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Neuroblastoma

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Opis
Neuroblastomas are tumors of the sympathetic nervous system. Unfortunately, this group of tumors has not shown the same remarkable progress in cure rate that has been achieved in most other childhood malignancies and this is one of the reasons why neuroblastomas have been studied so extensively by pediatric oncologists worldwide. This book summarizes the current state-of-the-art of neuroblastoma biology and therapy. The international authorship of this book illustrates the global interest in neuroblastomas by pediatric oncologists, surgeons, radiologists, biologists, pathologists and others. As it addresses all major areas from basic science to late effects of treatment, it will be a useful resource to a wide range of individuals in basic research, clinical investigation and treatment.
Szczegóły produktu
Butterworth-Heinemann
47928
9780444502223
9780444502223

Opis

Rok wydania
2000
Numer wydania
1
Oprawa
twarda
Liczba stron
610
Waga (g)
1234
  • Preface. List of Contributors.

    Chapter 1. Neuroblastoma: A Historical Perspective 1864--1998

    (A.E. Evans). 1. Initial description and histologic appearance. 2. Incidence. 3. Spontaneous regression. 4. Effect of stage and age. 5. Laboratory prognostic factors. 6. Genetic studies. 7. Success and failure of therapy. References.

    Chapter 2. Development of the Neural Crest and Sympathetic Nervous System

    (S. Pĺhlman, F. Hedborg). Introduction. 1. Neural crest formation and derived structures. 2. Lineage determination of neural crest cells. 3. The sympathetic nervous system. 3.1. Ganglionic and adrenal medullary development. 3.2. Development and physiology of the extra-adrenal chromaffin system. 4. Concluding remarks. References.

    Chapter 3. Concept of Tumorigenesis and Regression

    (P.F. Ambros, G.M. Brodeur). Introduction. 1. Genetics of neuroblastoma: an overview. 1.1. Neuroblastoma subtypes according to the DNA content. 1.2. Structural chromosome aberrations found in diploid and near-triploid tumors. 2. Tumor initiation in neuroblastoma: an unsolved question. 3. MYCN amplification and chromosome 1p deletion: initial events or acquired during tumor evolution? 4. Model of tumorigenesis in neuroblastomas. 5. Spontaneous tumor regression. 5.1. Prerequisites: age and genetics. 5.2. Mechanisms of spontaneous regression. 6. Concluding remarks. References.

    Chapter 4. Epidemiology of Neuroblastoma

    (A.F. Olshan, G.R. Bunin). Introduction. 1. Incidence. 2. Environmental risk factors. 2.1. Parental occupation. 2.2. Medication use. 2.3. Pregnancy history and birth characteristics. 2.4. Lifestyle exposures. 2.5. Association with birth defects. 3. Conclusions and future directions. References.

    Chapter 5. Ploidy and Cytogenetics of Neuroblastoma

    (Y. Kaneko, S.L. Cohn). Introduction. 1. Constitutional chromosome abnormalities in patients with neuroblastoma. 2. Double minutes (dmin) and homogeneously staining regions (hsr) in tumor cells. 3. Deletions of the short arm of chromosome 1 (1p) and gains of the long arm of chromosome 17 (17q). 4. Chromosome abnormalities determined by comparative genomic hybridization (CGH). 5. Ploidy determined by flow cytometric analysis. 6. Ploidy determined by cytogenetic analysis. 7. Multivariate analyses of ploidy and cytogenetic abnormalities. Conclusion. References.

    Chapter 6. Allelic Loss and Neuroblastoma Suppressor Genes

    (P.S. White, R. Versteeg). Introduction. 1. Chromosome 1. 1.1. Deletions of 1p36. 1.2. Proximal 1p and 1q. 1.3. Association of 1p and 17q abnormalities. 2. Chromosomes 2, 3, and 4. 3. Chromosome 9. 4. Chromosome 11. 5. Chromosome 14. 6. Chromosome 17. 7. Chromosome 18. 8. Additional loci. 9. Patterns of chromosomal defects. Summary. References.

