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Advances in cancer drug targets . Volume 1 / / editor, Atta-ur-Rahman
| Advances in cancer drug targets . Volume 1 / / editor, Atta-ur-Rahman |
| Autore | Rahman Atta-ur |
| Edizione | [1st ed.] |
| Pubbl/distr/stampa | Sharjah, United Arab Emirates ; ; Oak Park, Ill., : Bentham Science Publishers, [2013?] |
| Descrizione fisica | 1 online resource (316 p.) |
| Disciplina | 615/.19 |
| Altri autori (Persone) | RahmanAtta-ur- <1942-> |
| Collana | Advances in cancer drug targets |
| Soggetto topico |
Cancer - Chemotherapy
Drug targeting |
| ISBN |
9781608054749
1608054748 |
| Formato | Materiale a stampa  |
| Livello bibliografico | Monografia |
| Lingua di pubblicazione | eng |
| Nota di contenuto | Title; EUL; Contents; Foreword; List of Contributors; Chapter 01; Chapter 02; Chapter 03; Chapter 04; Chapter 05; Chapter 06; Chapter 07; Chapter 08; Index |
| Record Nr. | UNINA-9910962333503321 |
Rahman Atta-ur
|
||
| Sharjah, United Arab Emirates ; ; Oak Park, Ill., : Bentham Science Publishers, [2013?] | ||
| Materiale a stampa | ||
| Lo trovi qui: Univ. Federico II | ||
| ||
Advances in cancer drug targets . Volume 3 / / Atta-ur-Rahman, editor ; contributors Alain J. P. Alix [and thirty seven others]
| Advances in cancer drug targets . Volume 3 / / Atta-ur-Rahman, editor ; contributors Alain J. P. Alix [and thirty seven others] |
| Pubbl/distr/stampa | Sharjah, United Arab Emirates : , : Bentham Science Publishers, , 2016 |
| Descrizione fisica | 1 online resource (278 p.) |
| Disciplina | 616.994061 |
| Collana | Advances in Cancer Drug Targets |
| Soggetto topico |
Cancer - Chemotherapy
Drug targeting Drug delivery systems |
| Soggetto genere / forma | Electronic books. |
| ISBN | 1-68108-233-0 |
| Formato | Materiale a stampa |
| Livello bibliografico | Monografia |
| Lingua di pubblicazione | eng |
| Nota di contenuto |
CONTENTS; PREFACE ; List of Contributors ; Neutrophil Elastase as a Target in Lung Cancer: the State of the Art ; 1. INTRODUCTION: NEUTROPHIL ELASTASE/Α-1ANTITRYPSIN IMBALANCE AS A LINK BETWEEN CHRONIC OBSTRUCTIVE PULMONARY DISEASE AND LUNG CANCER; 2. MULTIFACETED FUNCTIONS OF NEUTROPHIL ELASTASE IN LUNG CANCER; 3. ENDEGNENOUS NEUTROPHIL ELASTASE INHIBITORS; 3.1. Proteinaceous Inhibitors; 3.2. Natural Compounds; 3.2.1. Glycosaminoglycans; 3.2.2. Phenolics; 3.2.3. Triterpenoids ; 3.2.4. Fatty Acids and Peptide Derivatives; 4. DESIGN OF DUAL NEUTROPHIL ELASTASE / MMP INHIBITORS
DESIGN OF DUAL HNE-MMP INHIBITORSCONCLUDING REMARKS; ADDITIONAL MATERIAL; 1. Molecular Modeling and Molecular Graphics; 2. Ligand and Receptor Preparation; 3. Docking Protocol; CONFLICT OF INTEREST; DISCLOSURE; ACKNOWLEDGEMENTS; ABBREVIATIONS; REFERENCES; Inhibition of Membrane Complement Inhibitor Expression (CD46, CD55, CD59) by siRNA Sensitizes Tumor Cells to Complement Attack ; INTRODUCTION; MATERIALS AND METHODS; Cell Culture; SiRNA Sequences; SiRNA Transfection; Flow Cytometry; Complement-mediated Cytotoxicity Assay (CDC); C3-binding Studies; Real-Time RT-PCR; Statistical Analysis RESULTSDesign of siRNAs Specific for