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2017 oncology nursing drug handbook / / Gail M. Wilkes, MS, APRN-BC, AOCN, oncology nursing consultant Kilauea, Hawaii, Margaret Barton-Burke PhD, RN, FAAN, director of Nursing Research Memorial Sloan Kettering Cancer Center New York, New York
2017 oncology nursing drug handbook / / Gail M. Wilkes, MS, APRN-BC, AOCN, oncology nursing consultant Kilauea, Hawaii, Margaret Barton-Burke PhD, RN, FAAN, director of Nursing Research Memorial Sloan Kettering Cancer Center New York, New York
Autore Wilkes Gail M.
Pubbl/distr/stampa Burlington, MA : , : Jones & Bartlett, , [2017]
Descrizione fisica 1 online resource (3,329 pages) : illustrations
Disciplina 616.994061
Soggetto topico Cancer - Chemotherapy
Antineoplastic agents
Cancer - Nursing
ISBN 1-284-11719-7
Formato Materiale a stampa
Livello bibliografico Monografia
Lingua di pubblicazione eng
Record Nr. UNINA-9910162769603321
Wilkes Gail M.  
Burlington, MA : , : Jones & Bartlett, , [2017]
Materiale a stampa
Lo trovi qui: Univ. Federico II
Opac: Controlla la disponibilità qui
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
Opac: Controlla la disponibilità qui
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
Opac: Controlla la disponibilità qui
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
Opac: Controlla la disponibilità qui
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
Opac: Controlla la disponibilità qui
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
Opac: Controlla la disponibilità qui
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-9910814601403321
Sharjah, United Arab Emirates ; ; Oak Park, Ill., : Bentham Science Publishers, [2013?]
Materiale a stampa
Lo trovi qui: Univ. Federico II
Opac: Controlla la disponibilità qui
Advances in cancer research . Volume 125 ABC transporters and cancer / / edited by John D. Schuetz, Toshihisa Ishikawa ; contributors Suresh V. Ambudkar [and thirty one others]
Advances in cancer research . Volume 125 ABC transporters and cancer / / edited by John D. Schuetz, Toshihisa Ishikawa ; contributors Suresh V. Ambudkar [and thirty one others]
Edizione [First edition.]
Pubbl/distr/stampa London, England : , : Academic Press, , 2015
Descrizione fisica 1 online resource (280 p.)
Disciplina 616.9940072
Soggetto topico Cancer - Research
Drug resistance in cancer cells
Cancer - Chemotherapy
Soggetto genere / forma Electronic books.
ISBN 0-12-801361-3
Formato Materiale a stampa
Livello bibliografico Monografia
Lingua di pubblicazione eng
Nota di contenuto Front Cover; ABC Transporters and Cancer; Copyright; Dedication; Contents; Contributors; Preface; Chapter 1: Apical ABC Transporters and Cancer Chemotherapeutic Drug Disposition; 1. Introduction to Apical ABC Transporters; 2. Impact of Apical ABC Transporters on Intestinal Absorption of Oral Chemotherapeutic Drugs; 2.1. Apical ABC transporters affecting the oral bioavailability of taxanes; 2.1.1. ABCB1 and oral taxane availability; 2.1.2. ABCC2 and oral taxane availability; 2.1.3. ABCB1 inhibitors to improve taxane oral availability
2.1.4. Assessing CNS toxicity risks of using ABCB1 inhibitors to improve oral taxane availability2.1.5. Possible effects of ABCB1 inhibitors on enhancing taxane antitumor efficacy; 2.2. Apical ABC transporters in the oral bioavailability of rationally designed anticancer drugs; 2.2.1. Tyrosine kinase inhibitors; 2.2.2. PARP inhibitors; 2.2.3. Chemical inhibition of transporters to increase oral availability of rationally designed anticancer drugs; 2.2.4. Importance of the sensitivity and specificity of in vitro assays used to assess ABC transporter substrates
3. Impact of Apical ABC Transporters on Brain Disposition of Oral Chemotherapeutic Drugs3.1. Does the BBB matter in drug delivery to brain tumors?; 3.2. Apical efflux transporters in the BBB affecting brain accumulation of anticancer drugs; 3.2.1. Drugs affected mostly by Abcb1a but also by Abcg2 in their brain accumulation; 3.2.2. Drugs only affected by Abcb1a in their brain accumulation; 3.2.3. Drugs affected mostly by Abcg2 but also by Abcb1a in their brain accumulation; 3.2.4. Three different apical BBB ABC efflux transporters affect brain accumulation of some camptothecins
3.2.5. Models to explain the disproportionate effect of combined deficiency of Abcb1 and Abcg2 on brain accumulation of s...3.2.6. Why are many rationally designed anticancer drugs still ABCB1 and/or ABCG2 substrates?; 3.2.7. Limitations of knockout mouse models to study ABC transporter functions at the BBB; 3.2.8. Tissue and cellular context may affect the in vivo impact of apical ABC efflux transporters; 3.2.9. Use of chemical inhibitors to enhance brain accumulation of ABC transporter substrate drugs; 4. Concluding Remarks; References
