Acute Myeloid Leukemia: Diagnosis, Prognosis, Treatment and Outcomes

Name: Acute Myeloid Leukemia: Diagnosis, Prognosis, Treatment and Outcomes
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This book is written by multidisciplinary specialists who diagnose and treat acute myeloid leukemia (AML) patients and is meant for anyone interested in the clinical care of patients with hematologic malignancies, including students and trainees. The 21 contributors for this book include expert clinicians in leukemia and hematologic malignancies, infectious diseases, pharmacological drug administration, pathology, cytogenetics, molecular genetics, and artificial intelligence, and one medical student and advanced trainees. The book comprises nine chapters, starting with a comprehensive overview of the global epidemiology, etiology, prognosis, treatment, and outcomes in patients with AML. Chapter 2 describes the classification of myeloid neoplasms, including AML, with a historical perspective and current diagnostic criteria. This chapter describes the fifth edition of the World Health Organization (WHO) classification and the updates from the revised fourth edition of the WHO classification. It compares the similarities and differences from the International Consensus Classification. Chapter 3 is focused on genetic evaluation in AML, emphasizing cytogenetic techniques, with numerous illustrations depicting genetic abnormalities in AML. Chapter 4 discusses measurable residual disease (MRD) in AML and explains the approaches and current guidelines for MRD detection by multiparametric flow cytometry and molecular techniques, emphasizing the pre-analytical, analytical, and post-analytical factors in evaluating MRD, with illustrations for essential concepts. Chapter 5 describes clonal hematopoiesis and its role in the development of myeloid neoplasms. Chapter 6 discusses inherited germline predisposition to myeloid malignancies, including inherited bone marrow failure syndromes and syndromic and non-syndromic predisposition syndromes for hematologic malignancies. Chapter 7 describes and illustrates novel therapeutic agents in AML, including genetically-targeted therapies, non-genetically targeted therapies, and immunotherapies. Chapter 8 covers the management of infectious complications in patients with AML, and Chapter 9 introduces the reader, with many illustrations, to the emerging applications of artificial intelligence in diagnostic hematopathology.

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Intro
Contents
Preface
Acknowledgments
Chapter 1
Acute Myeloid Leukemia: A Global Perspective of Epidemiology, Prognosis, Treatment and Outcomes
Abstract
Abbreviations
1.1. Introduction
1.2. Epidemiology
1.2.1. Incidence
1.2.2. Disease Burden
1.2.3. Patient Age
1.2.4. Genetics
1.3. Etiology
1.3.1. Environmental Factors
1.3.2. Previous Treatment for Cancer
1.3.3. Patients' Predisposing Factors
1.4. Pathogenesis
1.4.1. Driver Mutations
1.4.2. Leukemia Stem Cells
