BH3-mimetics and BET-inhibitors elicit enhanced lethality in malignant glioma
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Georg Karpel-Massler | Chang Shu | M. Halatsch | M. Westhoff | G. Karpel-Massler | Chiaki Tsuge Ishida | Elena Bianchetti | Marc-Eric Halatsch | M. Andrew Westhoff | Markus D. Siegelin | M. Siegelin | C. T. Ishida | E. Bianchetti | C. Shu | C. Ishida
[1] C. Wirtz,et al. Artesunate enhances the antiproliferative effect of temozolomide on U87MG and A172 glioblastoma cell lines. , 2014, Anti-cancer agents in medicinal chemistry.
[2] Aaron N. Chang,et al. Functional genomics identifies therapeutic targets for MYC-driven cancer , 2012, Proceedings of the National Academy of Sciences.
[3] P. Sandy,et al. Targeting MYC dependence in cancer by inhibiting BET bromodomains , 2011, Proceedings of the National Academy of Sciences.
[4] G. Gordon,et al. Venetoclax in relapsed or refractory chronic lymphocytic leukaemia with 17p deletion: a multicentre, open-label, phase 2 study. , 2016, The Lancet. Oncology.
[5] C. Wirtz,et al. Olanzapine inhibits proliferation, migration and anchorage-independent growth in human glioblastoma cell lines and enhances temozolomide’s antiproliferative effect , 2015, Journal of Neuro-Oncology.
[6] J. Engelman,et al. The BCL2 Family: Key Mediators of the Apoptotic Response to Targeted Anticancer Therapeutics. , 2015, Cancer discovery.
[7] A. Ross,et al. Exploiting the mitochondrial unfolded protein response for cancer therapy in mice and human cells. , 2011, The Journal of clinical investigation.
[8] William B. Smith,et al. Selective inhibition of BET bromodomains , 2010, Nature.
[9] C. Tse,et al. ABT-263: a potent and orally bioavailable Bcl-2 family inhibitor. , 2008, Cancer research.
[10] A. Harris,et al. Targeting the ATF4 pathway in cancer therapy , 2012, Expert opinion on therapeutic targets.
[11] P. Canoll,et al. Inhibition of deubiquitinases primes glioblastoma cells to apoptosis in vitro and in vivo , 2016, Oncotarget.
[12] Derek Y. Chiang,et al. The landscape of somatic copy-number alteration across human cancers , 2010, Nature.
[13] P. Canoll,et al. PI3K and Bcl-2 Inhibition Primes Glioblastoma Cells to Apoptosis through Downregulation of Mcl-1 and Phospho-BAD , 2014, Molecular Cancer Research.
[14] P. Canoll,et al. Metabolic reprogramming of glioblastoma cells by L-asparaginase sensitizes for apoptosis in vitro and in vivo , 2016, Oncotarget.
[15] J. Maris,et al. ATF4 regulates MYC-mediated neuroblastoma cell death upon glutamine deprivation. , 2012, Cancer cell.
[16] S. Lowe,et al. RNAi screen identifies Brd4 as a therapeutic target in acute myeloid leukaemia , 2011, Nature.
[17] P. Canoll,et al. Combined inhibition of Bcl-2/Bcl-xL and Usp9X/Bag3 overcomes apoptotic resistance in glioblastoma in vitro and in vivo , 2015, Oncotarget.
[18] T. W. Fawcett,et al. Complexes containing activating transcription factor (ATF)/cAMP-responsive-element-binding protein (CREB) interact with the CCAAT/enhancer-binding protein (C/EBP)-ATF composite site to regulate Gadd153 expression during the stress response. , 1999, The Biochemical journal.
[19] T. Kuwana,et al. BH3 Domains other than Bim and Bid Can Directly Activate Bax/Bak* , 2010, The Journal of Biological Chemistry.
[20] M. Feldman,et al. ATF4-dependent induction of heme oxygenase 1 prevents anoikis and promotes metastasis. , 2015, The Journal of clinical investigation.
[21] S. Kaufmann,et al. Mitochondrial apoptosis and BH3 mimetics , 2016, F1000Research.
