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Childhood acute lymphoblastic leukemia [electronic resource]

Childhood acute lymphoblastic leukemia [electronic resource]

자료유형
E-Book(소장)
개인저자
Vora, Ajay.
서명 / 저자사항
Childhood acute lymphoblastic leukemia [electronic resource] / Ajay Vora, editor.
발행사항
Cham :   Springer,   c2017.  
Switzerland.  
형태사항
1 online resource (ix, 342 p.) : ill. (some col.).
ISBN
9783319397078 9783319397085 (eBook)
요약
This book provides a comprehensive and up-to-date review of all aspects of childhood Acute Lymphoblastic Leukemia, from basic biology to supportive care. It offers new insights into the genetic pre-disposition to the condition and discusses how response to early therapy and its basic biology are utilized to develop new prognostic stratification systems and target therapy. Readers will learn about current treatment and outcomes, such as immunotherapy and targeted therapy approaches.  Supportive care and management of the condition in resource poor countries are also discussed in detail. This is an indispensable guide for  research and laboratory scientists, pediatric hematologists as well as specialist nurses involved in the care of childhood leukemia.
일반주기
Title from e-Book title page.  
서지주기
Includes bibliographical references and index.
이용가능한 다른형태자료
Issued also as a book.  
일반주제명
Hematology. Pediatrics. Oncology .
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URL
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020 ▼a 9783319397078
020 ▼a 9783319397085 (eBook)
040 ▼a 211009 ▼c 211009 ▼d 211009
050 4 ▼a RB45
082 0 4 ▼a 618.92/99419 ▼2 23
084 ▼a 618.9299419 ▼2 DDCK
090 ▼a 618.9299419
245 0 0 ▼a Childhood acute lymphoblastic leukemia ▼h [electronic resource] / ▼c Ajay Vora, editor.
260 ▼a Cham : ▼b Springer, ▼c c2017.
260 ▼a Switzerland.
300 ▼a 1 online resource (ix, 342 p.) : ▼b ill. (some col.).
500 ▼a Title from e-Book title page.
504 ▼a Includes bibliographical references and index.
520 ▼a This book provides a comprehensive and up-to-date review of all aspects of childhood Acute Lymphoblastic Leukemia, from basic biology to supportive care. It offers new insights into the genetic pre-disposition to the condition and discusses how response to early therapy and its basic biology are utilized to develop new prognostic stratification systems and target therapy. Readers will learn about current treatment and outcomes, such as immunotherapy and targeted therapy approaches.  Supportive care and management of the condition in resource poor countries are also discussed in detail. This is an indispensable guide for  research and laboratory scientists, pediatric hematologists as well as specialist nurses involved in the care of childhood leukemia.
530 ▼a Issued also as a book.
538 ▼a Mode of access: World Wide Web.
650 0 ▼a Hematology.
650 0 ▼a Pediatrics.
650 0 ▼a Oncology .
700 1 ▼a Vora, Ajay.
856 4 0 ▼u https://oca.korea.ac.kr/link.n2s?url=https://doi.org/10.1007/978-3-319-39708-5
945 ▼a KLPA
991 ▼a E-Book(소장)

소장정보

No. 소장처 청구기호 등록번호 도서상태 반납예정일 예약 서비스
No. 1 소장처 중앙도서관/e-Book 컬렉션/ 청구기호 CR 618.9299419 등록번호 E14013738 도서상태 대출불가(열람가능) 반납예정일 예약 서비스 M

