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[null,"1.","Record Nr.",null,"UNINA9911019793003321"]
[null,null,"Autore",null,"Vickers Elaine"]
[null,null,"Titolo",null,"A Beginner's Guide to Targeted Cancer Treatments and Cancer Immunotherapy"]
[null,null,"Pubbl/distr/stampa",null,"Newark : , : John Wiley & Sons, Incorporated, , 2024"]
[{"$nulls":4},"©2024"]
[null,null,"ISBN",null,"9781119834090"]
[{"$nulls":4},"1119834090"]
[{"$nulls":4},"9781119834083"]
[{"$nulls":4},"1119834082"]
[{"$nulls":4},"9781119834076"]
[{"$nulls":4},"1119834074"]
[null,null,"Edizione",null,"[2nd ed.]"]
[null,null,"Descrizione fisica",null,"1 online resource (463 pages)"]
[null,null,"Disciplina",null,"616.994061"]
[null,null,"Soggetti",null,"Immunotherapy"]
[{"$nulls":4},"Drug targeting"]
[null,null,"Lingua di pubblicazione",null,"Inglese"]
[null,null,"Formato",null,"Materiale a stampa"]
[null,null,null,"Livello bibliografico","Monografia"]
[null,null,"Nota di contenuto",null,"Cover -- Title Page -- Copyright Page -- Contents -- Acknowledgments -- Praise For The First Edition -- About The author -- How To use This Book -- Chapter 1 An Introduction To cancer Cell Biology And genetics -- 1.1 Introduction -- 1.2 Dna Damage Is The cause Of every Cancer -- 1.2.1 Causes Of Dna Mutations -- 1.2.2 Types Of Dna Mutations -- 1.2.3 Numbers And Patterns Of dna Mutations In Cancer cells -- 1.2.4 Driver Mutations - Those That Affect Cancer Cell Behavior -- 1.2.5 The \"usual Suspects\" - Genes Commonly Mutated In many Cancers -- 1.3 The Defining Features (hallmarks) Of cancer Cells -- 1.3.1 Ten Hallmarks Of Cancer (plus Four Enabling Characteristics) -- 1.4 Variation Among Cancer Cells In a Single Tumor -- 1.4.1 Causes Of genetic Heterogeneity -- 1.4.2 Other Types Of heterogeneity -- 1.5 Cancer's Relationship With our Immune System -- 1.5.1 How Our Immune System Monitors For signs Of damage And destroys Faulty Cells -- 1.5.2 The Cancer-immunity Cycle -- 1.5.3 How Cancer Cells Avoid Destruction By The immune system -- 1.5.4 How Cancer Cells Ultimately Survive, And thrive, Among White Blood Cells -- 1.5.5 Elimination, Equilibrium, And escape -- 1.6 The Cancer Microenvironment -- 1.6.1 The Role Of white Blood cells -- 1.6.2 The "]
[{"$nulls":4},"Role Of other Cell Types -- 1.6.3 Angiogenesis -- 1.6.4 Two Examples Of the Importance Of the Tumor Microenvironment -- 1.7 Cancer Spread/metastasis -- 1.7.1 Routes Through Which Cancers Spread -- 1.7.2 Locations To which Cancers spread -- 1.7.3 Reasons Why Cancers Spread -- 1.8 Cancer Stem Cells -- 1.9 Unique Properties Of Hematological Cancers -- 1.9.1 Introducing Hematological Cancers -- 1.9.2 Most Of Them Develop From faulty B Cells -- 1.9.3 Certain Translocations Are Common To each Type And subtype -- 1.9.4 They Have Cd Antigens On their Surface -- 1.9.5 They Live In close Proximity To other White Blood Cells."]
[{"$nulls":4},"1.10 Obstacles That Prevent Us From curing Cancer -- 1.10.1 The Similarity Between Healthy Cells And cancer Cells -- 1.10.2 Differences Between Different Cancer Types -- 1.10.3 Cancer Spread -- 1.10.4 Intratumoral Heterogeneity -- 1.10.5 The Cancer Microenvironment -- 1.11 Final Thoughts -- References -- Chapter 2 Monoclonal Antibodies And small Molecules As cancer Treatments -- 2.1 Introduction -- 2.2 Antibody-based Cancer Treatments -- 2.2.1 Why Antibodies Make Good Cancer Treatments -- 2.2.2 How Antibody Therapies Have Changed Over The years -- 2.2.3 Mechanisms Of action Of antibody-based Cancer Treatments -- 2.2.4 Antibodies That Kill Cancer Cells Directly -- 2.2.5 Antibodies That Create A cancer-fighting Immune Response -- 2.2.6 Limitations Of antibody Treatments And reasons For side Effects -- 2.2.7 Uses Of monoclonal Antibody Treatments For cancer -- 2.2.8 Antibody Biosimilars -- 2.3 Small Molecule Cancer Treatments -- 2.3.1 Why Small Molecules Make Good Cancer Treatments -- 2.3.2 How Small Molecule Drugs Have Changed Over The years -- 2.3.3 Small Molecules That Block Kinases -- 2.3.4 Different Types Of kinase Inhibitors -- 2.3.5 Common Targets And uses Of kinase Inhibitors -- 2.3.6 Limitations Of kinase Inhibitors And reasons Why They Cause Side Effects -- 2.3.7 Small Molecules With Non-kinase Targets -- 2.4 Treatment Combinations -- 2.5 Final Thoughts -- References -- Chapter 3 Treatments That Target Cell Communication -- 3.1 Introduction -- 3.2 Growth Factor-controlled Signaling Pathways -- 3.2.1 Growth Factor Receptors: Some Basics -- 3.2.2 Growth Factor Receptors Activate Signaling Pathways -- 3.2.3 A Few Extra Things To know About Signaling Pathways -- 3.2.4 Signaling Pathways In cancer Cells -- 3.3 Growth Factor Receptors In cancer -- 3.3.1 Reasons For overactive Growth Factor Receptors On cancer Cells -- 3.4 Drugs That Target Egfr."]