1.4.3. Pre-Leukemia Cells
1.5. Clinical Features
1.6. Diagnosis
1.6.1. Diagnosis and Classification
1.7. Prognostic Factors
1.7.1. Cytogenetic and Molecular Aberrations
1.7.2. Treatment Response
1.8. Treatment
1.8.1. Therapy for Adult AML
1.8.1.1. The Incorporation of Novel Agents in the Frontline Therapy of AML
1.8.1.2. The Stratified Post-Remission Treatments
1.8.1.3. Maintenance Therapies
1.8.1.4. AML in China: Specific Aspects
1.8.1.4.1. Diagnosis
1.8.1.4.2. Genetic Risk Stratification
1.8.1.4.3. Homoharringtonine Used in China
1.8.1.4.4. Unrelated Cord Blood Transplantation
1.8.2. Therapy for Older Patients with AML
1.8.3. Therapy for Relapsed or Refractory AML
1.8.4. Therapy for Acute Promyelocytic Leukemia (APL)
1.8.5. Summary of Significant Clinical Trials Discussed in This Chapter for Treating Patients with AML
1.9. Outcomes
10. Future Perspectives
Conclusion
References
Chapter 2
The Diagnostic Classification of Myeloid Neoplasms with Emphasis on Acute Myeloid Leukemia
Abstract
Abbreviations
2.1. Introduction
2.1.1. Epidemiologic Characteristics of Acute Myeloid Leukemia and Myelodysplastic Neoplasms in the U.S.A
2.2. Historical Background
2.2.1. Early Descriptions: Hematology and Genetics in Acute Myeloid Leukemia
2.2.2. The Diagnostic Classifications of Acute Myeloid Leukemia from 1976 to 2017
2.2.2.1. Acute Myeloid Leukemia Diagnosis and Classification by the FAB Group: Primarily Morphology-Based
2.2.2.2. Flow Cytometric Immunophenotypic Analysis in Acute Leukemias: Earliest Incorporation in the Diagnosis of AML
2.2.2.3. Myeloid Neoplasms in the World Health Organization Classification in 2001: Incorporation of Cytogenetics and Molecular Genetics in the Diagnostic Classification of Acute Myeloid Leukemia
2.2.2.3.1. Types of Acute Myeloid Leukemia Recognized by the WHO 2001 Classification, as Shown in Table 2
2.2.2.3.2. Types of Myelodysplastic Syndromes Recognized by the WHO 2001 Classification, as Shown in Table 2
2.2.2.4. The Fourth Edition 2008 WHO Classification of Tumors of the Hematopoietic and Lymphoid Tissues
2.2.2.4.1. Types of AML Recognized by the WHO 2008 Classification (in the Context of Other Myeloid Neoplasms Recognized by WHO 2008)
2.2.2.4.2. Acute Leukemias of Ambiguous Lineage Recognized by the WHO 2008 Classification
2.2.2.4.3. Types of MDS Recognized by the WHO 2008 Classification
2.2.2.4.4. Other Myeloid Neoplasms Recognized by the WHO 2008 Classification
2.2.2.5. The Revised Fourth Edition 2017 WHO Classification of Tumors of the Hematopoietic and Lymphoid Tissues
2.2.2.5.1. Types of AML and Related Precursor Neoplasms Recognized by the WHO 2017 Classification
2.2.2.5.2. Acute Leukemias of Ambiguous Lineage Recognized by the WHO 2017 Classification
2.2.2.5.3. Nomenclature Changes for the Types of MDS in the WHO 2017 Classification
2.2.2.5.4. Other Myeloid Neoplasms Recognized by the WHO 2017 Classification
2.2.2.5.5. Myeloid Neoplasms with Germline Predisposition in the WHO 2017 Classification
2.3. The Fifth Edition of the WHO Classification of Tumors
