Activation of executioner caspases is a predictor of progression-free survival in glioblastoma patients: a systems medicine approach
暂无分享,去创建一个
V. Seifert | M. Rehm | D. Kögel | J. Prehn | H. Huber | C. Senft | M. Mittelbronn | B. Murphy | J H M Prehn | C Senft | M Rehm | J. Weissenberger | V Seifert | J Weissenberger | D Kögel | J. Schmid | Á C Murphy | B Weyhenmeyer | J Schmid | S M Kilbride | H J Huber | M Dunst | M Mittelbronn | B M Murphy | M. Dunst | Á. Murphy | S. M. Kilbride | B. Weyhenmeyer
[1] Xiaodong Wang,et al. Smac, a Mitochondrial Protein that Promotes Cytochrome c–Dependent Caspase Activation by Eliminating IAP Inhibition , 2000, Cell.
[2] T. Boeckers,et al. Small-molecule XIAP inhibitors enhance gamma-irradiation-induced apoptosis in glioblastoma. , 2009, Neoplasia.
[3] Alan G. Porter,et al. Caspase-3 Is Required for DNA Fragmentation and Morphological Changes Associated with Apoptosis* , 1998, The Journal of Biological Chemistry.
[4] D. Louis. WHO classification of tumours of the central nervous system , 2007 .
[5] X. Liu,et al. An APAF-1·Cytochrome c Multimeric Complex Is a Functional Apoptosome That Activates Procaspase-9* , 1999, The Journal of Biological Chemistry.
[6] Xiaodong Wang,et al. Apaf-1, a Human Protein Homologous to C. elegans CED-4, Participates in Cytochrome c–Dependent Activation of Caspase-3 , 1997, Cell.
[7] M. Rehm,et al. Intracellular signaling dynamics during apoptosis execution in the presence or absence of X-linked-inhibitor-of-apoptosis-protein. , 2008, Biochimica et biophysica acta.
[8] Scar,et al. Inactivation of the DNA-repair gene MGMT and the clinical response of gliomas to alkylating agents. , 2000, The New England journal of medicine.
[9] R. Mirimanoff,et al. Radiotherapy plus concomitant and adjuvant temozolomide for glioblastoma. , 2005, The New England journal of medicine.
[10] T. van Dyke,et al. Differential Apaf-1 levels allow cytochrome c to induce apoptosis in brain tumors but not in normal neural tissues , 2007, Proceedings of the National Academy of Sciences.
[11] R. Mirimanoff,et al. MGMT gene silencing and benefit from temozolomide in glioblastoma. , 2005, The New England journal of medicine.
[12] A. Kung,et al. Anti-apoptosis mechanisms in malignant gliomas. , 2008, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[13] A. Strasser,et al. Deciphering the rules of programmed cell death to improve therapy of cancer and other diseases , 2011, The EMBO journal.
[14] Pedro Martínez,et al. Identification of survival‐related genes of the phosphatidylinositol 3′‐kinase signaling pathway in glioblastoma multiforme , 2008, Cancer.
[15] Xiaodong Wang,et al. Structural and biochemical basis of apoptotic activation by Smac/DIABLO , 2000, Nature.
[16] Markus Rehm,et al. APOPTO-CELL - a simulation tool and interactive database for analyzing cellular susceptibility to apoptosis , 2007, Bioinform..
[17] M. Weller,et al. Apoptosis in malignant glioma cells triggered by the temozolomide-induced DNA lesion O6-methylguanine , 2007, Oncogene.
[18] T. Boeckers,et al. Small-Molecule XIAP Inhibitors Enhance γ-Irradiation-Induced Apoptosis in Glioblastoma , 2009 .
[19] K. Black,et al. Proteasome inhibitor PS-341 causes cell growth arrest and apoptosis in human glioblastoma multiforme (GBM) , 2005, Oncogene.
[20] S. Srinivasula,et al. Cytochrome c and dATP-Dependent Formation of Apaf-1/Caspase-9 Complex Initiates an Apoptotic Protease Cascade , 1997, Cell.
[21] R. Mirimanoff,et al. Effects of radiotherapy with concomitant and adjuvant temozolomide versus radiotherapy alone on survival in glioblastoma in a randomised phase III study: 5-year analysis of the EORTC-NCIC trial. , 2009, The Lancet. Oncology.