    Chapter 7. MYCN Amplification in Neuroblastoma

    (M. Schwab). Introduction. 1. Amplification of MYCN 1.1. Identification of amplified MYCN 1.2. Mechanism of amplification. 1.3. Non-syntenic amplification of MYCN and MDM2 2. Expression of MYCN 3. Cellular consequence of enhanced MYCN expression. 3.1. Cell transformation. 3.2. Advancement of cell cycle progression. 3.3. Sensitizing cells for apoptosis. Acknowledgements. References.

    Chapter 8. Structure of theMYCN Amplicon

    (R.E. George, J.A. Squire). Introduction. 1. Gene amplification. 2. The MYCN amplicon . 2.1. Amplicon size. 2.2. Amplicon structure. 2.3. Rearrangements within the amplicon. 2.4. Presence of coamplified genes. 3. Gene coamplification with MYCN in neuroblastoma. 3.1. Ornithine decarboxylase. 3.2. Ribonucleotide reductase (RRM2). 3.3. Syndecan 1. 3.4. TheN-cym gene. 3.5. pG21/DDX1 3.6. NAS2 and NAS3. 4. The DDX1 gene. 4.1. The DEAD box family. 4.2. The DDX1 gene: structure and function. 4.3. Position of DDX1relative to MYCN. 4.4. DDX1 coamplification with MYCN in neuroblastoma. 4.5. The transforming potential of DDX1. 4.6. Significance ofDDX1coamplification with MYCN in neuroblastoma. 5. Conclusions. Acknowledgments. References.

    Chapter 9. Imprinting of 1p, MYCN and Other Loci

    (H.N. Caron, M.D. Hogarty). Introduction. 1. Genomic Imprinting in Mammals. 1.1. Evidence for mammalian imprinting. 1.2. Molecular characteristics of imprinting. 1.3. Genomic imprinting and cancer. 2. Chromosome 1p tumor suppressor loci in neuroblastoma. 2.1. Evidence for an imprinted 1p suppressor locus in MYCN single-copy neuroblastoma. 2.2. TP73: a candidate gene for the imprinted NBL tumor suppressor locus? 3. MYCN and parent-of-origin effects. 4. Other genes and chromosome regions. Conclusions. References.

    Chapter 10. 17q Gain in Neuroblastoma

    (F. Speleman, N. Bown). Introduction. 1. Cytogenetics and molecular cytogenetics of chromosome 17 abnormalities. 1.1. Classical cytogenetics. 1.2. Molecular cytogenetics. 1.3. Comparative genomic hybridization (CGH) analyses of chromosome 17. 1.4. Analysis of 17q breakpoints in neuroblastoma. 2. 17q Gain as a prognostic factor in neuroblastoma. 2.1. Relationship with known predictive factors. 2.2. Survival analyses: independent predictive power of 17q status. 3. Biological significance of 17q gain in neuroblastoma. Conclusions. References.

    Chapter 11. Genetics of Familial Neuroblastoma

    (J.M. Maris, G.P. Tonini). Introduction. 1. Clinical and etiologic considerations. 1.1. Genetic hypothesis. 2. Associated conditions and constitutional chromosomal abnormalities. 3. Identification of a familial neuroblastoma predisposition locus. 3.1. Pedigree ascertainment. 3.2. Candidate locus approaches. 3.3. Genome-wide approaches. Conclusions. Acknowledgments. References.

    Chapter 12. Expression of MYCN mRNA and Protein

    (S.L. Cohn, N. Ikegaki). Introduction. 1. MYCN amplification and concomitant high levels of MYCN expression. 1.1. The MYCN protein product. 2.MYCN expression correlates with tumor phenotype in vitro. 3. Targeted expression of MYCN in transgenic mice. 4. MYCN expression and its clinical implications. 4.1. Expression of MYCN in primary neuroblastomas. 4.2. Prognostic significance of MYCN expression in neuroblastoma. Acknowledgments. References.

    Chapter 13. Expression and Function of Trk and its Related Genes in Human Neuroblastoma

    (A. Nakagawara, P. Kogner). Introduction. 1. Molecular mechanism of neural crest development. 2. Role of neurotrophins and their receptors in normal nervous system. 3. Role of neurotrophins and their receptors in neuroblastoma. 3.1. Expression and function of Trk family tyrosine kinase receptors in neuroblastoma. 3.1. Expression of neurotrophins in neuroblastoma. 3.2. NGF-induced differentiation of neuroblastoma cells in primary culture. 3.3. TrkA as a prognostic indicator. 3.4. Therapeutic application. 3.5. Role of p75 NTR in neuroblastoma. 4. Other neurotrophic factors and receptors in neuroblastoma . 4.1. GDNF families. 4.2. Midkine/pleiotrophin families. Conclusions. References.