2.3.1. The Creation of Two Parallel Classifications in 2022 for Hematolymphoid Tumors
2.3.2. The Fifth Edition WHO Classification of Hematolymphoid Tumors in 2022
2.3.2.1. The Fifth Edition WHO Classification of Myeloid Proliferations and Neoplasms
2.3.2.1.1. Tables 18-19: Myeloid Proliferations and Neoplasms, and Histiocytic/Dendritic Cell Neoplasms in the WHO 2022 Classification
2.3.2.1.2. Clonal Hematopoiesis (CH), Age-Related CH, CH of Indeterminate Potential (CHIP), and Clonal Cytopenia of Undetermined Significance (CCUS)
2.3.2.1.3. Chronic Myeloid Leukemia (CML)
2.3.2.1.4. BCR::ABL1-Negative Myeloproliferative Neoplasms (MPN)
2.3.2.1.5. Types of Mastocytosis
2.3.2.1.6. Myelodysplastic Neoplasms (Previously Termed Myelodysplastic Syndromes)
2.3.2.1.6.1. Tables 22-23: Types of Myelodysplastic Neoplasms
2.3.2.1.7. Myelodysplastic/Myeloproliferative Neoplasms
2.3.2.1.8. Acute Myeloid Leukemia Diagnosis and Classification by WHO-HAEM5 Criteria
2.3.2.1.8.1. Significant Changes in AML Classification in the Fifth Edition Compared with the Fourth Edition of the WHO Classification
2.3.2.1.9. Acute Leukemias of Ambiguous Lineage by the Fifth Edition of the WHO Classification
2.3.2.1.10. Blastic Plasmacytoid Dendritic Cell Neoplasms Are Now Included in the Histiocytic/Dendritic Cell Neoplasms Category
2.3.2.1.11. Secondary Myeloid Neoplasms in the Fifth Edition of the WHO Classification
2.3.2.1.11.1. Myeloid Neoplasms Post-Cytotoxic Therapy
2.3.2.1.11.2. Myeloid Neoplasms Associated with Germline Predisposition in the Fifth Edition of the WHO Classification
2.3.2.1.11.3. Down Syndrome-Associated Myeloid Neoplasms in the Fifth Edition of the WHO Classification
2.3.2.2. The Fifth Edition WHO Classification Compared with the International Consensus Classification of Hematolymphoid Tumors
2.3.2.2.1. The ICC of Myeloid Neoplasms and Acute Leukemia
2.3.2.2.2. Pre-Neoplastic Myeloid Precursor States, Myelodysplastic Neoplasms, and AML Classification Comparison (WHO-HAEM5 and ICC)
2.3.2.2.2.1. Pre-Neoplastic Myeloid Precursor States in WHO-HAEM5 and the ICC
2.3.2.2.2.2. Types of Myelodysplastic Neoplasms (Previously Myelodysplastic Syndromes) in WHO-HAEM5 and the ICC
2.3.2.2.2.3. Diagnostic Criteria for the Genetically Defined Types of Myelodysplastic Neoplasms (Previously Myelodysplastic Syndromes) in WHO-HAEM5 and the ICC
2.3.2.2.2.4. Terminology Changes in MDS with Increased Blasts Compared across the Fourth and Fifth Editions of the WHO Classification and the ICC
2.3.2.2.2.5. Table 36: Comparison of the Types of AML in WHO-HAEM5 and the ICC
2.3.2.2.3. Myeloproliferative Neoplasms and Myeloproliferative/Myelodysplastic Neoplasms Classification Comparison (WHO-HAEM5 and ICC)
2.3.2.2.3.1. Chronic Myeloid Leukemia (WHO-HAEM5 and ICC)
2.3.2.2.3.2. BCR::ABL1-Negative Myeloproliferative Neoplasms (WHO-HAEM5 and ICC)
2.3.2.2.3.3. Myelodysplastic/Myeloproliferative Neoplasms by WHO-HAEM5 and the ICC
2.4. The Other Chapters in this Book
2.5. Future Perspectives