[22] G. Weiss,et al. A Randomized Phase I and Pharmacological Trial of Sequences of 1,3-bis(2-Chloroethyl)-1-Nitrosourea and Temozolomide in Patients with Advanced Solid Neoplasms , 2004, Clinical Cancer Research.
[23] J C Reed,et al. IAPs block apoptotic events induced by caspase‐8 and cytochrome c by direct inhibition of distinct caspases , 1998, The EMBO journal.
[24] G. Núñez,et al. Role of cytochrome c and dATP/ATP hydrolysis in Apaf‐1‐mediated caspase‐9 activation and apoptosis , 1999, The EMBO journal.
[25] Survival signalling and apoptosis resistance in glioblastomas: opportunities for targeted therapeutics , 2010, Molecular Cancer.
[26] D. Vaux,et al. Alterations in the apoptotic machinery and their potential role in anticancer drug resistance , 2003, Oncogene.
[27] M. Weller,et al. Targeting apoptosis pathways in glioblastoma. , 2013, Cancer letters.
[28] Michael Weller,et al. Smac agonists sensitize for Apo2L/TRAIL- or anticancer drug-induced apoptosis and induce regression of malignant glioma in vivo , 2002, Nature Medicine.
[29] S. Fulda,et al. Therapeutic exploitation of apoptosis and autophagy for glioblastoma. , 2010, Anti-cancer agents in medicinal chemistry.
[30] V. Seifert,et al. Pharmacological inhibition of Bcl-2 family members reactivates TRAIL-induced apoptosis in malignant glioma , 2008, Journal of Neuro-Oncology.
[31] R. DePinho,et al. Malignant glioma: genetics and biology of a grave matter. , 2001, Genes & development.
[32] M. Weller,et al. Macrophage migration inhibitory factor (MIF) expression in human malignant gliomas contributes to immune escape and tumour progression , 2011, Acta Neuropathologica.
[33] G. Reifenberger,et al. Molecular predictors of progression-free and overall survival in patients with newly diagnosed glioblastoma: a prospective translational study of the German Glioma Network. , 2009, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[34] L. Chin,et al. Bcl2L12 inhibits post-mitochondrial apoptosis signaling in glioblastoma. , 2007, Genes & development.
[35] B. Scheithauer,et al. The 2007 WHO classification of tumours of the central nervous system , 2007, Acta Neuropathologica.
[36] S. Baird,et al. IAP-targeted therapies for cancer , 2008, Oncogene.
[37] Emad S. Alnemri,et al. Ordering the Cytochrome c–initiated Caspase Cascade: Hierarchical Activation of Caspases-2, -3, -6, -7, -8, and -10 in a Caspase-9–dependent Manner , 1999, The Journal of cell biology.
[38] B. Funke,et al. Basal Caspase Activity Promotes Migration and Invasiveness in Glioblastoma Cells , 2007, Molecular Cancer Research.
[39] Jochen H M Prehn,et al. Systems analysis of effector caspase activation and its control by X‐linked inhibitor of apoptosis protein , 2006, The EMBO journal.
[40] O. Tachibana,et al. Frequent LOH at Chromosome 12q22‐23 and Apaf‐1 Inactivation in Glioblastoma , 2003, Brain pathology.
[41] D. Coppola,et al. Immunocytochemical detection of members of the caspase cascade of apoptosis in high-grade astrocytomas. , 2004, In vivo.
[42] P. Kleihues,et al. Population-based studies on incidence, survival rates, and genetic alterations in astrocytic and oligodendroglial gliomas. , 2005, Journal of neuropathology and experimental neurology.
[43] D. Cohen,et al. Activation of Mitochondrial Pathway is Crucial for Tumor Selective Induction of Apoptosis by LAQ824 , 2006, Cell cycle.
[44] B. O'neill,et al. Glioblastoma survival in the United States before and during the temozolomide era , 2012, Journal of Neuro-Oncology.
[45] S. Kügler,et al. Expression and biological activity of X-linked inhibitor of apoptosis (XIAP) in human malignant glioma , 1999, Cell Death and Differentiation.