    Chapter 14. Telomerase as a Biological and Prognostic Marker in Neuroblastoma

    (E. Hiyama, C.P. Reynolds). Introduction. 1. Basis of telomere and telomerase. 1.1. Telomere structure and telomere hypothesis. 1.2. Structure and function of telomerase. 2. Telomere and telomerase in neuroblastoma. 2.1. Telomerase activity in neuroblastoma specimens. 2.2. Telomere length in neuroblastoma. 2.3. Telomerase activity and clinical stage. 2.4. Telomerase activity and other biological characteristics of neuroblastoma. 2.5. Telomerase RNA component and telomerase reverse transcriptase in neuroblastoma. 3. Telomere and telomerase in normal development of neuroblasts and in tumorigenesis of neuroblastomas. 4. Future aspects for telomerase in neuroblastoma. References.

    Chapter 15. Expression of Ha-RAS, TP53, and TP73 in Neuroblastoma

    (T. Tanaka, J. Bénard). Introduction. 1. Ha-ras gene expression in Neuroblastoma. 1.1. Immunohistochemistry and prognostic correlation of Ha-ras expression. 1.2. Prognostic discrimination of patients with clinical neuroblastomas. 1.3. Clinical significance of Ha-ras gene expression in neuroblastomas. 2. TP53 and homologs in neuroblastoma. 2.1. TP53 is not mutated in undifferentiated neuroblastomas but sequestered in the cytoplasm. 2.2. TP73 is altered not by mutation but by a specific mechanism in neuroblastoma. 2.3. Frequent but preferential TP73allelic loss in human neuroblastoma. 2.4. Disequilibrium of allelic expression of p73 gene in neuroblastoma tumors but not lymphocytes of patients. Concluding remarks and perspectives. References.

    Chapter 16. Retinoids and Neuroblastoma: Differentiation or Apoptosis?

    (G. Raschellŕ, G. Melino, C.J. Thiele). Introduction. 1. Differentiation pathways in neuroblastoma cells. 1.1. Retinoids. 1.2. Retinoic acid receptors in neuroblastoma. 2. Retinoids regulate apoptosis in neuroblastoma cells. 2.1. Expression of RARs/RXRs receptors in neuroblastoma cells and their regulation of tTG in apoptotic cells. 2.2. Caspases in apoptosis of neuroblastoma cells. 2.3. Bcl-2 family. 3. Retinoid therapy. References.

    Chapter 17. Apoptosis in Neuroblastoma and Pathways Involving Bcl-2 and Caspases

    (H. Ikeda, V.P. Castle). Introduction. 1. Pathways to apoptosis. 1.1. Apoptosis and neurogenesis. 1.2. Apoptosis in neuroblastoma. 2. Apoptosis-modulating gene product expression in neuroblastoma. 2.1. Expression of the anti-apoptotic proteins Bcl-2 and Bcl-xL. 2.2. Expression of caspases. 3. Pathways to apoptosis induction in neuroblastoma. 3.1. Induction of apoptosis by cytotoxic agents. 3.2. Future opportunities/challenges. References.

    Chapter 18. Multidrug Resistance Genes in Neuroblastoma

    (M. Haber, M. Kavallaris). Introduction. 1. ATP-binding cassette (abc) transporters. 1.1. The MDR1 gene/P-glycoprotein. 1.2. The MRP gene. 1.3. The cMOAT/MRP2 gene. 2. Genes involved in detoxification, apoptosis, DNA repair and drug sequestration. 3. The MYCN oncogene. 4. Modulation of multidrug resistance in neuroblastoma. Summary. References.

    Chapter 19. Adhesion Molecules Expression in Neuroblastoma

    (M.C. Favrot, N. Gross). Introduction. 1. Adhesion molecules. 2. Integrins. 3. CD44 hyaluronan receptor. 3.1. Clinical relevance of CD44 expression in neuroblastoma. 3.2. Function and regulation of CD44 expression in neuroblastoma. References.