Conclusion
References
Chapter 3
Genetic Evaluation in Acute Myeloid Leukemia
Abstract
Abbreviations
3.1. Introduction
3.2. Techniques and A Brief Overview of Methods
3.2.1. Karyotyping
3.2.1.1. Technique Overview for Obtaining Chromosomes for Karyotyping
3.2.1.2. Nomenclature: How to Read and Understand Karyotypes
3.2.1.3. Advantages/Limitations of Chromosome Analysis or Karyotyping
3.2.2. Fluorescence In Situ Hybridization
3.2.2.1. Technique Overview
3.2.2.2. FISH Probe Types and Uses
3.2.2.3. Figure 7: FISH Probe Designs
3.2.2.3.1. Dual-Color FISH Probes
3.2.2.3.2. Dual-Color, Extra Signal FISH Probe
3.2.2.3.3. Dual-Color, Dual-Fusion FISH Probe
3.2.2.3.4. Break-Apart FISH Probe
3.2.2.4. Nomenclature: How to Read and Understand FISH Results
3.2.2.4.1. Figure 8 (A-N)
FISH Abnormalities in Examples of AML
3.2.2.5. Advantages and Limitations of FISH
3.2.3. Chromosomal Microarray
3.2.3.1. Technique Overview and Concepts
3.2.3.2. Abnormalities Detected by Chromosomal Microarrays (CMAs)
3.2.3.3. Nomenclature: How to Read a Chromosomal Microarray Result
3.2.3.4. Advantages and Limitations of Chromosomal Microarrays
3.3. Integrating the Results of Different Cytogenetic Techniques and Assay Selection
3.3.1. TP53 Abnormalities in AML as an Example, as Detected by FISH and Chromosomal Microarray
3.4. Genetic Abnormalities Missed by Conventional Cytogenetic Methods
3.5. Detection of Recurrent Genetic Abnormalities in AML
3.5.1. Acute Promyelocytic Leukemia with PML::RARA Fusion
3.5.2. AML with RUNX1::RUNX1T1 Fusion
3.5.3. AML with CBFB::MYH11 Fusion
3.5.4. AML with DEK::NUP214 Fusion
3.5.5. AML with RBM15::MRTFA Fusion (Megakaryoblastic)
3.5.6. AML with BCR::ABL1 Fusion
3.5.7. AML with KMT2A Rearrangement
3.5.8. AML with MECOM Rearrangement
3.5.9. AML with NUP98 Rearrangement
3.5.10. AML with NPM1 Mutation
3.5.11. AML with CEBPA Mutation
3.5.12. AML with Other Defined Genetic Alterations/ AML with Other Rare Recurring Translocations
3.6. Recurrent Somatic Mutations in AML
3.7. Secondary AML
3.7.1. AML, Myelodysplasia-Related
3.7.2. Myeloid Neoplasm, Post-Cytotoxic Therapy
3.8. Future Perspectives
Conclusion
Acknowledgment
References
Chapter 4
Measurable Residual Disease in Acute Myeloid Leukemia
Abstract
Abbreviations
4.1. Introduction
4.2. Biology
4.2.1. Acute Myeloid Leukemia
4.2.2. Classification of AML
4.2.3. Risk Stratification and Prognosis
4.3. Diagnostic Techniques
4.3.1. Aspirate and Trephine Morphology
4.3.2. Flow Cytometry
4.3.3. Conventional Cytogenetics
4.3.4. Molecular Techniques
4.4. Treatment Aims
4.5. What Is Measurable Residual Disease?
4.6. An Overview of Measurable Residual Disease Analysis Techniques
4.6.1. Multiparameter Flow Cytometry: Two Approaches to MRD Evaluation
4.6.2. Molecular Techniques
4.7. Multiparametric Flow Cytometry for MRD Monitoring: Technical Considerations
4.7.1. Pre-Analytical Considerations
4.7.1.1. Sample Collection
4.7.1.1.1. Hemodilution
4.7.1.1.2. Sample Storage
4.7.1.1.3. Sample Transport
4.7.1.2. Sample Processing
