Bcl-2/Bcl-xL Inhibition Increases the Efficacy of MEK Inhibition Alone and in Combination with PI3 Kinase Inhibition in Lung and Pancreatic Tumor Models
暂无分享,去创建一个
J. Settleman | Leslie B. Lee | W. Fairbrother | D. Sampath | Rebecca Hong | Peng Yue | M. Nannini | K. Williams | L. Belmont | S. Price | Nguyen Tan | Maureen Wong | Pierre Pascal Savy
[1] S. Cook,et al. The BH3 mimetic ABT-263 synergizes with the MEK1/2 inhibitor selumetinib/AZD6244 to promote BIM-dependent tumour cell death and inhibit acquired resistance. , 2013, The Biochemical journal.
[2] Travis J Cohoon,et al. Synthetic lethal interaction of combined BCL-XL and MEK inhibition promotes tumor regressions in KRAS mutant cancer models. , 2013, Cancer cell.
[3] G. Giaccone,et al. Phase II Study of Single-Agent Navitoclax (ABT-263) and Biomarker Correlates in Patients with Relapsed Small Cell Lung Cancer , 2012, Clinical Cancer Research.
[4] N. Normanno,et al. The RAS/RAF/MEK/ERK and the PI3K/AKT signalling pathways: role in cancer pathogenesis and implications for therapeutic approaches , 2012, Expert opinion on therapeutic targets.
[5] T. Gilmer,et al. Combinations of BRAF, MEK, and PI3K/mTOR Inhibitors Overcome Acquired Resistance to the BRAF Inhibitor GSK2118436 Dabrafenib, Mediated by NRAS or MEK Mutations , 2012, Molecular Cancer Therapeutics.
[6] Gordon B Mills,et al. Inhibition of PI3K/mTOR leads to adaptive resistance in matrix-attached cancer cells. , 2012, Cancer cell.
[7] Hao Xiong,et al. Substantial susceptibility of chronic lymphocytic leukemia to BCL2 inhibition: results of a phase I study of navitoclax in patients with relapsed or refractory disease. , 2012, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[8] F. Peale,et al. Navitoclax (ABT-263) Reduces Bcl-xL–Mediated Chemoresistance in Ovarian Cancer Models , 2012, Molecular Cancer Therapeutics.
[9] B. Kholodenko,et al. Cross-talk between mitogenic Ras/MAPK and survival PI3K/Akt pathways: a fine balance. , 2012, Biochemical Society transactions.
[10] A. Tolcher,et al. The Clinical Effect of the Dual-Targeting Strategy Involving PI3K/AKT/mTOR and RAS/MEK/ERK Pathways in Patients with Advanced Cancer , 2012, Clinical Cancer Research.
[11] M. Konopleva,et al. MEK inhibition enhances ABT-737-induced leukemia cell apoptosis via prevention of ERK-activated MCL-1 induction and modulation of MCL-1/BIM complex , 2012, Leukemia.
[12] Mark Merchant,et al. Intermittent administration of MEK inhibitor GDC-0973 plus PI3K inhibitor GDC-0941 triggers robust apoptosis and tumor growth inhibition. , 2012, Cancer research.
[13] J. Holbrook,et al. Comprehensive Predictive Biomarker Analysis for MEK Inhibitor GSK1120212 , 2011, Molecular Cancer Therapeutics.
[14] E. Plise,et al. Preclinical pharmacokinetics of the novel PI3K inhibitor GDC-0941 and prediction of its pharmacokinetics and efficacy in human , 2011 .
[15] G. Tzivion,et al. FoxO transcription factors; Regulation by AKT and 14-3-3 proteins. , 2011, Biochimica et biophysica acta.
[16] Qiaojun He,et al. GDC-0941 sensitizes breast cancer to ABT-737 in vitro and in vivo through promoting the degradation of Mcl-1. , 2011, Cancer letters.
[17] C. Tse,et al. The Bcl-2/Bcl-XL/Bcl-w Inhibitor, Navitoclax, Enhances the Activity of Chemotherapeutic Agents In Vitro and In Vivo , 2011, Molecular Cancer Therapeutics.
[18] M. Deininger,et al. Advances in the treatment of chronic myeloid leukemia , 2011, BMC medicine.
[19] T. Mitchison,et al. Navitoclax (ABT-263) accelerates apoptosis during drug-induced mitotic arrest by antagonizing Bcl-xL. , 2011, Cancer research.
[20] Rodney J Hicks,et al. In Vivo Activity of Combined PI3K/mTOR and MEK Inhibition in a KrasG12D;Pten Deletion Mouse Model of Ovarian Cancer , 2011, Molecular Cancer Therapeutics.
[21] J. Engelman,et al. Potential Therapeutic Strategies to Overcome Acquired Resistance to BRAF or MEK Inhibitors in BRAF Mutant Cancers , 2011, Oncotarget.
[22] David B Solit,et al. Resistance to MEK Inhibitors: Should We Co-Target Upstream? , 2011, Science Signaling.