CD46, CD55 and CD59; SiRNA-mediated Downregulation of mCRP Expression; siRNA-mediated Augmentation of Tumor Cell Complement Lysis and Opsonization; Time-course of siRNA-induced mCRP Inhibition; Stable Downregulation of CD59 Using an Hairpin siRNA Expression Vector; DISCUSSION; CONFLICT OF INTEREST; DISCLOSURE; ACKNOWLEDGEMENT; ABBREVIATIONS; REFERENCES; Points of Therapeutic Intervention along the Wnt Signaling Pathway in Hepatocellular Carcinoma ; INTRODUCTION; THE WNT SIGNALING PATHWAY; Overview of the Wnt Signaling; The Wnt/β-catenin Pathway Aberrant Activation of the Wnt/β-catenin Pathway in HCCTARGETING THE WNT/Β-CATENIN PATHWAY IN HCC; Targeting the Upstream Components; Endogenous Inhibitors of the Ligand/Receptor Complex; Targeting Wnt Ligands and FZD Receptors ; Targeting the Dishevelled Protein; Cellular Trafficking and Targets; Targeting the β-catenin Destruction Complex; Targeting the β-catenin/TCF Transcriptional Complex; Pitfalls in Targeting the Wnt/β-catenin Pathway; CONCLUSIONS AND PERSPECTIVES ; CONFLICT OF INTEREST; DISCLOSURE; ACKNOWLEDGMENT; ABBREVIATIONS; REFERENCES Collaboration of Epithelial Mesenchymal Transition and Cancer Stem Cells: Sinister Routes for Chemoresistant Recurrent Ovarian Cancer INTRODUCTION; PATHOLOGY OF OVARIAN CANCER; TRANSITION FROM EPITHELIAL TO MESENCHYMAL PHENOTYPE AND THE PROGRESSION OF CANCER ; EVIDENCE OF EMT IN OVARIAN CANCER; STEM CELLS IN NORMAL OVARIES AND OVARIAN CANCER; SPHERE FORMATION AND THE CANCER STEM CELL PHENOTYPE OF THE OVARY; ASSOCIATION OF EMT AND CSCS: A MERGER FOR POTENTIAL CHEMORESISTANCE IN OVARIAN CANCER Cisplatin Induced EMT Generates Ovarian Cancer Stem-Like Cells: A Study on the OVCA 433 Cell Line as an Experimental Model |
| Record Nr. | UNINA-9910511486903321 |
| Sharjah, United Arab Emirates : , : Bentham Science Publishers, , 2016 | ||
| Materiale a stampa | ||
| Lo trovi qui: Univ. Federico II | ||
| ||
Advances in cancer drug targets . Volume 3 / / Atta-ur-Rahman, editor ; contributors Alain J. P. Alix [and thirty seven others]
| Advances in cancer drug targets . Volume 3 / / Atta-ur-Rahman, editor ; contributors Alain J. P. Alix [and thirty seven others] |
| Pubbl/distr/stampa | Sharjah, United Arab Emirates : , : Bentham Science Publishers, , 2016 |
| Descrizione fisica | 1 online resource (278 p.) |
| Disciplina | 616.994061 |
| Collana | Advances in Cancer Drug Targets |
| Soggetto topico |
Cancer - Chemotherapy
Drug targeting Drug delivery systems |
| ISBN | 1-68108-233-0 |
| Formato | Materiale a stampa |
| Livello bibliografico | Monografia |
| Lingua di pubblicazione | eng |
| Nota di contenuto |
CONTENTS; PREFACE ; List of Contributors ; Neutrophil Elastase as a Target in Lung Cancer: the State of the Art ; 1. INTRODUCTION: NEUTROPHIL ELASTASE/Α-1ANTITRYPSIN IMBALANCE AS A LINK BETWEEN CHRONIC OBSTRUCTIVE PULMONARY DISEASE AND LUNG CANCER; 2. MULTIFACETED FUNCTIONS OF NEUTROPHIL ELASTASE IN LUNG CANCER; 3. ENDEGNENOUS NEUTROPHIL ELASTASE INHIBITORS; 3.1. Proteinaceous Inhibitors; 3.2. Natural Compounds; 3.2.1. Glycosaminoglycans; 3.2.2. Phenolics; 3.2.3. Triterpenoids ; 3.2.4. Fatty Acids and Peptide Derivatives; 4. DESIGN OF DUAL NEUTROPHIL ELASTASE / MMP INHIBITORS
