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The Resource Chronic Myeloid Leukemia : Diagnosis and Treatment

Chronic Myeloid Leukemia : Diagnosis and Treatment

Label
Chronic Myeloid Leukemia : Diagnosis and Treatment
Title
Chronic Myeloid Leukemia
Title remainder
Diagnosis and Treatment
Creator
Subject
Language
eng
Member of
Cataloging source
MiAaPQ
Literary form
non fiction
Nature of contents
dictionaries
Series statement
Hematologic Malignancies Ser
Chronic Myeloid Leukemia : Diagnosis and Treatment
Label
Chronic Myeloid Leukemia : Diagnosis and Treatment
Link
http://libproxy.rpi.edu/login?url=https://ebookcentral.proquest.com/lib/rpi/detail.action?docID=4648528
Publication
Copyright
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Carrier category
online resource
Carrier category code
cr
Carrier MARC source
rdacarrier
Color
multicolored
Content category
text
Content type code
txt
Content type MARC source
rdacontent
Contents
  • Contents -- Introduction: Chronic Myeloid Leukemia (CML) in the Era of Tyrosine Kinase Inhibition -- 1: Cytogenetics of Chronic Myeloid Leukemia (CML) -- 1.1 The Discovery of the Philadelphia Chromosome (Ph) -- 1.2 The Translocation t(9 -- 22) -- 1.3 Relevance of Additional Cytogenetic Aberrations in a Ph-Positive Clone -- 1.4 Ph-Negative Clones -- 1.5 Significance of Cytogenetics for Current and Future Diagnosis and Monitoring of CML -- References -- 2: The Biology and Pathogenesis of Chronic Myeloid Leukemia -- 2.1 Clinical Overview -- 2.1.1 Diagnosis -- 2.1.2 CML Evolution and Prognosis -- 2.1.3 Treatment -- 2.2 The Molecular Biology of CML -- 2.2.1 The t(9 -- 22) Translocation and the BCR-ABL1 Gene -- 2.2.2 Protein Structure -- 2.2.3 The Consequence of BCR-ABL1 -- 2.3 Important Pathways Affected by BCR-ABL1 Activity -- 2.3.1 JAK/STAT -- 2.3.2 PI3K/AKT and Autophagy -- 2.3.3 Ras/MEK Pathway -- 2.3.4 Src Kinases -- 2.3.5 Crkl -- 2.3.6 Long Noncoding (lnc) RNA-BGL3 -- 2.3.7 Apoptosis Deregulation -- 2.4 CML Stem Cells -- 2.4.1 LSCs Are Refractory to TKIs -- 2.4.2 Ý-Catenin -- 2.4.3 Smo -- 2.4.4 PP2A-JAK2-SET -- 2.4.5 FoxO -- 2.4.6 Alox5 and Alox15 -- 2.4.7 Bone Marrow Microenvironment -- 2.5 Biology of Blast Crisis -- 2.5.1 BCR-ABL1 and BC-CML -- 2.5.1.1 DNA Damage/Repair -- 2.5.1.2 C/EBPÜ and hnRNP-E2 -- 2.5.1.3 IRF-8 -- 2.5.2 Examples of Important Pathways Involved in BC-CML -- 2.5.2.1 MYC -- 2.5.2.2 p53 -- 2.5.2.3 Musashi-2 (Msi2) -- 2.5.2.4 XPO1 -- 2.5.2.5 SIRT1 -- 2.5.2.6 ADAR1 -- 2.5.2.7 Screening for Novel BC Driver Genes -- 2.6 Concluding Remarks -- References -- 3: The Choice of First-Line Chronic Myelogenous Leukemia Treatment -- 3.1 Introduction -- 3.2 Second-Generation TKIs in First-Line Treatment -- 3.3 High-Dose Imatinib for First-{u00AD}Line Treatment
  • 3.4 Combination Therapy: Imatinib Plus Interferon Alpha -- Conclusions -- References -- 4: A Review and an Update of European LeukemiaNet Recommendations for the Management of Chronic Myeloid Leukemia -- 4.1 Chronic Phase (CP), Accelerated Phase (AP), and Blastic Phase -- 4.2 Risk, Baseline -- 4.3 Response to Treatment -- 4.4 First-Line Treatment -- 4.5 Second-Line Treatment -- 4.6 Treatment Continuation or Discontinuation, Treatment- Free Remission (TFR), Cure -- 4.7 Treatment of Accelerated and Blastic Phase -- Conclusions -- References -- 5: Management of Adverse Events Associated with ATP-Competitive BCR-ABL1 Tyrosine Kinase Inhibitors in Chronic Myeloid Leukemia -- 5.1 Introduction -- 5.2 Myelosuppression -- 5.3 Dermatologic Adverse Events -- 5.4 