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008			170707s2017 sz ob 001 0 eng d
020			_a3319568051 _q(electronic bk.)
020			_a9783319568058 _q(electronic bk.)
020			_z3319568043
020			_z9783319568041
040			_aYDX _cYDX _dN$T _dEBLCP _dN$T _dGW5XE _dYDX _dOCLCO _dN$T _dOCLCO _dOCLCF _dNJR _dUAB _dOCLCO _dESU _dAZU _dUPM _dIOG _dCOO _dOCLCQ _dMERER _dVT2 _dOCLCQ _dOCLCO _dJG0 _dOCLCO _dOCLCA _dES-MaUEC _bspa
050		4	_aRC270.8 _b2017 EB
245	0	0	_aTRAIL, Fas Ligand, TNF and TLR3 in cancer _cOlivier Micheau, editor.
264		1	_aCham _bSpringer _c2017.
300			_a1 recurso en línea
336			_aTexto _btxt _2rdacontent
337			_aelectrónico _bc _2rdamedia
338			_arecurso electrónico _bcr _2rdacarrier
347			_atext file _bPDF
490	0		_aResistance to targeted anti-cancer therapeutics _vv. 12
500			_aSpringerLink _bSpringer Biomedical and Life Sciences eBooks 2017 English+International
504			_aIncluye referencias bibliográficas e índice
505	0		_aPreface; Contents; Contributors; About the Editor; Chapter 1: Resistance to TRAIL Pathway-Targeted Therapeutics in Cancer; 1.1 Mechanisms of TRAIL-Induced Apoptosis; 1.1.1 TRAIL Ligand and TRAIL Receptors; 1.1.2 Engagement of the Extrinsic Pathway of Apoptosis; 1.1.3 Engagement of the Intrinsic Pathway of Apoptosis; 1.2 TRAIL's Impact on Metastasis; 1.3 Development of TRAIL Pathway-Targeted Therapeutics; 1.3.1 Optimization of TRAIL Delivery; 1.3.2 TRAIL Receptor Antibodies; 1.3.3 Small Molecules to Induce TRAIL and Upregulate DR5.
505	8		_a1.4 Mechanisms of Resistance to TRAIL Pathway-Targeted Therapeutics1.4.1 Aberration in Death Receptor Expression; 1.4.2 Strategies to Address Low Surface Levels of Death Receptors; 1.4.3 Expression of TRAIL Decoy Receptors; 1.4.4 Dysfunction in the DISC and FADD; 1.4.5 Perturbation in Downstream Pro-apoptotic Signals; 1.4.6 Strategies to Address Aberrations in Downstream Pathways of Apoptosis; 1.4.7 Resistance of Normal Cells; 1.5 Complex Nature of TRAIL Resistance; 1.5.1 Multiple Resistance Mechanisms; 1.5.2 Acquisition of Resistance.
505	8		_a1.6 Addressing Resistance to TRAIL Pathway-Targeted Therapeutics in the Clinic1.6.1 Single Agent; 1.6.2 Combinational; 1.7 Conclusion; References; Chapter 2: TRAIL-R3/R4 and Inhibition of TRAIL Signalling in Cancer; 2.1 Introduction; 2.2 The TRAIL Signalling System; 2.2.1 Structure of TRAIL; 2.2.2 Structure and Function of TRAIL Receptors; 2.2.3 TRAIL Receptor Signalling; 2.2.3.1 Apoptotic Signalling; 2.2.3.2 Necroptotic Signalling; 2.2.3.3 Non-cytotoxic Signalling; 2.2.4 TRAIL's Role In Vivo; 2.3 The TRAIL System in Cancer.
505	8		_a2.3.1 Predictive and Prognostic Significance of TRAIL Receptor Expression2.3.2 TRAIL Death Receptor Agonists; 2.3.3 The Role of TRAIL-R3 and TRAIL-R4 in Resistance to TRAIL-Mediated Apoptosis; 2.3.3.1 The Decoy Model for TRAIL-R3 and TRAIL-R4; 2.3.3.2 Formation of Heteromeric Complexes Affected in Signalling; 2.3.3.3 TRAIL-R3 and TRAIL-R4 Incorporation in Ligand Receptor Clusters; 2.3.3.4 Activation of Pro-Survival Pathways by TRAIL-R4; 2.4 Outlook; References; Chapter 3: IAPs and Resistance to Death Receptors in Cancer; 3.1 Introduction; 3.2 Structure and Molecular Functions.
505	8		_a3.3 Regulation of DR Signalling Pathways by IAPs3.3.1 Regulation of RIPK-Dependent Signalling Complex; 3.3.2 Regulation of DR-Induced Apoptosis by IAPs; 3.4 Sensitization to Death Receptor-Induced Cell Death by Smac Mimetics; 3.4.1 Smac Mimetics in Combination with Tumor Necrosis Factor (TNF); 3.4.2 Smac Mimetics in Combination with CD95; 3.4.3 Smac Mimetics in Combination with TNF-Related Apoptosis-Inducing Ligand (TRAIL); References; Chapter 4: Bcl-2 Proteins and TRAIL Resistance in Melanoma; 4.1 Apoptosis Deficiency: A Major Issue in Melanoma Therapy Resistance; 4.2 Control of Apoptosis.
520	3		_aThis volume provides the current understanding of death receptor's/TLR3 signaling regulation in cancer. Death receptors, including TRAIL-R1, TRAIL-R2, Fas and TNF-RI, owing to their ability to trigger apoptosis and to contribute to the elimination of cancer cells by the immune system have been considered, to variable extent, as important therapeutic targets for cancer therapy. But an increasing body of evidence suggests that some of these receptors may also contribute to tumorigenesis, or that new players such as TLR3 may be targeted for cancer therapy due to their ability to behave like death receptors.
650		7	_aApoptosis. _2fast _0(OCoLC)fst00811467 _9157983 _0comprobar BNE20004390141
700	1		_aMicheau, Olivier, _eeditor literario
856	4	0	_uhttps://go.openathens.net/redirector/universidadeuropea.es?url=http://link.springer.com/10.1007/978-3-319-56805-8 _zAcceso a este recurso digital (usuarios Universidad Europea de Madrid)
988			_aEBOOK, asignarmaterias, EBSPRINGER_2017D
998			_b02/2018 _dz _e- _zSI
999			_c96309 _d96309 _x1