DESIGN OF DUAL HNE-MMP INHIBITORSCONCLUDING REMARKS; ADDITIONAL MATERIAL; 1. Molecular Modeling and Molecular Graphics; 2. Ligand and Receptor Preparation; 3. Docking Protocol; CONFLICT OF INTEREST; DISCLOSURE; ACKNOWLEDGEMENTS; ABBREVIATIONS; REFERENCES; Inhibition of Membrane Complement Inhibitor Expression (CD46, CD55, CD59) by siRNA Sensitizes Tumor Cells to Complement Attack ; INTRODUCTION; MATERIALS AND METHODS; Cell Culture; SiRNA Sequences; SiRNA Transfection; Flow Cytometry; Complement-mediated Cytotoxicity Assay (CDC); C3-binding Studies; Real-Time RT-PCR; Statistical Analysis RESULTSDesign of siRNAs Specific for CD46, CD55 and CD59; SiRNA-mediated Downregulation of mCRP Expression; siRNA-mediated Augmentation of Tumor Cell Complement Lysis and Opsonization; Time-course of siRNA-induced mCRP Inhibition; Stable Downregulation of CD59 Using an Hairpin siRNA Expression Vector; DISCUSSION; CONFLICT OF INTEREST; DISCLOSURE; ACKNOWLEDGEMENT; ABBREVIATIONS; REFERENCES; Points of Therapeutic Intervention along the Wnt Signaling Pathway in Hepatocellular Carcinoma ; INTRODUCTION; THE WNT SIGNALING PATHWAY; Overview of the Wnt Signaling; The Wnt/β-catenin Pathway Aberrant Activation of the Wnt/β-catenin Pathway in HCCTARGETING THE WNT/Β-CATENIN PATHWAY IN HCC; Targeting the Upstream Components; Endogenous Inhibitors of the Ligand/Receptor Complex; Targeting Wnt Ligands and FZD Receptors ; Targeting the Dishevelled Protein; Cellular Trafficking and Targets; Targeting the β-catenin Destruction Complex; Targeting the β-catenin/TCF Transcriptional Complex; Pitfalls in Targeting the Wnt/β-catenin Pathway; CONCLUSIONS AND PERSPECTIVES ; CONFLICT OF INTEREST; DISCLOSURE; ACKNOWLEDGMENT; ABBREVIATIONS; REFERENCES Collaboration of Epithelial Mesenchymal Transition and Cancer Stem Cells: Sinister Routes for Chemoresistant Recurrent Ovarian Cancer INTRODUCTION; PATHOLOGY OF OVARIAN CANCER; TRANSITION FROM EPITHELIAL TO MESENCHYMAL PHENOTYPE AND THE PROGRESSION OF CANCER ; EVIDENCE OF EMT IN OVARIAN CANCER; STEM CELLS IN NORMAL OVARIES AND OVARIAN CANCER; SPHERE FORMATION AND THE CANCER STEM CELL PHENOTYPE OF THE OVARY; ASSOCIATION OF EMT AND CSCS: A MERGER FOR POTENTIAL CHEMORESISTANCE IN OVARIAN CANCER Cisplatin Induced EMT Generates Ovarian Cancer Stem-Like Cells: A Study on the OVCA 433 Cell Line as an Experimental Model |
| Record Nr. | UNINA-9910798274803321 |
| Sharjah, United Arab Emirates : , : Bentham Science Publishers, , 2016 | ||
| Materiale a stampa | ||
| Lo trovi qui: Univ. Federico II | ||
| ||
Advances in cancer drug targets . Volume 3 / / Atta-ur-Rahman, editor ; contributors Alain J. P. Alix [and thirty seven others]
| Advances in cancer drug targets . Volume 3 / / Atta-ur-Rahman, editor ; contributors Alain J. P. Alix [and thirty seven others] |
| Pubbl/distr/stampa | Sharjah, United Arab Emirates : , : Bentham Science Publishers, , 2016 |
| Descrizione fisica | 1 online resource (278 p.) |
| Disciplina | 616.994061 |
| Collana | Advances in Cancer Drug Targets |
| Soggetto topico |