4.7.1.3. Other Considerations
4.7.2. Analytical Considerations
4.7.2.1. Monoclonal Antibody Panel Selection
4.7.2.2. Selection of Control Samples
4.7.2.3. Instrument Setting and Zeroing
4.7.2.4. Sample Running and Cell Detection
4.7.2.5. Gating Approach
4.7.3. Post-Analytical Considerations
4.7.3.1. Data Analysis
4.7.3.2. Reporting
4.8. Technical Considerations in the Use of Molecular MRD Monitoring
4.8.1. Preanalytical Considerations
4.8.1.1. Sample Collection
4.8.1.2. Sample Source
4.8.1.3. Hemodilution
4.8.1.4. Duplicate and Self-Collected Samples
4.8.1.5. Sample Storage and Transport
4.8.1.6. Sample Processing
4.8.1.7. Unidirectional Compartmentalization of Preparation and Testing
4.8.2. Analytical Considerations
4.8.2.1. Assay Controls
4.8.2.2. Assessment of DNA Quantity and Quality
4.8.2.3. Agnostic MPS Approaches
4.8.2.4. Detection of Known Variants
4.8.3. Post-Analytical Considerations
4.8.3.1. Defining Sequence Quality and Separating Noise from Variants
4.8.3.2. Attributing Biological Risk and Clinical Significance via Variant Curation
4.8.3.3. Report Generation
4.9. Clinical Applications of MRD in Acute Myeloid Leukemia
4.9.1. Clinical Use of Molecular MRD Evaluation in AML
4.9.1.1. AML with NPM1 Mutation (WHO 2022)
4.9.1.2. Core Binding Factor AML
4.9.1.3. AML with KMT2A Rearrangement (WHO 2022)
4.9.1.4. FLT3-Mutated AML
4.9.1.5. AML with CEBPA Mutation (WHO 2022)
4.9.1.6. AML with IDH1 or IDH2 Mutations
4.9.1.7. AML with DNMT3A, TET2, or ASXL1 Mutations
4.9.2. Clinical Use of MRD Evaluation by MPFC in AML
4.9.2.1. MRD Evaluation by MPFC Post-Intensive Chemotherapy
4.9.2.2. MRD Evaluation by MPFC Post-Allogeneic Stem Cell Transplant
4.10. Future Perspectives
Conclusion
References
Chapter 5
Clonal Hematopoiesis and Acute Myeloid Leukemia
Abstract
Abbreviations
5.1. Introduction
5.2. An Aging Hematopoietic System and Clonal Hematopoiesis
5.3. Definitions: Clonal Hematopoiesis (CH), Clonal Hematopoiesis of Indeterminate Potential (CHIP), and Clonal Cytopenia of Uncertain Significance (CCUS)
5.4. How Did We Learn about Clonal Hematopoiesis?
5.5. Most Common Clonal Hematopoiesis Mutations
5.5.1. Regulation of Gene Expression/Epigenetic Modifiers
5.5.2. RNA Splicing
5.5.3. Cell Signaling Pathway
5.5.4. Cell Cycle/DNA Damage Response
5.6. Why Do Clonal Populations Expand?
5.6.1. Intrinsic Mechanisms
5.6.2. Extrinsic Mechanisms
5.7. Clonal Hematopoiesis and Clinical Associations
5.7.1. Cardiovascular Disease
5.7.2. Other Diseases
5.7.3. Risk of Myeloid Malignancies
5.8. Clinical Evaluation of Clonal Hematopoiesis
5.9. Future Perspectives
Conclusion
References
Chapter 6
Inherited Germline Predisposition in Hematological Malignancy
Abstract
Abbreviations
6.1. Introduction
6.2. Non-Syndromic Hematological Malignancy Predisposition
6.2.1. CEBPA
6.2.2. DDX41
6.2.3. 14q32.2 Genomic Duplication
6.2.4. Clonal Hematopoiesis-Predisposing Germline Genetic Variants
6.3. Inherited Thrombocytopenias
6.3.1. RUNX1-associated Familial Platelet Disorder