[{"$nulls":4},"3.4.1 Monoclonal Antibodies That target Egfr -- 3.4.2 Kinase Inhibitors That Target Egfr -- 3.5 Drugs That Target Her2 -- 3.5.1 Monoclonal Antibodies That Target Her2 -- 3.5.2 Kinase Inhibitors That Target Her2 -- 3.6 Drugs That Block Other Growth Factor Receptors -- 3.6.1 Pdgfr And Kit Inhibitors -- 3.6.2 Fgfr Inhibitors -- 3.6.3 Met Inhibitors -- 3.6.4 Ret Inhibitors -- 3.6.5 Alk And Ros1 Inhibitors -- 3.6.6 Trka/b/c Inhibitors -- 3.6.7 Her3 Inhibitors -- 3.6.8 Flt3 Inhibitors -- 3.7 Targeting The mapk Signaling Pathway -- 3.7.1 Things To remember -- 3.7.2 Defects In The Mapk Signaling Pathway In Cancer Cells -- 3.7.3 Drugs That Block The Mapk Pathway -- 3.7.4 K-ras Inhibitors -- 3.7.5 B-raf Inhibitors -- 3.7.6 A Bit Extra On Mek Inhibitors -- 3.8 Targeting The pi3k/akt/mtor Signaling Pathway -- 3.8.1 Defects In The Pi3k/akt/mtor Pathway In Cancer Cells -- 3.8.2 Drugs That Block The Pi3k/akt/mtor Pathway -- 3.8.3 Pi3k Inhibitors -- 3.8.4 Dual Pi3k And Mtor Inhibitors -- 3.8.5 Akt Inhibitors -- 3.8.6 Mtor Inhibitors -- 3.9 Targeting The jak-stat Pathway -- 3.9.1 Defects In The Jak-stat Pathway In Cancer Cells -- 3.9.2 Jak2 Inhibitors -- 3.10 Bcr-abl Inhibitors -- 3.10.1 The Bcr-abl Protein -- 3.10.2 Imatinib: The First Bcr-abl Inhibitor -- 3.10.3 Second- And third-generation Bcr-abl "]
[{"$nulls":4},"Inhibitors -- 3.10.4 Allosteric Inhibitors Of bcr-abl -- 3.11 Final Thoughts -- References -- Chapter 4 More Targets And treatments -- 4.1 Angiogenesis Inhibitors -- 4.1.1 How Tumors Trigger Angiogenesis -- 4.1.2 Tumor Blood Vessels Are Weird -- 4.1.3 Why Block Vegf? -- 4.1.4 Why Angiogenesis Inhibitors Sometimes Work -- 4.1.5 Drugs That target Vegf Or Vegf Receptors -- 4.1.6 Everolimus And Temsirolimus -- 4.1.7 Kidney Cancer - A special Case -- 4.1.8 Hif-2alpha Inhibitor - Belzutifan -- 4.1.9 Why Angiogenesis Inhibitors Don't Always Work."]