Cancer - Chemotherapy
Drug targeting Drug delivery systems |
| ISBN | 1-68108-233-0 |
| Formato | Materiale a stampa |
| Livello bibliografico | Monografia |
| Lingua di pubblicazione | eng |
| Nota di contenuto |
CONTENTS; PREFACE ; List of Contributors ; Neutrophil Elastase as a Target in Lung Cancer: the State of the Art ; 1. INTRODUCTION: NEUTROPHIL ELASTASE/Α-1ANTITRYPSIN IMBALANCE AS A LINK BETWEEN CHRONIC OBSTRUCTIVE PULMONARY DISEASE AND LUNG CANCER; 2. MULTIFACETED FUNCTIONS OF NEUTROPHIL ELASTASE IN LUNG CANCER; 3. ENDEGNENOUS NEUTROPHIL ELASTASE INHIBITORS; 3.1. Proteinaceous Inhibitors; 3.2. Natural Compounds; 3.2.1. Glycosaminoglycans; 3.2.2. Phenolics; 3.2.3. Triterpenoids ; 3.2.4. Fatty Acids and Peptide Derivatives; 4. DESIGN OF DUAL NEUTROPHIL ELASTASE / MMP INHIBITORS
DESIGN OF DUAL HNE-MMP INHIBITORSCONCLUDING REMARKS; ADDITIONAL MATERIAL; 1. Molecular Modeling and Molecular Graphics; 2. Ligand and Receptor Preparation; 3. Docking Protocol; CONFLICT OF INTEREST; DISCLOSURE; ACKNOWLEDGEMENTS; ABBREVIATIONS; REFERENCES; Inhibition of Membrane Complement Inhibitor Expression (CD46, CD55, CD59) by siRNA Sensitizes Tumor Cells to Complement Attack ; INTRODUCTION; MATERIALS AND METHODS; Cell Culture; SiRNA Sequences; SiRNA Transfection; Flow Cytometry; Complement-mediated Cytotoxicity Assay (CDC); C3-binding Studies; Real-Time RT-PCR; Statistical Analysis RESULTSDesign of siRNAs Specific for CD46, CD55 and CD59; SiRNA-mediated Downregulation of mCRP Expression; siRNA-mediated Augmentation of Tumor Cell Complement Lysis and Opsonization; Time-course of siRNA-induced mCRP Inhibition; Stable Downregulation of CD59 Using an Hairpin siRNA Expression Vector; DISCUSSION; CONFLICT OF INTEREST; DISCLOSURE; ACKNOWLEDGEMENT; ABBREVIATIONS; REFERENCES; Points of Therapeutic Intervention along the Wnt Signaling Pathway in Hepatocellular Carcinoma ; INTRODUCTION; THE WNT SIGNALING PATHWAY; Overview of the Wnt Signaling; The Wnt/β-catenin Pathway Aberrant Activation of the Wnt/β-catenin Pathway in HCCTARGETING THE WNT/Β-CATENIN PATHWAY IN HCC; Targeting the Upstream Components; Endogenous Inhibitors of the Ligand/Receptor Complex; Targeting Wnt Ligands and FZD Receptors ; Targeting the Dishevelled Protein; Cellular Trafficking and Targets; Targeting the β-catenin Destruction Complex; Targeting the β-catenin/TCF Transcriptional Complex; Pitfalls in Targeting the Wnt/β-catenin Pathway; CONCLUSIONS AND PERSPECTIVES ; CONFLICT OF INTEREST; DISCLOSURE; ACKNOWLEDGMENT; ABBREVIATIONS; REFERENCES Collaboration of Epithelial Mesenchymal Transition and Cancer Stem Cells: Sinister Routes for Chemoresistant Recurrent Ovarian Cancer INTRODUCTION; PATHOLOGY OF OVARIAN CANCER; TRANSITION FROM EPITHELIAL TO MESENCHYMAL PHENOTYPE AND THE PROGRESSION OF CANCER ; EVIDENCE OF EMT IN OVARIAN CANCER; STEM CELLS IN NORMAL OVARIES AND OVARIAN CANCER; SPHERE FORMATION AND THE CANCER STEM CELL PHENOTYPE OF THE OVARY; ASSOCIATION OF EMT AND CSCS: A MERGER FOR POTENTIAL CHEMORESISTANCE IN OVARIAN CANCER Cisplatin Induced EMT Generates Ovarian Cancer Stem-Like Cells: A Study on the OVCA 433 Cell Line as an Experimental Model |