[23] C. Rudin,et al. Phase I study of Navitoclax (ABT-263), a novel Bcl-2 family inhibitor, in patients with small-cell lung cancer and other solid tumors. , 2011, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[24] J. Zha,et al. Navitoclax Enhances the Efficacy of Taxanes in Non–Small Cell Lung Cancer Models , 2011, Clinical Cancer Research.
[25] E. Plise,et al. Preclinical pharmacokinetics of the novel PI3K inhibitor GDC-0941 and prediction of its pharmacokinetics and efficacy in human. , 2011, Xenobiotica; the fate of foreign compounds in biological systems.
[26] W. Wilson,et al. Navitoclax, a targeted high-affinity inhibitor of BCL-2, in lymphoid malignancies: a phase 1 dose-escalation study of safety, pharmacokinetics, pharmacodynamics, and antitumour activity. , 2010, The Lancet. Oncology.
[27] Aik Choon Tan,et al. Identification of Predictive Markers of Response to the MEK1/2 Inhibitor Selumetinib (AZD6244) in K-ras–Mutated Colorectal Cancer , 2010, Molecular Cancer Therapeutics.
[28] Deepak Sampath,et al. Pharmacokinetic-Pharmacodynamic Modeling of Tumor Growth Inhibition and Biomarker Modulation by the Novel Phosphatidylinositol 3-Kinase Inhibitor GDC-0941 , 2010, Drug Metabolism and Disposition.
[29] D. Elashoff,et al. Identification of Common Predictive Markers of In vitro Response to the Mek Inhibitor Selumetinib (AZD6244; ARRY-142886) in Human Breast Cancer and Non–Small Cell Lung Cancer Cell Lines , 2010, Molecular Cancer Therapeutics.
[30] B. Taylor,et al. Transcriptional pathway signatures predict MEK addiction and response to selumetinib (AZD6244). , 2010, Cancer research.
[31] Kwok-Kin Wong,et al. Targeting the PI3K signaling pathway in cancer. , 2010, Current opinion in genetics & development.
[32] Saul H. Rosenberg,et al. The Bcl-2 inhibitor ABT-263 enhances the response of multiple chemotherapeutic regimens in hematologic tumors in vivo , 2010, Cancer Chemotherapy and Pharmacology.
[33] C. Sander,et al. V600EBRAF is associated with disabled feedback inhibition of RAF–MEK signaling and elevated transcriptional output of the pathway , 2009, Proceedings of the National Academy of Sciences.
[34] A. Letai,et al. Control of mitochondrial apoptosis by the Bcl-2 family , 2009, Journal of Cell Science.
[35] Michael S. Cohen,et al. betaTrCP- and Rsk1/2-mediated degradation of BimEL inhibits apoptosis. , 2009, Molecular cell.
[36] Michael S. Cohen,et al. TrCP-and Rsk 1 / 2-Mediated Degradation of BimEL Inhibits Apoptosis , 2009 .
[37] A. Strasser,et al. Treatment of B-RAF mutant human tumor cells with a MEK inhibitor requires Bim and is enhanced by a BH3 mimetic. , 2008, The Journal of clinical investigation.
[38] Corey Nislow,et al. Combination chemical genetics. , 2008, Nature chemical biology.
[39] Gary Box,et al. The identification of 2-(1H-indazol-4-yl)-6-(4-methanesulfonyl-piperazin-1-ylmethyl)-4-morpholin-4-yl-thieno[3,2-d]pyrimidine (GDC-0941) as a potent, selective, orally bioavailable inhibitor of class I PI3 kinase for the treatment of cancer . , 2008, Journal of medicinal chemistry.
[40] C. Tse,et al. ABT-263: a potent and orally bioavailable Bcl-2 family inhibitor. , 2008, Cancer research.
[41] Alexei Degterev,et al. Identification of RIP1 kinase as a specific cellular target of necrostatins. , 2008, Nature chemical biology.
[42] G. Mills,et al. ERK promotes tumorigenesis by inhibiting FOXO3a via MDM2-mediated degradation , 2008, Nature Cell Biology.
[43] A. Brunet,et al. FOXO transcription factors , 2007, Current Biology.
[44] Miki Ebisuya,et al. Continuous ERK Activation Downregulates Antiproliferative Genes throughout G1 Phase to Allow Cell-Cycle Progression , 2006, Current Biology.
[45] Neal Rosen,et al. The BAD protein integrates survival signaling by EGFR/MAPK and PI3K/Akt kinase pathways in PTEN-deficient tumor cells. , 2005, Cancer cell.
[46] R. Craig,et al. MCL1 is phosphorylated in the PEST region and stabilized upon ERK activation in viable cells, and at additional sites with cytotoxic okadaic acid or taxol , 2004, Oncogene.
[47] V. Carey,et al. Mixed-Effects Models in S and S-Plus , 2001 .
[48] D. Bates,et al. Mixed-Effects Models in S and S-PLUS , 2001 .
[49] Andrius Kazlauskas,et al. Growth-factor-dependent mitogenesis requires two distinct phases of signalling , 2001, Nature Cell Biology.
[50] A. Brunet,et al. Nuclear translocation of p42/p44 mitogen‐activated protein kinase is required for growth factor‐induced gene expression and cell cycle entry , 1999, The EMBO journal.