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Targeting Cell Survival Pathways to Enhance Response to Chemotherapy /

"Targeting Cell Survival Pathways to Enhance Response to Chemotherapy encompasses recently developed molecular targeting agents and approaches that suppress cell survival signaling. Cell survival signaling attenuates the effectiveness of conventional chemotherapy and numerous mechanisms have be...

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Detalles Bibliográficos
Clasificación:Libro Electrónico
Autor principal: Johnson, Daniel E. (Professor) (Autor)
Formato: Electrónico eBook
Idioma:Inglés
Publicado: London, United Kingdom : Academic Press, an imprint of Elsevier, [2018]
Colección:Cancer sensitizing agents for chemotherapy ; v. 3.
Temas:
Acceso en línea:Texto completo

MARC

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245 0 0 |a Targeting Cell Survival Pathways to Enhance Response to Chemotherapy /  |c edited by Daniel E. Johnson. 
264 1 |a London, United Kingdom :  |b Academic Press, an imprint of Elsevier,  |c [2018] 
264 4 |c �2018 
300 |a 1 online resource 
336 |a text  |b txt  |2 rdacontent 
337 |a computer  |b c  |2 rdamedia 
338 |a online resource  |b cr  |2 rdacarrier 
490 1 |a Cancer sensitizing agents for chemotherapy ;  |v volume 3 
588 |a Online resource; title from PDF title page (EBSCO, viewed March 29, 2018). 
504 |a Includes bibliographical references and index. 
520 |a "Targeting Cell Survival Pathways to Enhance Response to Chemotherapy encompasses recently developed molecular targeting agents and approaches that suppress cell survival signaling. Cell survival signaling attenuates the effectiveness of conventional chemotherapy and numerous mechanisms have been described, and continue to be described, which contribute to cell survival in the face of chemotherapy treatment. Key pathways leading to chemoresistance emanate from growth factor receptors, PI3K, STAT3, anti-apoptotic Bcl-2 family members, autophagy, and the DNA damage response pathway. New advances have underscored the potential of targeting each of these cell survival mechanisms to improve responsiveness to chemotherapy. This book reviews these recent advances and provides a foundational background and hints of new opportunities for basic, translational, and clinical investigators focused on improving therapeutic responses to chemotherapy. Presents cutting-edge agents and approaches with proved success in different model systems that can be translated to a different type of cancerBrings updated information to be used to propose new clinical trials investigating innovative strategies for improving responses to chemotherapyProvides mechanistic details to help guide the design of laboratory studies associated with clinical trials"--  |c Provided by publisher 
505 0 |a Cover; Title Page; Copyright Page; Dedication; Contents; List of Contributors; Author Biography; Preface; Chapter 1 -- Targeting Members of the Epidermal Growth Factor Receptor Family to Improve Response to Chemotherapy; Abstract; 1.1 -- Introduction; 1.2 -- HER Family Receptors; 1.2.1 -- EGFR; 1.2.2 -- HER2; 1.2.3 -- HER3; 1.2.4 -- HER4; 1.3 -- Conclusions; Abbreviations; Acknowledgements; References; Chapter 2 -- Targeting the Hepatocyte Growth Factor Receptor to Overcome Resistance to Targeted Therapies; Abstract; 2.1 -- Discovery and Structure of Hepatocyte Growth Factor. 
505 8 |a 2.2 -- Activation of the HGF-MET Signaling Pathway2.2.1 -- Mitogen-Activated Protein Kinase Cascades; 2.2.2 -- PI3K-Akt; 2.2.3 -- STAT3; 2.2.4 -- HGF-Independent Activation and cMET Internalization; 2.2.5 -- Receptor Shedding; 2.3 -- HGF Functions; 2.3.1 -- Placenta; 2.3.2 -- Muscle; 2.3.3 -- Liver; 2.3.4 -- Kidney; 2.3.5 -- Nervous System; 2.3.6 -- Testis; 2.4 -- Dysregulation in Cancer; 2.4.1 -- cMET Mutations; 2.4.2 -- Amplification and Fusion Protein of cMET; 2.4.3 -- cMET Overexpression; 2.4.4 -- HGF Overexpression; 2.5 -- HGF Inhibitors for Cancer Therapy; 2.5.1 -- HGF Activation Inhibitors. 
505 8 |a 2.5.2 -- HGF Inhibitors2.5.3 -- MET Antagonists; 2.5.4 -- MET Kinase Inhibitors; 2.6 -- Targeting HGF-cMET Pathway in Solid Tumors to Overcome Drug Resistance; 2.6.1 -- Lung Cancer; 2.6.2 -- Renal Cancer; 2.6.3 -- Pancreatic Ductal Adenocarcinoma; 2.6.4 -- Colorectal Cancer; 2.7 -- Biomarkers for HGF/MET Inhibitors; 2.8 -- Conclusions and Future Directions; Abbreviations; Acknowledgments; References; Chapter 3 -- Roles for AXL and MERTK in Resistance to Cytotoxic and Targeted Therapies; Abstract; 3.1 -- Introduction; 3.2 -- Roles for TAM RTKs in Tumorigenesis. 
505 8 |a 3.2.1 -- TAM Receptor Expression and Signaling in Cancer3.2.2 -- Role of TAM RTKs in Mediating the Epithelial-to-Mesenchymal Transition; 3.2.3 -- Role of TAM RTKs in Angiogenesis; 3.3 -- Resistance to Therapy Mediated by TAM RTKs; 3.3.1 -- Role of TAM RTKs in Mediating Resistance to Traditional Chemotherapy; 3.3.2 -- Role of TAM RTKs in Mediating Resistance to Targeted Therapies; 3.3.3 -- Role of TAM RTKs in Immunosuppression; 3.4 -- Targeting AXL and Mertk; 3.4.1 -- Agents and Approaches to Inhibit TAM RTKs; 3.4.2 -- TAM RTKs as Dual Targets; 3.4.3 -- TAM RTK Biomarkers; 3.5 -- Summary; Abbreviations. 
650 0 |a Chemotherapy. 
650 0 |a Drug targeting. 
650 1 2 |a Molecular Targeted Therapy  |0 (DNLM)D058990 
650 1 2 |a Neoplasms  |x drug therapy  |0 (DNLM)D009369Q000188 
650 2 2 |a Antineoplastic Agents  |x therapeutic use  |0 (DNLM)D000970Q000627 
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650 2 |a Drug Delivery Systems  |0 (DNLM)D016503 
650 6 |a Chimioth�erapie.  |0 (CaQQLa)201-0034750 
650 6 |a M�edicaments  |x Ciblage.  |0 (CaQQLa)201-0196695 
650 7 |a MEDICAL  |x Pharmacology.  |2 bisacsh 
650 7 |a Chemotherapy  |2 fast  |0 (OCoLC)fst00853595 
650 7 |a Drug targeting  |2 fast  |0 (OCoLC)fst00898709 
655 4 |a Internet Resources. 
700 1 |a Johnson, Daniel E.  |c (Professor),  |e author. 
776 0 8 |i Print version:  |z 0128164328  |z 9780128164327  |w (OCoLC)1028888109 
830 0 |a Cancer sensitizing agents for chemotherapy ;  |v v. 3. 
856 4 0 |u https://sciencedirect.uam.elogim.com/science/book/9780128137536  |z Texto completo