    Chapter 20. The Role of Schwann Cells in Neuroblastoma

    (I.M. Ambros, P.F. Ambros). Introduction. 1. Schwann cells: embryology and physiology. 2. Maturation of neuroblastomas: genetic aspects. 3. Differentiation of neuroblastoma cells: are they pluripotent? 4. Maturation: biologic aspects. 5. A model of maturation in neuroblastomas. 6. Neuroblastoma cell -- Schwann cell cocultivation. 7. Concluding remarks. Acknowledgments. References.

    Chapter 21. Screening for Neuroblastoma in Infancy in Japan

    (T. Sawada, T. Takeda). 1. Introduction. 1. Milestones in the history of mass screening for neuroblastoma in Japan. 2. Methods and procedure. 3. Results of the Japanese experiences of neuroblastoma screening. 3.1. Present status in Japan. 3.2. Clinical analysis of the 1400 cases. 4. Discussion. 4.1. Incidence of neuroblastoma. 4.2. Changes in age and stage distributions. 4.3. Investigation of changes of number of neuroblastoma deaths. 4.4. Biological characters of cases detected by screening. 4.5. Spontaneous regression. 4.6. Timing and frequency of screening. Summary. References.

    Chapter 22. Mass Screening for Neuroblastoma: The North American Experience

    (B. Lemieux, W.G. Woods). Introduction. 1. Prescreening period. 1.1. Choice of the screened population (experimental group). 1.2. Choice of unscreened control population. 1.3. Choice of methodology. 1.4. Feasibility studies. 2. Screening period: (May 1989 to April 1994). 2.1. Design and implementation. 2.2. Results. 3. Post-screened period. 4. Discussion. Summary and conclusions. Acknowledgments. References.

    Chapter 23. Mass Screening for Neuroblastoma: The European Experience

    (F.H. Schilling, L. Parker). Introduction. 1. Screening before 10 months of age. 1.1. United Kingdom. 1.2. France. 1.3. Germany. 1.4. Austria. 2. Screening after 10 months of age. 2.1. Germany. 2.2. France. 3. Study for the evaluation of neuroblastoma screening in Europe (SENSE). 4. Epidemiological considerations. 5. Biology. 6. Outlook. References.

    Chapter 24. Symptoms of Neuroblastoma: Paraneoplastic Syndromes

    (H. Mugishima, M. Sakurai). Introduction. 1. Primary tumors. 2. Metastatic disease. 3. Paraneoplastic syndromes. References.

    Chapter 25. Imaging of Neuroblastoma and Metastasis

    (C.R. Staalman, C.A. Hoefnagel). Introduction. 1. Conventional imaging. 1.1. Plain radiography. 1.2. Intravenous urography. 1.3. Invasive procedures. 2. Computed tomography. 3. Ultrasonography. 3.1. Procedural aspects. 3.2. Sonographic results. 3.3 Clinical implications. 4. MIBG scintigraphy. 4.1. Procedural aspects. 4.2. Scintigraphic results. 4.3. Clinical implications. 4.4. Pitfalls in MIBG interpretation. 4.5. MIBG and bone scintigraphy. 4.6. Intraoperative detection of neuroblastoma. 4.7. Other tumour-seeking radiopharmaceuticals. 5. Magnetic resonance imaging. 5.1. Esthesioneuroblastoma (olfactory neuroblastoma). 5.2. Procedural aspects. 5.3. MRI results. 6. Comparison and imaging advice. References.

    Chapter 26. Detection of Microscopic Residual Tumors in Bone Marrow

    (N.-K.V. Cheung, M.D. Norris). Introduction. 1. Conventional histology and immunocytology. 1.1. Detection of metastatic neuroblastoma in bone marrow: when is routine marrow histology insensitive? 1.2. Detection of neuroblastoma in the bone marrow by immunocytology: is a single marrow aspirate adequate? 2. Molecular markers. 2.1. Detection of microscopic disease: comparison of histology, immunocytology and RT--PCR. 3. Use of blood for residual disease detection. 4. Summary. References.