[{"$nulls":4},"4.1.10 The Search For biomarkers -- 4.1.11 Combining Angiogenesis Inhibitors With Immunotherapy -- 4.2 Antibody Conjugates -- 4.2.1 The Structure Of Adcs -- 4.2.2 How Adcs Are Being Improved -- 4.2.3 An Example: Trastuzumab Deruxtecan -- 4.2.4 Common Targets Of Adcs And Treatment Examples -- 4.2.5 Who Are They Given To? -- 4.2.6 Reasons For Resistance To adcs -- 4.2.7 Side Effects Of Adcs -- 4.2.8 Other Types Of conjugate -- 4.3 Parp Inhibitors -- 4.3.1 What Is Parp? -- 4.3.2 How Do Parp Inhibitors Work? -- 4.3.3 What Are Brca Genes And Brca Proteins? -- 4.3.4 Why Are People With Inherited Brca Mutations So Likely To Develop Cancer? -- 4.3.5 Parp Inhibitors For People With Inherited Brca Gene Mutations And Breast Or Ovarian Cancer -- 4.3.6 Parp Inhibitors For Ovarian cancers In People Who Haven't Inherited A Brca gene Mutation -- 4.3.7 Parp Inhibitors As Treatments For Other Cancers -- 4.3.8 Biomarkers Of Response To Parp Inhibitors -- 4.3.9 Resistance Mechanisms To Parp Inhibitors -- 4.3.10 Overcoming Resistance To Parp Inhibitors -- 4.4 Cdk Inhibitors And other Cell Cycle-targeted Treatments -- 4.4.1 Cdks That Control The Cell cycle -- 4.4.2 Other Cdks -- 4.4.3 Why Cell Cycle Cdks Are Overactive In Cancer Cells -- 4.4.4 Cdk4/6 Inhibitors As Cancer treatments -- 4.4.5 Resistance To Cdk4/6 Inhibitors -- 4.4.6 Treatments That Target Other Cell Cycle Proteins -- 4.5 Hedgehog Pathway Inhibitors -- 4.5.1 Components Of the Hedgehog Pathway -- 4.5.2 Hedgehog Pathway Inhibitors -- 4.5.3 Smoothened Inhibitors As Treatments For basal Cell carcinoma And Medulloblastoma -- 4.5.4 Broadening The uses Of hedgehog Inhibitors -- 4.6 Targeting Epigenetic Enzymes -- 4.6.1 Epigenetic Control Of Our genes -- 4.6.2 Epigenetics And cancer -- 4.6.3 Treatments That Target Epigenetic Enzymes -- 4.7 Targeting Cell Survival -- 4.7.1 Bcl-2 Protects Cancer Cells From Apoptosis."]
[{"$nulls":4},"4.7.2 Mechanism Of Action Of Bcl-2 Inhibitors -- 4.7.3 How Else Can We trigger Apoptosis? -- 4.8 Targeting B Cell Receptor Signaling -- 4.8.1 The Normal Function Of Bcrs -- 4.8.2 How Bcr Signaling Goes Wrong In Cancer Cells -- 4.8.3 The Effects Of Blocking Bcr-controlled Signaling -- 4.8.4 Btk Inhibitors -- 4.8.5 Pi3k Inhibitors -- 4.8.6 Treatments That Target Cd79b Or Other Cell Surface Proteins -- 4.9 Nuclear Transport Inhibitors -- 4.9.1 Nuclear Transport And cancer -- 4.9.2 Exportin-1 inhibitors -- 4.10 Proteasome Inhibitors -- 4.10.1 About The proteasome -- 4.10.2 The Actions Of proteasome Inhibitors -- 4.10.3 Proteasome Inhibitors As Treatments For myeloma -- 4.10.4 Proteasome Inhibitors As treatments For other Cancers -- 4.11 Final Thoughts -- References -- Chapter 5 Immunotherapy With checkpoint Inhibitors -- 5.1 The Importance Of T Cells -- 5.1.1 The Importance Of T cells as a Target For immunotherapy -- 5.1.2 How Do The various T Cell-directed Immunotherapies Work? -- 5.2 An Introduction To Immune Checkpoint Inhibitors -- 5.2.1 The Normal Role Of checkpoint Proteins -- 5.2.2 Checkpoint Proteins Sometimes Suppress Cancer-fighting T Cells -- 5.3 How Checkpoint Inhibitors Work -- 5.3.1 Licensed Checkpoint Inhibitors -- 5.4 Lessons Learned From Checkpoint Inhibitor Trials -- 5.4.1 Some Patients With advanced "]
[{"$nulls":4},"Cancer Can effectively Be cured -- 5.4.2 Responders To checkpoint Inhibitor Monotherapy Are Usually In a Minority -- 5.4.3 The Earlier You can Give The Checkpoint Inhibitor The Better -- 5.4.4 There's Very Little Relationship Between Dose and response -- 5.4.5 Side Effects Are Unpredictable And can be life Long -- 5.4.6 There Are Various Possible Patterns Of response -- 5.4.7 Response Rates Are Highest In tumors With pd-l1/2 Gene Mutations -- 5.4.8 Early Data From Immunotherapy Trials Can be misleading."]
[{"$nulls":4},"5.5 Why Some Patients Benefit From Checkpoint Inhibitors And Others Don't."]
[null,null,null,"Sommario/riassunto","A Beginner's Guide to Targeted Cancer Treatments and Cancer Immunotherapy by Elaine Vickers provides a comprehensive introduction to the latest advancements in cancer treatment. This second edition, updated for 2025, offers insights into the biology and genetics of cancer, emphasizing the role of DNA damage and cancer cell hallmarks. The book explores modern therapies such as monoclonal antibodies, small molecules, and various immunotherapies, including checkpoint inhibitors and CAR T cell therapy. It also delves into specific treatments for different cancer types. Designed for healthcare professionals and those interested in oncology, the book aims to enhance understanding of targeted cancer treatments and their potential impact on patient care."]