Gastrointestinal Adverse Events -- 5.5 Hepatic and Pancreatic Disorders -- 5.6 Musculoskeletal Symptoms -- 5.7 Fluid Retention -- 5.8 Pulmonary Toxicity -- 5.9 Cardiovascular Toxicity -- 5.9.1 QT Interval Prolongation -- 5.9.2 Systemic Arterial Hypertension -- 5.9.3 Congestive Heart Failure -- 5.9.4 Arterial Occlusion -- 5.10 Metabolic and Endocrine Side Effects -- 5.11 Other Side Effects -- Conclusion -- References -- 6: Standardization of Molecular Monitoring for Chronic Myeloid Leukemia -- 6.1 Background -- 6.2 Measurement of Residual Disease in the Laboratory -- 6.3 Choice of Control Gene -- 6.4 The International Scale for BCR-ABL1 Measurement -- 6.5 Implementing the International Scale -- 6.6 Development of Reference Reagents and Calibrated Kits -- 6.7 What Is Achievable by Standardization? -- 6.8 Next Steps -- References -- 7: Epidemiology of Chronic Myeloid Leukemia -- 7.1 Population-Based Registries -- 7.2 Incidence -- 7.2.1 Incidence of CML in the Total Adult Population -- 7.2.2 Age and Sex Differences -- 7.2.3 Has the Incidence of CML Increased Over Time?
  • 7.3 Prevalence -- 7.4 Risk Factors for Developing CML -- 7.5 Survival Rates and Non-{u00AD}Disease-{u00AD}Related Prognostic Factors -- 7.5.1 Overall and Relative Survival in the Population-Based Setting -- 7.5.2 Age and Comorbidity -- 7.5.3 Socioeconomy and Health-{u00AD}Care Setting -- 7.6 Do CML Patients Have an Increased Risk to Develop Other Cancers? -- References -- 8: Prognostic Scores for Patients with Chronic Myeloid Leukemia Under Particular Consideration of Disease-Specific Death -- 8.1 What Are Prognostic Scores? -- 8.2 Relevance of Prognostic Scores -- 8.3 Baseline Prognostic Scores as Part of the ELN Recommendations -- 8.3.1 Sokal Score -- 8.3.2 Euro Score -- 8.3.3 EUTOS Score -- 8.3.4 Comparative Assessments of the Three Scores in Imatinib-Treated Patients -- 8.4 Growing Proportion of Deaths Unrelated to CML -- 8.4.1 EUTOS Long-Term Survival (ELTS) Score -- 8.4.2 Data of the German CML Study IV -- 8.5 Survival When "Death Due to CML Only" Is the Event of Interest -- 8.6 Probabilities of Dying of CML -- 8.7 Cumulative Incidence Probabilities of Death Due To CML in the Risk Groups of the Prognostic Scores -- 8.8 Prognostic Modeling Under Presence of Competing Risks -- 8.9 Software -- 8.10 Conclusions -- 8.10.1 Probabilities of Dying of CML -- 8.10.2 Comparative Assessment of the Prognostic Performance of the Baseline Scores -- 8.10.3 Regression Modeling -- References -- 9: Response-Related Predictors of Survival in CML -- 9.1 Introduction -- 9.2 The Correlation of Response and Prognosis -- 9.2.1 Prognostic Significance of Later Landmarks (at 6, 12, and 18 Months) Under First-{u00AD}Line Treatment with Imatinib -- 9.2.2 Early Prediction of Survival (at 3 Months) Using Absolute Landmarks Under First-Line Treatment with Imatinib -- 9.2.3 Early Prediction of Survival Using Relative Landmarks -- 9.3 Predicting Treatment-Free Remission
  • 9.4 First-Line Treatment with Second-Generation TKI -- 9.5 Second-Line Treatment After Imatinib Failure -- Conclusions -- References -- 10: CML Blast Crisis: Implications and Management -- 10.1 Introduction -- 10.2 Diagnosis -- 10.3 Pathogenetic Basis of Therapy -- 10.4 Intensive Chemotherapy -- 10.5 TKI Therapy -- 10.5.1 Imatinib -- 10.5.2 Dasatinib -- 10.5.3 Nilotinib -- 10.5.4 Imatinib in Combination -- 10.5.5 Dasatinib or Nilotinib in Combination -- 10.5.6 Bosutinib and Ponatinib -- 10.6 Allo-SCT -- 10.7 Investigational Agents -- 10.8 Prevention -- 10.9 Early Prediction of Progression -- 10.10 Conclusion -- 10.11 Summary -- References -- 11: Managing Pregnancy in Chronic Myeloid Leukemia -- 11.1 Introduction -- 11.2 Animal Studies -- 11.2.1 Imatinib -- 11.2.2 Dasatinib -- 11.2.3 Nilotinib -- 11.2.4 Bosutinib -- 11.2.5 Ponatinib -- 11.3 Pregnancy Outcomes on Tyrosine Kinase Inhibitors -- 11.3.1 Male Patients -- 11.3.2 Female Patients -- 11.4 Planning Pregnancy in CML -- 11.5 Treating CML in Pregnancy -- 11.6 Breastfeeding -- 11.7 Management of the Patient Presenting in Pregnancy -- 11.8 Management of Fertility at Diagnosis -- Conclusion -- References -- 12: The Role of Hematopoietic Stem Cell Transplantation in Chronic Myeloid Leukemia -- 12.1 Evolution of HSCT for CML -- 12.1.1 Historical Perspective: The Role Model of CML for HSCT -- 12.1.2 HSCT for CML in 2015 -- 12.2 Outcome of HSCT for CML -- 12.2.1 Factors Associated with Outcome -- 12.2.2 Impact of Pretransplant Treatment -- 12.2.3 Impact of HSCT Methodology -- 12.2.4 Graft Versus Host: Graft Versus Leukemia Effects -- 12.2.5 Economic Factors, Center Effects, and Outcome -- 12.3 HSCT Versus Non-transplant Therapy Studies -- 12.3.1 "Randomized Comparisons" -- 12.3.2 "Non-randomized Comparisons": A Look to the Future of "Precision Medicine"
  • 12.4 Current Recommendations -- 12.4.1 European LeukemiaNet -- 12.4.2 Other Recommendations -- 12.4.3 Critical Appraisal -- 12.5 Concluding Remarks -- References -- 13: Discontinuation or Cessation of Tyrosine Kinase Inhibitor Treatment in Chronic Myeloid Leukemia Patients with Deep Molecular Response -- 13.1 Introduction -- 13.2 Which Clinical and Biological Factors Might Predict TFR? -- 13.3 Can We Cure CML? -- 13.4 Side Effects -- References -- 14: The Interferon Alpha Revival in CML -- 14.1 Mechanisms of IFNÜ Antitumor Effects -- 14.2 IFNÜ Induces Apoptosis -- 14.3 IFNÜ Inhibits Cell Growth -- 14.4 IFNÜ Suppresses Angiogenesis -- 14.5 IFNÜ Activates Immune Effector Cells -- 14.6 IFNÜ Suppresses Hematopoiesis -- 14.7 IFNÜ Mechanism of Action in MPNs -- 14.8 Molecular Markers of Response to IFNÜ -- 14.9 Experience with IFNÜ Before TKIs -- 14.10 Durable Responses and Unmaintained Remissions with IFN Therapy -- 14.11 Introduction of Imatinib -- 14.12 Combination Therapy with TKIs and IFNÜ -- 14.13 IFNÜ Maintenance Therapy -- 14.14 IFNÜ Activity in Ph- MPNs -- Conclusion -- References -- 15: Changing the Cost of Care for Chronic Myeloid Leukemia: The Availability of Generic Imatinib in the USA and the EU -- 15.1 Will the Arrival of Generic Imatinib Revolutionize the Economics of Treating Chronic Myeloid Leukemia? -- 15.2 Background on Patent Protection and Generic Entry -- 15.3 Molecule Characteristics Associated with Generic Drug "Success" -- 15.4 Patient, Physician, and Health System Factors Determine the Use of Imatinib to Treat CML After Generic Entry -- 15.5 The Role of Health Technology Assessment in the Use of Generic Imatinib for CML -- 15.6 A US-Specific Empirical Analysis of the Potential Impact of Generic Imatinib on the Cost-Effective Treatment of Incident CML in Chronic Phase -- 15.6.1 Empirical Methods
  • 15.6.1.1 Effectiveness
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1 online resource (261 pages)
Form of item
online
Isbn
9783319331980
Media category
computer
Media MARC source
rdamedia
Media type code
c
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unknown sound
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remote

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