Contemporary Hematology/Oncology

1 Clonal and Stem Cell Origin of Blood Cell Neoplams.- 1.1. Introduction.- 1.2. Mosaic Systems.- 1.2.1. X-Chromosome Inactivation Mosaicism.- 1.2.2. G6PD Markers.- 1.3. Myeloproliferative Disorders.- 1.3.1. Chronic Myelogenous Leukemia.- 1.3.2. Polycythemia Vera.- 1.3.3. Agnogenic Myeloid Metaplasia with Myelofibrosis.- 1.4. Miscellaneous Myeloid Cell Disorders.- 1.4.1. Paroxysmal Nocturnal Hemoglobinuria.- 1.4.2. Sideroblastic Anemia.- 1.5. Blood Cell Lymphoproliferative Neoplasms.- 1.5.1. Immunoglobulin Mosaicism.- 1.5.2. Chronic Lymphocytic Leukemia.- 1.5.3. Plasma Cell Neoplasms.- 1.5.4. Waldenstrom Macroglobulinemia.- 1.5.5. Idiopathic Cold Agglutinin Disease.- 1.6. Lymphoma.- 1.6.1. Burkitt Lymphoma.- 1.6.2. Other B-Cell Lymphomas.- 1.7. Acute Leukemia.- 1.7.1. Acute Lymphoblastic Leukemia.- 1.7.2. Acute Nonlymphoblastic Leukemia.- 1.7.3. Posttransplantation Recurrences of Acute Leukemia.- 1.8. Summary and Concluding Remarks.- 1.8.1. Pluripotent Stem Cell Origin.- 1.8.2. Clonal Origin.- 1.8.3. Pathogenic Implications.- 1.8.4. Diagnostic and Therapeutic Implications.- 1.8.5. Recurrences.- 1.8.6. Second Malignancies in Patients with Chronic Hematopoietic Neoplasms.- 1.8.7. Future Studies.- References.- 2 Interactions of Vessel Wall with Formed Blood Elements.- 2.1. Introduction.- 2.2. Thrombus Formation within the Blood Vessel.- 2.2.1. Blood Flow.- 2.3. The Blood Vessel.- 2.3.1. Endothelial Cells.- 2.3.2. The Subendothelial Zone.- 2.4. Thrombosis on the Subendothelium.- 2.4.1. The Media and Smooth Muscle Cell.- 2.4.2. Adventitia.- 2.5. Endothelial Damage.- 2.6. The Platelet Response.- 2.7. Vascular Response to the Hemostatic Mechanism.- 2.8. Hypercoagulability and Atherogenesis.- 2.9. The Endothelium and Atherogenesis.- 2.10. Control of the Lesion.- 2.11. Summary.- References.- 3 The Effect of Heparin upon Complement Activation.- 3.1. Introduction.- 3.1.1. Pharmacology of Heparin.- 3.1.2. Mechanism of Complement Activation.- 3.1.3. Role of Complement Activation in Human Diseases.- 3.2. Heparin as a Complement Inhibitor.- 3.2.1. Historical Aspects.- 3.2.2. Heparin and the Classic Complement Pathway.- 3.2.3. Heparin and the Alternative Pathway.- 3.2.4. Heparin and the Final Common Complement Pathway.- 3.3. Clinical Implications.- 3.3.1. Paroxysmal Nocturnal Hemoglobinuria.- 3.3.2. Immune Hemolytic Anemia.- 3.3.3. Hypocomplementemic Glomerulonephritis.- 3.3.4. Hereditary Angioneurotic Edema.- 3.3.5. Interaction between Complement and Human Granulocytes.- 3.4. Summary.- References.- 4 The Molecular Genetics of Thalassemia.- 4.1. Introduction.- 4.2. The Thalassemias: The Range of Potential Molecular Defects.- 4.3. Globin Gene Expression.- 4.3.1. Biogenesis, Metabolism, and Structure of Globin Messenger RNAs.- 4.3.2. In Vitro Globin Gene Expression and Chromatin Structure.- 4.4. The Organization of Eukaryotic Genes.- 4.5. The Organization of Globin Genes in Human DNA.- 4.6. Molecular Defects in Thalassemia Syndromes.- 4.6.1. Deletion of Globin Structural Genes.- 4.6.2. Gene Deletion Associated with Abnormal Globin Chains.- 4.6.3. State of the ß Globin Gene in ?0-Thalassemias.- 4.6.4. Nondeletion Thalassemic Defects in Globin Genes.- 4.6.5. Abnormal Globin Messenger RNAs in Thalassemias.- 4.7. Conclusions and Future Prospects.- References.- 5 Blood Group Alterations in Cancer.- 5.1. Introduction.- 5.2. Blood Groups: An Overview.- 5.2.1. Blood Group Serology: Techniques of Antigen Detection and Quantitation.- 5.2.2. Genetic Aspects.- 5.2.3. Blood Group Structure and Biosynthesis.- 5.3. Serologic Studies of Blood Groups in Malignancy.- 5.3.1. Associations of Blood Groups with Cancer.- 5.3.2. Loss of Erythrocytic Blood Groups in Leukemia.