Chapter 2: Regulation of ABC Transporters Blood-Brain Barrier: The Good, the Bad, and the Ugly1. Introduction; 2. Blood-Brain Barriers; 2.1. Assessing blood-brain barrier function; 3. ABC Transporters at the Blood-Brain Barrier; 4. The Bad and the Ugly: Mechanisms that Increase Transporter Expression and Reduce Drug Delivery to the CNS; 4.1. Xenobiotic-activated transcription factors; 4.2. Stress-activated transcription factors; 4.3. Disease; 5. The Good: Mechanisms that Reduce Transporter Activity/Expression and Have the Potential to Improve Drug Delivery to th...; 5.1. P-glycoprotein
5.2. BCRP
Record Nr. UNINA-9910460672103321
London, England : , : Academic Press, , 2015
Materiale a stampa
Lo trovi qui: Univ. Federico II
Opac: Controlla la disponibilità qui
Advances in cancer research . Volume 125 ABC transporters and cancer / / edited by John D. Schuetz, Toshihisa Ishikawa ; contributors Suresh V. Ambudkar [and thirty one others]
Advances in cancer research . Volume 125 ABC transporters and cancer / / edited by John D. Schuetz, Toshihisa Ishikawa ; contributors Suresh V. Ambudkar [and thirty one others]
Edizione [First edition.]
Pubbl/distr/stampa London, England : , : Academic Press, , 2015
Descrizione fisica 1 online resource (280 p.)
Disciplina 616.9940072
Soggetto topico Cancer - Research
Drug resistance in cancer cells
Cancer - Chemotherapy
ISBN 0-12-801361-3
Formato Materiale a stampa
Livello bibliografico Monografia
Lingua di pubblicazione eng
Nota di contenuto Front Cover; ABC Transporters and Cancer; Copyright; Dedication; Contents; Contributors; Preface; Chapter 1: Apical ABC Transporters and Cancer Chemotherapeutic Drug Disposition; 1. Introduction to Apical ABC Transporters; 2. Impact of Apical ABC Transporters on Intestinal Absorption of Oral Chemotherapeutic Drugs; 2.1. Apical ABC transporters affecting the oral bioavailability of taxanes; 2.1.1. ABCB1 and oral taxane availability; 2.1.2. ABCC2 and oral taxane availability; 2.1.3. ABCB1 inhibitors to improve taxane oral availability
2.1.4. Assessing CNS toxicity risks of using ABCB1 inhibitors to improve oral taxane availability2.1.5. Possible effects of ABCB1 inhibitors on enhancing taxane antitumor efficacy; 2.2. Apical ABC transporters in the oral bioavailability of rationally designed anticancer drugs; 2.2.1. Tyrosine kinase inhibitors; 2.2.2. PARP inhibitors; 2.2.3. Chemical inhibition of transporters to increase oral availability of rationally designed anticancer drugs; 2.2.4. Importance of the sensitivity and specificity of in vitro assays used to assess ABC transporter substrates
3. Impact of Apical ABC Transporters on Brain Disposition of Oral Chemotherapeutic Drugs3.1. Does the BBB matter in drug delivery to brain tumors?; 3.2. Apical efflux transporters in the BBB affecting brain accumulation of anticancer drugs; 3.2.1. Drugs affected mostly by Abcb1a but also by Abcg2 in their brain accumulation; 3.2.2. Drugs only affected by Abcb1a in their brain accumulation; 3.2.3. Drugs affected mostly by Abcg2 but also by Abcb1a in their brain accumulation; 3.2.4. Three different apical BBB ABC efflux transporters affect brain accumulation of some camptothecins
3.2.5. Models to explain the disproportionate effect of combined deficiency of Abcb1 and Abcg2 on brain accumulation of s...3.2.6. Why are many rationally designed anticancer drugs still ABCB1 and/or ABCG2 substrates?; 3.2.7. Limitations of knockout mouse models to study ABC transporter functions at the BBB; 3.2.8. Tissue and cellular context may affect the in vivo impact of apical ABC efflux transporters; 3.2.9. Use of chemical inhibitors to enhance brain accumulation of ABC transporter substrate drugs; 4. Concluding Remarks; References
Chapter 2: Regulation of ABC Transporters Blood-Brain Barrier: The Good, the Bad, and the Ugly1. Introduction; 2. Blood-Brain Barriers; 2.1. Assessing blood-brain barrier function; 3. ABC Transporters at the Blood-Brain Barrier; 4. The Bad and the Ugly: Mechanisms that Increase Transporter Expression and Reduce Drug Delivery to the CNS; 4.1. Xenobiotic-activated transcription factors; 4.2. Stress-activated transcription factors; 4.3. Disease; 5. The Good: Mechanisms that Reduce Transporter Activity/Expression and Have the Potential to Improve Drug Delivery to th...; 5.1. P-glycoprotein
5.2. BCRP
Record Nr. UNINA-9910787425603321
London, England : , : Academic Press, , 2015
Materiale a stampa
Lo trovi qui: Univ. Federico II
Opac: Controlla la disponibilità qui
Advances in cancer research . Volume 125 ABC transporters and cancer / / edited by John D. Schuetz, Toshihisa Ishikawa ; contributors Suresh V. Ambudkar [and thirty one others]
Advances in cancer research . Volume 125 ABC transporters and cancer / / edited by John D. Schuetz, Toshihisa Ishikawa ; contributors Suresh V. Ambudkar [and thirty one others]
Edizione [First edition.]