컨텐츠정보

목차

Intro -- Contents -- Contributors -- Chapter 1: Epidemiology and Etiology of Childhood ALL -- 1.1 Introduction -- 1.2 General Epidemiology -- 1.3 Natural History -- 1.4 Environmental Risk Factors -- 1.4.1 Infectious Disease and Immune Stimulation -- 1.4.2 Other Risk Factors -- 1.5 Heritability of ALL -- 1.6 High-Penetrance Genetic Predisposition -- 1.6.1 Syndromes Where ALL Is a Dominant Cancer Phenotype -- 1.6.2 Syndromes Where ALL Is Part of a Mixed Cancer Phenotype -- 1.7 Low-Penetrance Genetic Predisposition -- 1.8 Future Directions -- References -- Chapter 2: Clinical Presentation and Prognostic Factors -- 2.1 Clinical Presentation -- 2.1.1 Introduction -- 2.1.2 Symptoms and Signs Related to Bone Marrow Involvement -- 2.1.3 Symptoms and Signs Related to Extensive Bulk Disease -- 2.1.4 Central Nervous System -- 2.1.5 The Eye -- 2.1.6 Genitourinary System -- 2.1.7 Cardiovascular System -- 2.1.8 The Skin -- 2.1.9 Head and Neck -- 2.1.10 Gastrointestinal System -- 2.1.11 Hypercalcaemia -- 2.1.12 Haemophagocytic Lymphohistiocytosis (HLH) -- 2.1.13 Aplastic Presentation -- 2.1.14 Rare Presentations -- 2.1.15 Asymptomatic Pancytopenia -- 2.1.16 The Diagnostic Interval and Pathway -- 2.1.17 Differential Diagnosis -- 2.2 Laboratory Features -- 2.2.1 Haematology -- 2.2.2 Biochemistry -- 2.2.3 Bone Marrow Aspirate -- 2.2.4 Lumbar Puncture -- 2.3 Diagnostic Workup -- 2.4 Prognostic Factors -- 2.5 Individual Prognostic Factors -- 2.5.1 Age -- 2.5.2 White Cell Count -- 2.5.3 NCI Risk Score -- 2.5.4 Gender -- 2.5.5 CNS Disease -- 2.5.6 Disease Bulk -- 2.5.7 Immunophenotype -- 2.5.8 Genetics -- 2.5.9 Response to Treatment -- References -- Chapter 3: Diagnostic Flow Cytometry and Immunophenotypic Classification -- 3.1 Introduction -- 3.2 Immunophenotype of T-Lymphoblastic Leukemia/Lymphoma -- 3.3 Early T-Cell Precursor ALL -- 3.4 Immunophenotype of B-Lymphoblastic Leukemia/Lymphoma -- 3.5 Acute Leukaemia of Ambiguous Lineage -- 3.6 Antigen Expression: Correlation to Prognosis and Cytogenetics -- 3.7 Extended Leukaemia Immunophenotyping -- 3.8 Conclusions and Perspective -- References -- Chapter 4: Cytogenetics and Molecular Genetics -- 4.1 Introduction -- 4.2 Abnormality Detection Methodologies -- 4.3 Chromosomal Abnormalities in BCP-ALL -- 4.3.1 Favourable Risk Abnormalities -- 4.3.1.1 High Hyperdiploidy -- 4.3.1.2 t(12 -- 21)(p13 -- q22)/ETV6-RUNX1 -- 4.3.1.3 t(1 -- 19)(q23 -- p13)/TCF3-PBX1 -- 4.3.2 Poor-Risk Chromosomal Abnormalities -- 4.3.2.1 t(9 -- 22)(q34 -- q11.1)/BCR-ABL1 -- 4.3.2.2 t(17 -- 19)(q22 -- p13)/TCF3-HLF -- 4.3.2.3 11q23/KMT2A Gene Rearrangements -- 4.3.2.4 Near-Haploidy and Low Hypodiploidy -- 4.3.2.5 Intrachromosomal Amplification of Chromosome 21 (iAMP21) -- 4.3.3 B-ALL Lacking Sentinel Chromosomal Rearrangements -- 4.3.3.1 Ph-Like or BCR-ABL1-Like ALL -- 4.3.3.2 CRLF2 Rearrangements and Janus Kinase Mutations in ALL -- 4.3.3.3 DUX4 and ERG-Deregulated ALL -- 4.3.3.4 Translocations Involving the IGH Locus -- 4.3.3.5 PAX5 Rearrangement.