- 5.3.3. Alterations of Tissue Blood Group Antigens in Carcinoma.- 5.3.4. Other Malignancies.- 5.3.5. Naturally Occurring Blood Group Agglutinins—Loss in Malignancy.- 5.4. Immunologic Effects of Tumor-Associated Blood Group Alterations.- 5.5. Studies of Cellular Blood Group Structure and Biosynthesis in Malignancy.- 5.5.1. Abnormalities of Cellular Blood Group Glycoconjugates.- 5.5.2. Deficient Production of Glycosyltransferase Enzymes.- 5.5.3. Masking of Antigens by Excessive Neuraminic Acid.- 5.5.4. Relationships of Blood Groups to Carcinoembryonic Antigen.- 5.6. Studies of Blood Groups on Cultured Transformed Cells and Cell-Cell Hybrids: Structure-Function Relationships.- 5.6.1. Relationships of H-Gene-Specified ?-2-Fucosyltransferase and H-Antigen Expression to Growth Patterns of HeLa Cells.- 5.6.2. Cell-Cell Hybrids for Studies of Blood Group Alteration.- 5.6.3. In Vitro Approaches to Structure-Function Relationships of Blood Group Antigens.- 5.7. Discussion.- 5.8. Summary.- References.- 6 Rational Approach to Granulocyte Transfusion Therapy.- 6.1. Introduction.- 6.2. Granulocyte Collection.- 6.2.1. Differential Centrifugation Leukopheresis.- 6.2.2. Filtration Leukopheresis.- 6.3. Therapeutic Granulocyte Transfusion.- 6.4. Histocompatibility Testing.- 6.5. Prophylactic Granulocyte Transfusion.- 6.6. Future Research Methodology.- References.- 7 Mechanisms and Functions of Capping in Lymphocytes.- 7.1. Introduction.- 7.2. Surface Immunoglobulin on B Cells.- 7.3. Kinetics and Pharmacology of sIg Capping.- 7.4. Capping and Cell Motility.- 7.5. Events after Capping.- 7.6. Capping of Other Molecules and Cells.- 7.7. Capping and Membrane Structure: The Fluid Mosaic Model.- 7.8. Capping and the Immune Response.- 7.9. Capping Induced by Antigen.- 7.10. Capping and Chemotaxis.- 7.11. Abnormalities of Capping and Motility.- References.- 8 Amyloidosis.- 8.1. Introduction.- 8.2. Pathology.- 8.2.1. Gross Appearance.- 8.2.2. Tinctorial Properties.- 8.2.3. Light Microscopic Appearance.- 8.2.4. Ultrastructure.- 8.3. Biochemistry of Amyloid.- 8.4. Pathogenesis.- 8.4.1. Secondary, Transfer, and Age-Associated Amyloidosis.- 8.4.2. Serum Amyloid Precursors.- 8.4.3. Immunoregulatory Dysfunction Amyloidosis.- 8.4.4. Macrophages and Bone Marrow Dysfunction.- 8.5. Clinical Aspects.- 8.5.1. Diagnosis.- 8.5.2. General Clinical Manifestations.- 8.5.3. Prognosis.- 8.5.4. Treatment.- References.- 9 The Significance of Terminal Transferase in Normal and Neoplastic Hematopoietic Cells.- 9.1. Introduction.- 9.2. Original Discovery and Biochemistry of TdT.- 9.3. Discovery of TdT in Human Leukemia Cells.- 9.4. Procedures for the Assay of TdT.- 9.5. Characteristics of TdT-Positive Human Leukemias.- 9.6. Significance of TdT in Leukemia Cells.- 9.7. TdT in Leukemia-in-Remission.- 9.8. TdT in Malignant Lymphomas.- 9.9. TdT in Murine Leukemias.- 9.10. Anatomy and Physiology of Normally Occurring TdT-Positive Cells.- References.- 10 Kinin-Releasing Mechanisms in Hemostasis.- 10.1. Introduction.- 10.2. Kinin Release.- 10.3. Surface-Initiated Blood Clotting.- 10.4. Kinin-Releasing Mechanisms and Blood Clotting.- 10.5. The Clot-Promoting Actions of Kinin-Releasing Substances.- 10.6. Prekallikrein: Fletcher Factor.- 10.7. Kininogens and Clotting.- 10.8. Nature of Plasma Kininogens.- 10.9. High-Molecular-Weight Kininogen and Hageman-Factor-Dependent Reactions.- 10.10. What Is Activated Hageman Factor?.- 10.11. Bovine High-Molecular-Weight Kininogen.- 10.12. Kinin-Releasing Mechanisms and Fibrinolysis.- 10.13. The Role of Kinin-Releasing Mechanisms in Collaborative Actions between Intrinsic and Extrinsic Clotting Mechanisms.- 10.14. Concluding Remarks.- References.