Pubbl/distr/stampa London, England : , : Academic Press, , 2015
Descrizione fisica 1 online resource (280 p.)
Disciplina 616.9940072
Soggetto topico Cancer - Research
Drug resistance in cancer cells
Cancer - Chemotherapy
ISBN 0-12-801361-3
Formato Materiale a stampa
Livello bibliografico Monografia
Lingua di pubblicazione eng
Nota di contenuto Front Cover; ABC Transporters and Cancer; Copyright; Dedication; Contents; Contributors; Preface; Chapter 1: Apical ABC Transporters and Cancer Chemotherapeutic Drug Disposition; 1. Introduction to Apical ABC Transporters; 2. Impact of Apical ABC Transporters on Intestinal Absorption of Oral Chemotherapeutic Drugs; 2.1. Apical ABC transporters affecting the oral bioavailability of taxanes; 2.1.1. ABCB1 and oral taxane availability; 2.1.2. ABCC2 and oral taxane availability; 2.1.3. ABCB1 inhibitors to improve taxane oral availability
2.1.4. Assessing CNS toxicity risks of using ABCB1 inhibitors to improve oral taxane availability2.1.5. Possible effects of ABCB1 inhibitors on enhancing taxane antitumor efficacy; 2.2. Apical ABC transporters in the oral bioavailability of rationally designed anticancer drugs; 2.2.1. Tyrosine kinase inhibitors; 2.2.2. PARP inhibitors; 2.2.3. Chemical inhibition of transporters to increase oral availability of rationally designed anticancer drugs; 2.2.4. Importance of the sensitivity and specificity of in vitro assays used to assess ABC transporter substrates
3. Impact of Apical ABC Transporters on Brain Disposition of Oral Chemotherapeutic Drugs3.1. Does the BBB matter in drug delivery to brain tumors?; 3.2. Apical efflux transporters in the BBB affecting brain accumulation of anticancer drugs; 3.2.1. Drugs affected mostly by Abcb1a but also by Abcg2 in their brain accumulation; 3.2.2. Drugs only affected by Abcb1a in their brain accumulation; 3.2.3. Drugs affected mostly by Abcg2 but also by Abcb1a in their brain accumulation; 3.2.4. Three different apical BBB ABC efflux transporters affect brain accumulation of some camptothecins
3.2.5. Models to explain the disproportionate effect of combined deficiency of Abcb1 and Abcg2 on brain accumulation of s...3.2.6. Why are many rationally designed anticancer drugs still ABCB1 and/or ABCG2 substrates?; 3.2.7. Limitations of knockout mouse models to study ABC transporter functions at the BBB; 3.2.8. Tissue and cellular context may affect the in vivo impact of apical ABC efflux transporters; 3.2.9. Use of chemical inhibitors to enhance brain accumulation of ABC transporter substrate drugs; 4. Concluding Remarks; References
Chapter 2: Regulation of ABC Transporters Blood-Brain Barrier: The Good, the Bad, and the Ugly1. Introduction; 2. Blood-Brain Barriers; 2.1. Assessing blood-brain barrier function; 3. ABC Transporters at the Blood-Brain Barrier; 4. The Bad and the Ugly: Mechanisms that Increase Transporter Expression and Reduce Drug Delivery to the CNS; 4.1. Xenobiotic-activated transcription factors; 4.2. Stress-activated transcription factors; 4.3. Disease; 5. The Good: Mechanisms that Reduce Transporter Activity/Expression and Have the Potential to Improve Drug Delivery to th...; 5.1. P-glycoprotein
5.2. BCRP
Record Nr. UNINA-9910811415603321
London, England : , : Academic Press, , 2015
Materiale a stampa
Lo trovi qui: Univ. Federico II
Opac: Controlla la disponibilità qui