s -- MEF2D and ZNF384 Gene Fusions -- ETV6-RUNX1-Like -- 4.3.4 Secondary Genetic Alterations in BCP-ALL -- 4.4 Genetic Rearrangements in T-Lineage ALL -- 4.4.1 TAL1/LMO2 Rearranged T-ALL -- 4.4.2 TLX1/TLX3 Rearranged T-ALL -- 4.4.3 Early T-Cell Precursor ALL -- 4.4.4 Other T-ALL Genetic Subtypes: KMT2A Rearranged and PICALM-MLLT10 -- 4.5 Relapsed ALL -- 4.6 Inherited Genetic Variation and ALL Risk -- 4.7 Future Strategies/Conclusions -- References -- Chapter 5: Pharmacokinetics, Pharmacodynamics and Pharmacogenetics of Antileukemic Drugs -- 5.1 Introduction -- 5.2 Pharmacokinetics and Pharmacodynamics -- 5.3 Pharmacogenetics -- 5.4 Glucocorticosteroid -- 5.5 Vincristine -- 5.6 Anthracyclines -- 5.7 Asparaginase -- 5.8 Thiopurines -- 5.9 Methotrexate -- 5.10 Cytosine Arabinoside -- 5.11 Cyclophosphamide and Ifosfamide -- 5.12 Epipodophyllotoxins -- 5.13 Intrathecal Chemotherapy and Central Nervous System Leukemia -- 5.14 Patient Adherence and Physician Compliance -- 5.15 Treatment of Infants -- 5.16 Treatment of Adolescents -- 5.17 Treatment of Obese Patients -- 5.18 ALL Predisposition Syndromes and Chemotherapy -- 5.19 Conclusions and Future Perspectives -- References -- Chapter 6: Minimal Residual Disease (MRD) Diagnostics: Methodology and Prognostic Significance -- 6.1 Introduction -- 6.2 Standard MRD Methods -- 6.2.1 Quantitative PCR of Immunoglobulin and T Cell Receptor Gene Re-arrangement (IG-TR) Targets (DNA Level) -- 6.2.2 Classical Multicolor (4–6-Color) Flow-MRD -- 6.2.3 Real-Time Quantitative Reverse Transcriptase (RQ-RT)-PCR of Fusion Gene Transcripts -- 6.3 Sample Requirements -- 6.3.1 Monitoring of Bone Marrow Samples, Not Blood Samples -- 6.3.2 Homogeneous Distribution of ALL Cells over BM During Treatment -- 6.3.3 Always Use the First Pull Aspirate for Obtaining Reliable MRD Measurements -- 6.4 Prognostic Value of MRD Diagnostics -- 6.4.1 Frontline Treatment -- 6.4.2 Treatment Reduction in MRD-Based Low-Risk Patients? -- 6.4.3 Stem Cell Transplantation, Relapse Treatment, and Innovative Drugs -- 6.4.4 Continuous Monitoring After Induction Treatment? -- 6.5 New High Throughput MRD Technologies -- 6.5.1 EuroFlow-Based (≥8-Color) Next Generation Flow-­MRD (NGF-MRD) -- 6.5.2 High-Throughput Sequencing (HTS) of IG-TCR Targets (DNA Level) -- 6.6 Conclusions -- References -- Chapter 7: First Line Treatment: Current Approach -- 7.1 Introduction -- 7.1.1 Drugs and Protocols -- 7.1.2 Historical Background -- 7.1.2.1 Intensification Therapy -- 7.1.2.2 CNS Directed Therapy: Is Cranial Radiotherapy Essential? -- 7.1.2.3 Intravenous Methotrexate -- 7.1.2.4 Steroid, Asparaginase and Thiopurine Formulation -- 7.1.2.5 Purine Analogues and Proteasome Inhibitors -- 7.1.2.6 Haemopoietic Stem Cell Transplant (HSCT) -- 7.1.3 Current UK Strategy -- 7.1.3.1 Risk Stratification -- 7.1.3.2 Treatment -- 7.1.3.3 Induction and Consolidation -- 7.1.3.4 Interim Maintenance and Delayed Intensification -- 7.1.3.5 Continuation Therapy -- 7.1.3.6 Steroid and Asparag.