6.3.2. ANKRD26--related Thrombocytopenia
6.3.3. ETV6-related Thrombocytopenia
6.4. Inherited or Familial Syndromic MDS
6.4.1. GATA2 Deficiency
6.4.2. SAMD9/SAMD9L
6.5. Inherited Bone Marrow Failure
6.5.1. Diamond-Blackfan Anemia
6.5.2. Fanconi Anemia
6.5.3. Shwachman-Diamond Syndrome
6.5.4. Short Telomere Syndromes
6.5.5. Congenital Neutropenia
6.5.6. Germline ERCC6L2 Mutation
6.5.7. SRP72
6.6. Cell Cycle Pathway: The p53 Pathway
6.6.1. Li-Fraumeni Syndrome (LFS)
6.7. DNA Damage Response and DNA Repair Deficiency Syndromes
6.7.1. Lynch Syndrome
6.7.2. Constitutional Mismatch Repair Deficiency (CMMRD)
6.7.3. Hereditary Breast and Ovarian Cancer
6.7.4. Rare DNA Repair Syndromes
6.7.4.1. Bloom Syndrome
6.7.4.2. Werner Syndrome
6.7.4.3. Nijmegen Breakage Syndrome
6.7.4.4. LIG-4 Syndrome
6.7.4.5. Xeroderma Pigmentosum
6.8. Syndromes with Increased Risk for Hematologic Malignancy
6.8.1. Down Syndrome
6.8.2. RASopathies: RAS/Mitogen-Activated Protein Kinase (RAS/MAPK) Pathway Germline Mutations
6.9. Guidelines and Testing
6.10. Future Perspectives
Conclusion
Acknowledgments
References
Chapter 7
Novel Therapeutics in the Treatment of Acute Myeloid Leukemia
Abstract
Abbreviations
7.1. Introduction
7.1.1. Biological Background
7.1.2. Clinical Discussion
7.2. Novel Therapeutics in AML
7.2.1. Genetically Targeted Therapies
7.2.1.1. Fms-like Tyrosine Kinase 3 (FLT3)
7.2.1.1.1. Midostaurin
7.2.1.1.2. Gilteritinib
7.2.1.1.3. Quizartinib
7.2.1.1.4. Crenolanib
7.2.1.2. Isocitrate Dehydrogenase 1 and 2 (IDH1 and IDH2)
7.2.1.2.1. Enasidenib
7.2.1.2.2. Ivosidenib
7.2.1.2.3. Olutasidenib
7.2.1.2.4. Vorasidenib
7.2.1.3. TP53
7.2.1.3.1. APR-246 (Eprenetapopt)
7.2.1.3.2. MDM2 Inhibitors
7.2.1.4. Other Genetic Drivers Ripe for Targeted Therapies
7.2.1.5. Table 1: Summary of Genetically Targeted Therapies for AML
7.2.2. Non-genetically Targeted Therapies
7.2.2.1. Cellular Transport Pathway Protein XPO1
7.2.2.1.1. Selinexor
7.2.2.1.2. Eltanexor
7.2.2.2. Hypomethylation or Demethylation
7.2.2.2.1. Hypomethylating Agents
7.2.2.2.2. DNMT1 Inhibitors
7.2.2.3. DNA Replication and Repair
7.2.2.3.1. Topoisomerase II
7.2.2.3.1.1. CPX-351 (Vyxeos)
7.2.2.3.1.2. Vosaroxin
7.2.2.3.1.3. Annamycin
7.2.2.4. Apoptosis Pathway
7.2.2.4.1. B-Cell Lymphoma Protein 2 (BCL2)
7.2.2.4.1.1. Navitoclax
7.2.2.4.1.2. Venetoclax
7.2.2.4.2. MCL1 Inhibitors
7.2.2.4.2.1. AZD5991
7.2.2.4.2.2. S63845 and S64315
7.2.2.5. Menin Inhibitors
7.2.2.5.1. SNDX-5613 (Revumenib)
7.2.2.5.2. KO-539 (Ziftomenib)
7.2.2.6. Hedgehog Signaling Pathway
7.2.2.6.1. Glasdegib
7.2.2.7. Table 2: Summary of Novel Non-Genetically Targeted Therapies for AML
7.2.3. Immunotherapies
7.2.3.1. Antibody-Drug Conjugates
7.2.3.1.1. Gemtuzumab ozogamycin
7.2.2.1.2. Tagraxofusp
7.2.2.1.3. IMGN632
7.2.3.2. Bispecific Antibodies
7.2.3.2.1. Flotetuzumab
7.2.3.2.2. XmAb14045 (Vibecotamab)
7.2.3.3. Immune Checkpoint Inhibitors (ICIs)
7.2.3.3.1. Magrolimab
7.2.3.3.2. Sabatolimab
7.2.3.3.3. Nivolumab and Pembrolizumab
7.2.3.3.4. Ipilimumab
7.2.3.4. Cellular Therapy
