|1.||Chen, Ching-Shih: 12 articles (12/2012 - 02/2006)|
|2.||Dent, Paul: 7 articles (08/2015 - 08/2006)|
|3.||Booth, Laurence: 5 articles (08/2015 - 02/2012)|
|4.||Grant, Steven: 5 articles (10/2014 - 08/2006)|
|5.||Kulp, Samuel K: 4 articles (06/2009 - 11/2007)|
|6.||Roberts, Jane L: 3 articles (08/2015 - 10/2014)|
|7.||Park, Margaret A: 3 articles (01/2013 - 08/2006)|
|8.||Yacoub, Adly: 3 articles (02/2012 - 08/2006)|
|9.||Wang, Yu-Chieh: 3 articles (04/2008 - 11/2006)|
|10.||Poklepovic, Andrew: 2 articles (08/2015 - 10/2014)|
|1.||Glioblastoma (Glioblastoma Multiforme)
08/01/2006 - "In glioblastoma cells, OSU-03012 seemed to induce apoptosis via endoplasmic reticulum stress-induced PERK-dependent signaling. "
08/01/2006 - "OSU-03012 in the treatment of glioblastoma."
08/01/2006 - "These are important findings because they start to identify a new mechanism to sensitize glioblastoma cells and also suggest that OSU-03012 could be combined with existing inhibitors to further sensitize tumor cells. "
10/01/2015 - "Molecular docking and molecular dynamics studies reveal structural basis of inhibition and selectivity of inhibitors EGCG and OSU-03012 toward glucose regulated protein-78 (GRP78) overexpressed in glioblastoma."
10/01/2014 - "Collectively, our data demonstrate that PDE5 inhibitors recruit death receptor signaling to enhance OSU-03012 toxicity in glioblastoma multiforme (GBM) cells."
08/01/2013 - "Ser-15 of p53 was phosphorylated after 24 h of treatment of the cancer cells with OSU-03012. "
02/15/2012 - "We have further defined mechanism(s) by which the drug OSU-03012 (OSU) kills tumor cells. "
02/15/2012 - "OSU-03012 suppresses GRP78/BiP expression that causes PERK-dependent increases in tumor cell killing."
04/15/2008 - "These data suggest that the concomitant modulation of Akt and ER stress pathways with the OSU-03012/EGFR inhibitor combination represents a unique approach to overcoming EGFR inhibitor resistance in NSCLC and perhaps other types of cancer with elevated basal Akt activities."
09/17/2007 - "PDK-1/AKT pathway may be an attractive therapeutic target for cancer intervention in RMS using OSU-03012."
|3.||Breast Neoplasms (Breast Cancer)
04/01/2008 - "Here, we use OSU-03012, a small-molecule inhibitor of phosphoinositide-dependent protein kinase-1 (PDK-1) to address the hypothesis that PDK-1/Akt signaling represents a therapeutically relevant target to sensitize ER-negative breast cancer to tamoxifen. "
01/01/2013 - "In the present studies, estrogen receptor (ER) positive and ER negative breast cancer cells were genetically manipulated to up- or downregulate eIF2-alpha, its phospho-mutant, Nck1, or Nck2, then treated with OSU-03012, lapatinib or the combination and assayed for cytotoxicity/cytostaticity using clonogenic assays. "
01/01/2013 - "Treatment of breast cancer cell lines with lapatinib and OSU-03012 (a small molecule derivative of the Cox-2 inhibitor celecoxib) induced synergistic cytotoxic/cytostatic effects. "
11/01/2006 - "Here, we investigated the effect of OSU-03012 on trastuzumab-mediated apoptosis in four breast cancer cell lines with different HER2 expression and trastuzumab-resistance status, including MDA-MB-231, BT474, SKBR3, and insulin-like growth factor-I receptor-overexpressing SKBR3 (SKBR3/IGF-IR). "
04/01/2008 - "Sensitizing estrogen receptor-negative breast cancer cells to tamoxifen with OSU-03012, a novel celecoxib-derived phosphoinositide-dependent protein kinase-1/Akt signaling inhibitor."
|4.||Prostatic Neoplasms (Prostate Cancer)
03/01/2007 - "These data suggest that Akt signalling pathway inhibition is a potential strategy for the treatment of dogs with prostate cancer and that canine prostate cancer is a relevant large animal model for evaluating Akt pathway inhibitors such as OSU-03012 for use in people."
03/01/2007 - "In this study, we treated the novel canine prostate cancer cell line, Ace-1, with OSU-03012 or dimethyl sulphoxide in vitro. "
03/01/2007 - "We found that Akt was constitutively phosphorylated in the canine prostate cancer cell line Ace-1 and that there was a dose-dependent decrease in cell viability, and Akt and glycogen synthase kinase-3beta phosphorylation, in response to OSU-03012 treatment. "
|5.||Melanoma (Melanoma, Malignant)
|3.||sorafenib (BAY 43-9006)
|4.||Neurofibromin 2 (Merlin)
|7.||Dimethyl Sulfoxide (DMSO)
|10.||erlotinib (CP 358,774)
|1.||Heterologous Transplantation (Xenotransplantation)