inase Formulations, Doses and Schedules -- 7.1.3.7 Central Nervous System (CNS) Directed Therapy -- 7.1.3.8 Allogeneic Haemopoietic Stem Cell Transplantation (HSCT) -- 7.2 Current Outcomes -- 7.3 Treatment of Distinct Sub-groups -- 7.3.1 Young People (Age 16–25 Years) -- 7.3.2 Infants -- 7.3.3 Down Syndrome -- 7.4 Future Strategies and Conclusions -- References -- Chapter 8: Targeted Therapy and Precision Medicine -- 8.1 Introduction -- 8.2 Precision Medicine for B-ALL -- 8.2.1 Kinase Inhibition for BCR-ABL1-Rearranged (Ph+) ALL -- 8.2.2 Kinase Inhibition for BCR-ABL1-Like (Ph-Like) ALL -- 8.2.3 FLT3 Receptor Kinase Inhibition for KMT2A (MLL)-Rearranged ALL -- 8.2.4 MAP Kinase Inhibition for RAS Pathway-Mutant ALL -- 8.3 Precision Medicine for T-ALL -- 8.3.1 Kinase Inhibition for T-ALL -- 8.3.2 Gamma Secretase Inhibition for Notch1-Mutant T-ALL -- 8.4 Future Strategies/Conclusions -- References -- Chapter 9: Monoclonal Antibodies in Pediatric Acute Lymphoblastic Leukemia -- 9.1 Monoclonal Antibodies -- 9.1.1 Introduction -- 9.1.2 Structure of Monoclonal Antibodies (moAbs) -- 9.1.3 Clinical Use of moAbs -- 9.2 Target Antigens in Acute Lymphoblastic Leukemia -- 9.3 Naked moAbs -- 9.3.1 CD52 -- 9.3.1.1 Alemtuzumab -- 9.3.2 CD20 -- 9.3.2.1 Rituximab -- 9.3.2.2 Ofatumomab -- 9.3.2.3 Other Anti-CD20 moAbs -- 9.3.3 CD22 -- 9.3.3.1 Epratuzumab -- 9.4 MoAb-Drug Conjugates -- 9.4.1 CD22 -- 9.4.1.1 Moxetumomab -- 9.4.1.2 Inotuzumab Ozogamicin -- 9.4.2 CD19 -- 9.4.2.1 SAR3419 -- 9.4.3 CD19/CD22 -- 9.4.3.1 Combotox -- 9.4.3.2 DT2219 -- 9.5 Radioimmunotherapy -- 9.5.1 CD20 -- 9.5.2 CD22 -- 9.6 T Cell Engaging Antibodies/MoAb T Cell Conjugates -- 9.6.1 CD19 -- 9.6.1.1 Blinatumomab -- 9.6.2 CD20 -- 9.7 T Cell Targets -- 9.7.1 CD7 -- 9.7.2 CD5 -- 9.7.3 CD2 -- 9.8 Inhibitory T Cell Pathways -- 9.8.1 CTLA-4 -- 9.8.1.1 Ipilimumab -- 9.8.2 PD-1 Inhibitors -- 9.8.2.1 Nivolumab -- 9.8.2.2 Pembrolizumab -- 9.8.2.3 Pidilizumab -- 9.8.3 PD-L1 Inhibitors -- 9.8.3.1 AMP-224 -- 9.8.3.2 MPDL3280A -- 9.8.4 CD137 -- 9.8.5 CCR4 -- 9.9 Future Strategies/Conclusions -- References -- Chapter 10: Cellular Therapy -- 10.1 Introduction -- 10.2 Non-gene Engineered Cellular Therapies -- 10.2.1 Donor Leucocyte Infusions -- 10.2.2 Cytokine Induced Killer Cells -- 10.3 CAR-Engineered Cellular Therapies -- 10.3.1 Basic Principles -- 10.3.2 CD19 as a Target Antigen for CAR Therapy -- 10.3.3 T Cell Populations for CD19 CAR Transduction -- 10.3.4 CD19 CAR T Cell Therapy in B-ALL -- 10.3.5 Lessons Learnt from ALL Studies -- 10.3.5.1 Clinical Outcomes in Relation to CD19 CAR Design -- 10.3.5.2 Factors Associated with Improved Outcomes Following CD19CAR Therapy -- 10.3.5.3 Toxicity -- B Cell Aplasia -- Cytokine Release Syndrome (CRS) -- Neurotoxicity -- 10.4 Other CAR T Cell Targets in ALL -- 10.5 Future Directions -- References -- Chapter 11: Relapsed Acute Lymphoblastic Leukemia of Childhood -- 11.1 Introduction -- 11.2 Pathogenesis of Relapsed ALL -- 11.2.1 CNS Relapses -- 11.2.2 Bone Marrow R.

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