|1.||Dent, Paul: 12 articles (04/2012 - 01/2002)|
|2.||Grant, Steven: 12 articles (04/2012 - 01/2002)|
|3.||Dai, Yun: 7 articles (04/2012 - 11/2002)|
|4.||Kohno, Michiaki: 5 articles (04/2013 - 05/2003)|
|5.||Tanimura, Susumu: 5 articles (04/2013 - 05/2003)|
|6.||Yacoub, Adly: 5 articles (08/2011 - 11/2005)|
|7.||Mitchell, Clint: 4 articles (08/2011 - 11/2005)|
|8.||Rahmani, Mohamed: 4 articles (11/2009 - 01/2002)|
|9.||Watanabe, Kazushi: 3 articles (04/2013 - 02/2010)|
|10.||Grant, S: 3 articles (07/2011 - 07/2001)|
04/01/2007 - "However, in vivo studies show that anti-tumor efficacy of combining the CI-1040 and Tam was similar to single agent(s). "
05/08/2008 - "We obtained the following in vitro and in vivo evidence to support the above expression data: (1) cotransfection of ERK5wt and MEK5D constructs in PC3 cells results in predominant ERK5 nuclear localization, similar to that observed in aggressive clinical disease; (2) ERK5-overexpressing PC3 cells have enhanced proliferative, migrative and invasive capabilities in vitro (P<0.0001), and were dramatically more efficient in forming tumors, with a shorter mean time for tumors to reach a critical volume of 1000 mm(3), in vivo (P<0.0001); (3) the MEK1 inhibitor, PD184352, blocking ERK1/2 activation at low dose, did not suppress proliferation but did significantly decrease proliferation at a higher dose required to inhibit ERK5 activation. "
05/15/2007 - "CI-1040 treatment also led to dramatic tumor shrinkage in murine lung tumors driven by a mutant KRas allele. "
04/01/2007 - "This suggests that the combination of CI-1040 and Tam may not be synergistic in inhibiting E2-induced tumor growth. "
04/01/2007 - "Furthermore, sequential treatment with Tam followed by CI-1040 or CI-1040 followed by Tam did not significantly reduce E2-induced tumor growth. "
|2.||Breast Neoplasms (Breast Cancer)
04/01/2007 - "Our data show that both MEK-inhibitor CI-1040 and Tam blocked E2-induced MAPK phosphorylation and cell proliferation in MCF-7 breast cancer cells in vitro. "
11/01/2005 - "In vitro colony formation studies demonstrated that UCN-01 and the MEK1/2 inhibitor PD184352 interacted to synergistically kill human mammary carcinoma cells (MDA-MB-231, MCF7) with similar combination index values. "
12/01/2009 - "Response of EGFR downstream signaling pathways was assessed by Western blot and clonogenic cell survival assays in breast tumor cells after irradiation (5Gy), lapatinib, CI-1040, or combined treatment. "
10/01/2006 - "In vitro colony formation studies demonstrated that Taxotere and the MEK1/2 inhibitor PD184352 interacted in a sequence dependent fashion to synergistically kill human mammary carcinoma cells (MDA-MB-231, MCF7) as well as in other tumor cell types; e.g. "
11/15/2004 - "This multicenter, open-label, phase II study was undertaken to assess the antitumor activity and safety of the oral mitogen-activated extracellular signal regulated kinase kinase (MEK) inhibitor, CI-1040, in breast cancer, colon cancer, non-small-cell lung cancer (NSCLC), and pancreatic cancer. "
10/18/2007 - "This study afforded several compounds which were either equipotent or more potent than the clinical candidate CI-1040 (1) in an isolated enzyme assay, as well as murine colon carcinoma (C26) cells, as measured by suppression of phosphorylated ERK substrate. "
04/01/2005 - "Here, we report the development and molecular characterization of CI-1040 resistance in the murine colon 26 (C26) carcinoma cell line. "
01/01/2013 - "By the inhibition of LY294002 and PD184352, we confirm that hydronephrotic urine promotes urothelial carcinoma cell (T24) and immortalized normal urothelial cells (E6) proliferation, migration and invasion in a dose-dependent manner through the activation of the mTORC2-AKT and ERK signaling pathways. "
08/01/2011 - "Multiple MEK1/2 inhibitors (PD184352, AZD6244 (ARRY-142886)) interacted with multiple CHK1 inhibitors (UCN-01 (7-hydroxystaurosporine), AZD7762) to kill mammary carcinoma cells and transformed fibroblasts. "
04/01/2009 - "Because RET/PTC rearrangements are unique to thyroid carcinomas and a high percentage of PTCs possess either mutation, these findings support the clinical evaluation of CI-1040 for patients with PTC."
09/01/2005 - "Interactions between the histone deacetylase inhibitor SAHA and the pharmacologic MEK1/2 inhibitor PD184352 were examined in Bcr/Abl+ human leukemia cells. "
04/01/2012 - "Finally, we tested the combination of ABT-737 and CI-1040 in a murine xenograft model using MOLM-13 human leukemia cells.Whereas"
03/01/2014 - "Consistently, ERK inhibitor PD184352 suppressed LC3-II activation induced by Tan IIA, whereas PD184352 and PD98059 did not affect poly (ADP-ribose) polymerase cleavage and sub-G1 accumulation induced by Tan IIA in KBM-5 leukemia cells. "
12/01/2003 - "Previous studies have demonstrated that cotreatment with mitogen activated-protein kinase kinase (MEK) 1/2 inhibitors (e.g., PD184352) and the checkpoint abrogator 7-hydroxystaurosporine (UCN-01) dramatically induces apoptosis in a variety of human leukemia and multiple myeloma cell types. "
04/01/2006 - "To characterize interactions between the heat shock protein 90 antagonist 17-dimethylaminoethylamino-17-demethoxygeldanamycin (DMAG) and the mitogen-activated protein kinase/extracellular signal-regulated kinase (ERK) kinase 1/2 inhibitor PD184352 in Bcr/abl(+) leukemia cells sensitive and resistant to imatinib mesylate. "
|5.||Acute Myeloid Leukemia (Acute Myelogenous Leukemia)
09/01/2001 - "In this study we demonstrate that small-molecule MEK inhibitors (PD98059 and PD184352) profoundly impair cell growth and survival of acute myeloid leukemia (AML) cell lines and primary samples with constitutive MAPK activation. "
06/01/2006 - "We found that MEK1 inhibitor PD184352 strikingly increased apoptosis induced by arsenic trioxide (ATO) in 21 of 25 patients with primary acute myelogenous leukemia (AML). "
03/01/2007 - "Here, we demonstrate that simultaneous retinoid receptor ligation and blockade of the MEK/ERK signaling module, using the small-molecule inhibitor CI-1040, result in a strikingly synergistic induction of apoptosis in both acute myeloid leukemia (AML) and acute promyelocytic leukemia (APL) cells with constitutive ERK activation. "
11/12/2009 - "Inhibition of these pathways using the MEK inhibitor PD184352 or U0126 and the PI3K/Akt inhibitor perifosine strikingly induced apoptosis in multiple malignant human hematopoietic cells, and substantially reduced the colony-forming capacity of primary acute myeloblastic leukemia, but not normal CD34+ cells. "
|2.||soblidotin (TZT 1027)
|5.||7-hydroxystaurosporine (UCN 01)
|6.||2- (2- chloro- 4- iodophenylamino)- N- cyclopropylmethoxy- 3,4- difluorobenzamide
|7.||Protein Kinases (Protein Kinase)
|10.||sorafenib (BAY 43-9006)
|1.||Heterologous Transplantation (Xenotransplantation)