "
04/01/2010 - "In contrary to the expected, the data indicate that PI-103 induced immunosuppression promoting in vivo tumor growth and inhibiting apoptosis. "
07/01/2009 - "Furthermore, p53, the tumor suppressor which transcriptionally regulates p21, was also upregulated with PI-103 treatment. "
07/15/2008 - "Here, we tested the possibility of achieving specific tumor cell radiosensitization with a pharmacologic inhibitor of class I PI3K, the pyridinylfuranopyrimidine inhibitor PI-103. "
01/01/2011 - "To our knowledge, this is the first study that reveals the antitumor effect of PI-103 in intracranial gliomas. "
05/01/2011 - "We showed that the dual PtdIns3K-mTOR inhibitor PI-103 induces autophagy in therapy-resistant, PTEN-mutant glioma, with blockade of mTOR complex 1 (mTORC1) and complex 2 (mTORC2) contributing independently to autophagy. "
01/01/2011 - "Establishing cocultures of neural stem cells (NSC) and glioma cells, we show that PI-103 augments the response of glioma cells to stem cell-delivered S-TRAIL. "
01/01/2011 - "A dual PI3K/mTOR inhibitor, PI-103, cooperates with stem cell-delivered TRAIL in experimental glioma models."
01/01/2010 - "Here, we show that the dual PI3K-mTOR inhibitor PI-103 induces autophagy in a form of glioma that is resistant to therapy. "
02/15/2013 - "Furthermore, PI3K/mTOR inhibitors (e.g., BEZ235 and PI-103) synergistically increased ABT-737-mediated cell death in multiple leukemia cell lines and reduced colony formation in leukemic, but not normal, CD34+ cells. "
10/01/2011 - "Furthermore, the combined As(2)S(2)/PI-103 treatment effectively reduced leukemia cell repopulation and eradicated non-APL LSCs partially via induction of differentiation while sparing normal hematopoietic stem cells. "
05/01/2013 - "In addition, the level of myeloid cell leukemia 1 (Mcl-1) protein was markedly decreased by gefitinib/PI-103 combination in the BL TNBC cells, but showed no significant change by this combination in MSL subtype cells. "
10/01/2011 - "We found that a combined As(2)S(2)/PI-103 treatment synergized strongly to kill non-APL leukemia cells and promote their differentiation in vitro. "
09/01/2008 - "A dual inhibitor of PI3K and mTOR, PI-103, was more effective than rapamycin at suppressing proliferation of mouse pre-B-ALL and human CD19+CD34+)Ph+ ALL leukemia cells treated with the ABL kinase inhibitor imatinib. "
01/01/2014 - "We hypothesized that during autophagy induced in cancer cells by i) starvation through serum and amino acid deprivation or ii) treatment with PI-103, a class I PI3K/mTOR inhibitor, glycolytic metabolism would be affected, reducing flux to lactate, and that this effect may be reversible. "
01/01/2014 - "24 hr PI103-treatment or starvation caused significant reduction in the apparent forward rate constant (k(PL)) for pyruvate to lactate exchange compared with controls in HT29 (100 μM PI-103: 82%, p = 0.05) and HCT116 Bax-ko cells (10 μM PI-103: 53%, p = 0.05; 20 μM PI-103: 42%, p<0.0001; starvation: 52%, p<0.001), associated with reduced lactate excretion and intracellular lactate in all cases, and unchanged lactate dehydrogenase (LDH) activity and increased NAD+/NADH ratio following PI103 treatment or decreased LDH activity and unchanged NAD+/NADH ratio following starvation. "
|5.||Sarcoma (Soft Tissue Sarcoma)
01/01/2012 - "We report that the dual PI3K/mTOR inhibitor PI103 enhances the efficacy of DOX in several sarcoma cell lines and interacts with DOX in the induction of apoptosis. "
01/01/2012 - "Instead, the combination treatment of DOX plus PI103 activated Bax, the mitochondrial apoptosis pathway, and caspase 3. Caspase 3 activation was also observed in xenografts of sarcoma cells in nude mice upon combination of DOX with the specific PI3K inhibitor GDC-0941. "
|2.||erlotinib (CP 358,774)
|5.||Tumor Necrosis Factor-alpha (Tumor Necrosis Factor)
|6.||Phosphatidylinositol 3-Kinase (1 Phosphatidylinositol 3 Kinase)
|8.||Pyruvic Acid (Pyruvate)
|9.||Biological Markers (Surrogate Marker)
|10.||Epidermal Growth Factor Receptor (EGF Receptor)
|1.||Drug Therapy (Chemotherapy)
|2.||Heterologous Transplantation (Xenotransplantation)