| Record Nr. | UNINA-9910822427603321 |
| Sharjah, United Arab Emirates : , : Bentham Science Publishers, , 2016 | ||
| Materiale a stampa | ||
| Lo trovi qui: Univ. Federico II | ||
| ||
Advances in cancer drug targets [[electronic resource] ] . Volume 1 / / editor, Atta-ur-Rahman
| Advances in cancer drug targets [[electronic resource] ] . Volume 1 / / editor, Atta-ur-Rahman |
| Pubbl/distr/stampa | Sharjah, United Arab Emirates ; ; Oak Park, Ill., : Bentham Science Publishers, [2013?] |
| Descrizione fisica | 1 online resource (316 p.) |
| Disciplina | 615/.19 |
| Altri autori (Persone) | RahmanAtta-ur- <1942-> |
| Collana | Advances in cancer drug targets |
| Soggetto topico |
Cancer - Chemotherapy
Drug targeting |
| Soggetto genere / forma | Electronic books. |
| ISBN | 1-60805-474-8 |
| Formato | Materiale a stampa |
| Livello bibliografico | Monografia |
| Lingua di pubblicazione | eng |
| Nota di contenuto | Title; EUL; Contents; Foreword; List of Contributors; Chapter 01; Chapter 02; Chapter 03; Chapter 04; Chapter 05; Chapter 06; Chapter 07; Chapter 08; Index |
| Record Nr. | UNINA-9910452673003321 |
| Sharjah, United Arab Emirates ; ; Oak Park, Ill., : Bentham Science Publishers, [2013?] | ||
| Materiale a stampa | ||
| Lo trovi qui: Univ. Federico II | ||
| ||
Advances in cancer drug targets [[electronic resource] ] . Volume 1 / / editor, Atta-ur-Rahman
| Advances in cancer drug targets [[electronic resource] ] . Volume 1 / / editor, Atta-ur-Rahman |
| Pubbl/distr/stampa | Sharjah, United Arab Emirates ; ; Oak Park, Ill., : Bentham Science Publishers, [2013?] |
| Descrizione fisica | 1 online resource (316 p.) |
| Disciplina | 615/.19 |
| Altri autori (Persone) | RahmanAtta-ur- <1942-> |
| Collana | Advances in cancer drug targets |
| Soggetto topico |
Cancer - Chemotherapy
Drug targeting |
| ISBN | 1-60805-474-8 |
| Formato | Materiale a stampa |
| Livello bibliografico | Monografia |
| Lingua di pubblicazione | eng |
| Nota di contenuto | Title; EUL; Contents; Foreword; List of Contributors; Chapter 01; Chapter 02; Chapter 03; Chapter 04; Chapter 05; Chapter 06; Chapter 07; Chapter 08; Index |
| Record Nr. | UNINA-9910779510903321 |
| Sharjah, United Arab Emirates ; ; Oak Park, Ill., : Bentham Science Publishers, [2013?] | ||
| Materiale a stampa | ||
| Lo trovi qui: Univ. Federico II | ||
| ||
A Beginner's Guide to Targeted Cancer Treatments and Cancer Immunotherapy
| A Beginner's Guide to Targeted Cancer Treatments and Cancer Immunotherapy |
| Autore | Vickers Elaine |
| Edizione | [2nd ed.] |
| Pubbl/distr/stampa | Newark : , : John Wiley & Sons, Incorporated, , 2024 |
| Descrizione fisica | 1 online resource (463 pages) |
| Disciplina | 616.994061 |
| Soggetto topico |
Immunotherapy
Drug targeting |
| ISBN |
9781119834090
1119834090 9781119834083 1119834082 9781119834076 1119834074 |
| Formato | Materiale a stampa |
| Livello bibliografico | Monografia |
| Lingua di pubblicazione | eng |
| Nota di contenuto |
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 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.