7.2.3.5. Vaccines
7.2.3.6. Table 3: Summary of Novel Immunotherapies for AML
7.3. Future Perspectives
Conclusion
References
Chapter 8
Acute Myeloid Leukemia and the Propensity for Infectious Complications
Abstract
Abbreviations
8.1. Introduction
8.2. Febrile Neutropenia
8.2.1. Risk Factor Assessment
8.2.2. Approach to a Patient with Febrile Neutropenia
8.2.2.1. Initial Assessment
8.2.2.2. Initial Empiric Antibiotics
8.2.3. Duration of Antibiotic Therapy
8.3. Common Infectious Syndromes
8.3.1. Oral and Esophageal Infections
8.3.2. Enterocolitis
8.3.3. Catheter or Vascular Access Device (VAD) Bloodstream Infections
8.3.4. Cellulitis, Skin and Soft Tissue Infection
8.3.5. Clostridioides difficile-Associated Diarrhea
8.3.6. Invasive Fungal Infections
8.4. Infections Associated with Targeted Therapies
8.4.1. IDH Inhibitors
8.4.2. Midostaurin and Giltertinib
8.4.3. Veneteoclax
8.4.4. Gemtuzumab
8.4.5. Glasdegib
8.5. Antimicrobial Prophylaxis in AML
8.5.1. Bacterial Prophylaxis
8.5.1.1. Fluoroquinolones
8.5.1.2. Cephalosporins
8.5.2. Fungal Prophylaxis
8.5.2.1. Fluconazole
8.5.2.2. Voriconazole
8.5.2.3. Posaconazole
8.5.2.4. Isavuconazole
8.5.2.5. Echinocandins
8.5.3. Pneumocystis Prophylaxis
8.5.4. Herpes simplex Virus Prophylaxis
8.5.5. Hepatitis B prophylaxis
8.5.6. Summary of Antimicrobial Prophylaxis in Adult Hematology Patients
8.6. Other
8.6.1. Strongyloidiasis
8.7. Future Perspectives
Conclusion
References
Chapter 9
Clearing Barriers to the Application of Artificial Intelligence in Hematopathology
Abstract
Abbreviations
9.1. Introduction
9.2. Current Obstacles
9.3. The Solution
9.4. Artificial Intelligence (AI) Algorithms in Hematology
9.4.1. Framework of AI in Hematology
9.4.1.1. Logic Nesting Among Different AI Applications
9.4.2. Some Common Artificial Intelligence Models in Hematology
9.4.2.1. Cell or Blood Smear Image Retrieval
9.4.2.2. Cell or Blood Smear Image Classification
9.4.2.3. Whole Slide Imaging Feature Extraction
9.4.2.4. Cell or Blood Smear Image Segmentation
9.5. Directions of Artificial Intelligence (AI) Application Development in Hematology
9.5.1. Searching and Counting the Rare Cells with Diagnostic Value
9.5.2. A Quick Screen and Quantitative Evaluation of Myelodysplastic Syndromes or Myelodysplastic Neoplasms (MDS)
9.5.3. A Quick Hint of Acute Promyelocytic Leukemia
9.5.4. Universal Differential Count for Bone Marrow Cells
9.5.5. Measurable Residual Disease (MRD) Monitoring
9.5.6. Long-Term Comparative Monitoring of Chronic Lymphocytic Leukemia
9.5.7. Artificial Intelligence Can Detect Molecular Genetic Abnormalities in Myeloproliferative Neoplasms and Acute Myeloid Leukemia
9.6. Future Perspectives
Conclusion
Appendix
CSFA (Curved Surface Focus Algorithm)
Whole Slide Imaging Scanner for Hematopathology
Quantitative Morphology Feature Analysis
Hash Function
Online Virtual Slide Gallery for AI Training (www.digihema.com)
Conflict of Interest
References
Index
Editor's Contact Information
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