[22] Michael R. Green,et al. A genome-wide RNA interference screen reveals an essential CREB3L2/ATF5/MCL1 survival pathway in malignant glioma with therapeutic implications , 2010, Nature Medicine.
[23] 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.
[24] S. Korsmeyer,et al. Distinct BH3 domains either sensitize or activate mitochondrial apoptosis, serving as prototype cancer therapeutics. , 2002, Cancer cell.
[25] L. Lam,et al. ABT-199, a potent and selective BCL-2 inhibitor, achieves antitumor activity while sparing platelets , 2013, Nature Medicine.
[26] S. Fulda,et al. Interference with the HSF1/HSP70/BAG3 Pathway Primes Glioma Cells to Matrix Detachment and BH3 Mimetic–Induced Apoptosis , 2016, Molecular Cancer Therapeutics.
[27] C. Wirtz,et al. Combined Inhibition of HER1/EGFR and RAC1 Results in a Synergistic Antiproliferative Effect on Established and Primary Cultured Human Glioblastoma Cells , 2013, Molecular Cancer Therapeutics.
[28] Qiuyan Wang,et al. ERAD inhibitors integrate ER stress with an epigenetic mechanism to activate BH3-only protein NOXA in cancer cells , 2009, Proceedings of the National Academy of Sciences.
[29] P. Canoll,et al. TIC10/ONC201 synergizes with Bcl-2/Bcl-xL inhibition in glioblastoma by suppression of Mcl-1 and its binding partners in vitro and in vivo , 2015, Oncotarget.
[30] P. Ekert,et al. Programmed Anuclear Cell Death Delimits Platelet Life Span , 2007, Cell.
[31] L. Greene,et al. A Synthetic Cell-Penetrating Dominant-Negative ATF5 Peptide Exerts Anticancer Activity against a Broad Spectrum of Treatment-Resistant Cancers , 2016, Clinical Cancer Research.
[32] B. Teh,et al. Dual modulation of MCL-1 and mTOR determines the response to sunitinib , 2017, The Journal of clinical investigation.
[33] S. Fulda,et al. Pan-Mammalian Target of Rapamycin (mTOR) Inhibitor AZD8055 Primes Rhabdomyosarcoma Cells for ABT-737-induced Apoptosis by Down-regulating Mcl-1 Protein* , 2013, The Journal of Biological Chemistry.
[34] S. Korsmeyer,et al. An inhibitor of Bcl-2 family proteins induces regression of solid tumours , 2005, Nature.
[35] Paul S Mischel,et al. Single-Cell Phosphoproteomics Resolves Adaptive Signaling Dynamics and Informs Targeted Combination Therapy in Glioblastoma. , 2016, Cancer cell.
[36] Jiangbin Ye,et al. The GCN2‐ATF4 pathway is critical for tumour cell survival and proliferation in response to nutrient deprivation , 2010, The EMBO journal.
[37] J. Engelman,et al. Apoptosis in targeted therapy responses: the role of BIM. , 2012, Advances in pharmacology.
[38] M. Christmann,et al. Apoptosis induced by temozolomide and nimustine in glioblastoma cells is supported by JNK/c-Jun-mediated induction of the BH3-only protein BIM , 2015, Oncotarget.
[39] Reid C Thompson,et al. Inhibition of BET Bromodomain Targets Genetically Diverse Glioblastoma , 2013, Clinical Cancer Research.
[40] L. Ouafik,et al. OTX015 (MK‐8628), a novel BET inhibitor, displays in vitro and in vivo antitumor effects alone and in combination with conventional therapies in glioblastoma models , 2016, International journal of cancer.
[41] O. Wiestler,et al. Apoptosis-based treatment of glioblastomas with ABT-737, a novel small molecule inhibitor of Bcl-2 family proteins , 2008, Oncogene.
[42] P. Canoll,et al. PARP Inhibition Restores Extrinsic Apoptotic Sensitivity in Glioblastoma , 2014, PloS one.
[43] R. Mirimanoff,et al. MGMT gene silencing and benefit from temozolomide in glioblastoma. , 2005, The New England journal of medicine.