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. 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 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. 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. 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 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. 5.5 Why Some Patients Benefit From Checkpoint Inhibitors And Others Don't. |
| Record Nr. | UNINA-9911019793003321 |
|
Vickers Elaine
|
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| Newark : , : John Wiley & Sons, Incorporated, , 2024 | ||
| Materiale a stampa | ||
| Lo trovi qui: Univ. Federico II | ||
| ||
Core-shell nanostructures for drug delivery and theranostics : challenges, strategies and prospects for novel carrier systems / / edited by Maria Focarete and Anna Tampieri
| Core-shell nanostructures for drug delivery and theranostics : challenges, strategies and prospects for novel carrier systems / / edited by Maria Focarete and Anna Tampieri |
| Pubbl/distr/stampa | Duxford, United Kingdom : , : Woodhead Publishing, imprint of Elsevier, , [2018] |
| Descrizione fisica | 1 online resource (467 pages) |
| Disciplina | 615.7 |
| Collana | Woodhead Publishing Series in Biomaterials |
| Soggetto topico |
Drug targeting
Nanomedicine |
| ISBN | 0-08-102199-2 |
| Formato | Materiale a stampa |
| Livello bibliografico | Monografia |
| Lingua di pubblicazione | eng |
| Record Nr. | UNINA-9910583399503321 |
| Duxford, United Kingdom : , : Woodhead Publishing, imprint of Elsevier, , [2018] | ||
| Materiale a stampa | ||
| Lo trovi qui: Univ. Federico II | ||
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Designing multi-target drugs / / edited by J. Richard Morphy, C. John Harris
| Designing multi-target drugs / / edited by J. Richard Morphy, C. John Harris |
| Edizione | [1st ed.] |
| Pubbl/distr/stampa | Cambridge [England], : RSC Pub., 2012 |
| Descrizione fisica | 1 online resource (395 p.) |
| Disciplina | 615.19 |
| Altri autori (Persone) |
MorphyJ. Richard
HarrisC. John |
| Collana | RSC drug discovery series |
| Soggetto topico | Drug targeting |
| ISBN |
9781621981435
1621981436 9781849734912 1849734917 |
| Formato | Materiale a stampa |
| Livello bibliografico | Monografia |
| Lingua di pubblicazione | eng |
| Nota di contenuto | i-iv; v-x; xi-xiv; xv-xviii; xix-xxviii; 1-13; 14-31; 32-49; 50-65; 66-85; 86-93; 94-110; 111-129; 130-140; 141-154; 155-180; 181-205; 206-220; 221-242; 243-262; 263-269; 270-289; 290-315; 316-334; 335-352; 353-355; 356-366 |
| Record Nr. | UNINA-9911007090703321 |
| Cambridge [England], : RSC Pub., 2012 | ||
| Materiale a stampa | ||
| Lo trovi qui: Univ. Federico II | ||
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Drug delivery
| Drug delivery |
| Pubbl/distr/stampa | Orlando, FL, : Academic Press, 1993- |
| Descrizione fisica | 1 online resource |
| Disciplina | 615 |
| Soggetto topico |
Drug delivery systems
Drug targeting Drug Administration Routes Drug Evaluation Pharmaceutical Preparations - administration & dosage Systèmes d'administration de médicaments Médicaments - Ciblage Pharmacology |
| Soggetto genere / forma |
Periodical
Fulltext Internet Resources. Periodicals. |
| ISSN | 1521-0464 |
| Formato | Materiale a stampa |
| Livello bibliografico | Periodico |
| Lingua di pubblicazione | eng |
| Record Nr. | UNINA-9910154531203321 |
| Orlando, FL, : Academic Press, 1993- | ||
| Materiale a stampa | ||
| Lo trovi qui: Univ. Federico II | ||
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Soggetto topico
-
Drug targeting
(43)
- Drug delivery systems (9)
- Cancer - Chemotherapy (7)
- Drug Therapy (5)
- G proteins (5)