    Chapter 27. Histology: Tumors of the Neuroblastoma Group

    (H. Shimada, B. Roald). Introduction. 1. Basic morphology. 1.1.Neuroblastoma (Schwannian stroma-poor). 1.2. Ganglioneuroblastoma, intermixed (Schwannian stroma-rich). 1.3. Ganglioneuroma (Schwannian stroma-dominant). 1.4. Ganglioneuroblastoma, nodular (composite, Schwannian stroma-rich/ stroma-dominant and stroma-poor). 2. Prognostic classification. 3. Biological relevance. 3.1. Schwannian development in neuroblastic tumors. 3.2. MYCN amplification and morphology. 3.3. trkA expression and morphology. 3.4. Composite tumor. Summary. References.

    Chapter 28. Genetic and Biological Markers of Prognosis in Neuroblastoma

    (G.M. Brodeur, P.F. Ambros). Introduction. 1. Ploidy, allelic gain and oncogene activation. 1.1. Tumor cell DNA content or ploidy. 1.2. Amplification of MYCN and other loci . 1.3. Trisomy for 17q. 2. Allelic loss and tumor suppressor genes. 2.1. Chromosome deletion or allelic loss at 1p. 2.2. Allelic loss at 11q, 14q and other sites. 2.3. Involvement of TP53, CDK inhibitor, and NF1 gene. 3. Abnormal patterns of gene expression. 3.1. Expression of neurotrophin receptors. 3.2. Telomerase expression and activity. 3.3. Expression of RAS genes. 3.4. Expression of apoptosis genes. 3.5. Expression of the multidrug resistance genes. 3.6. Expression of CD44 glycoprotein. 3.7. Serum markers. 4. Biologically based risk groups. 5. Genetic model of neuroblastoma development. Acknowledgments. References.

    Chapter 29. Serum Markers and Prognosis in Neuroblastoma: Ferritin, LDH, and NSE

    (H.-W.L. Hann, E. Bombardieri). Introduction. 1. Ferritin. 1.1. Serum ferritin as a prognostic marker. 1.2. Serum ferritin as a tumor marker. 1.3. Biology of ferritin in neuroblastoma. 2. Lactic dehydrogenase (LDH). 3. Neuron-specific enolase (NSE). 3.1. Serum NSE as a prognostic marker. 3.2. Serum NSE as a tumor marker. References.

    Chapter 30. Experimental Therapeutics and New Agents for Neuroblastoma

    (G. Vassal and C.R. Pinkerton). Introduction. 1. New cytotoxic agents in clinical development. 1.1. Topoisomerase I inhibitors. 1.2. Taxanes. 2. Alternative treatment strategies in neuroblastoma. 2.1. Multidrug resistance (MDR) modulators. 2.2. Gene therapy. 2.3. Modulation of apoptosis. 2.4. Inhibitors of angiogenesis. 2.5. Glutathione inhibition (depletion). References.

    Chapter 31. Preclinical Models for Neuroblastoma Therapy

    (D.S. Middlemas, P.J. Houghton). 1. In-vitro models. 1.1. Evaluation of differentiating agents. 1.2. Identification of cellular factors involved in radiation and drug sensitivity. 1.3. Evaluation of novel drugs and resistance mechanisms. 2. In-vivo models. 2.1. Syngeneic models. 2.2. Heterotransplantation models. 3. Models for therapy. 3.1. Specialized rat models. 3.2. Mouse xenografts for chemotherapy studies. Acknowledgements. References.

    Chapter 32. Treatment of Localized Neuroblastoma

    (T. Matsumura, J.Michon). Introduction. 1. Biology of neuroblastoma. 1.1. MYCN gene amplification. 1.2. Histopathology. 2. Treatment. 2.1. General aspects. 2.2. Surgery. 2.3. Chemotherapy. 2.4. Radiotherapy. 2.5. Dumbbell-type neuroblastoma. 3. Screened neuroblastoma and a wait-and-see strategy for localized disease. 4. Future considerations. References.

    Chapter 33. Treatment of Advanced Neuroblastoma: The US Experience

    (K.K. Matthay, R.P. Castleberry). Introduction. 1. Principles of therapy. 2. Induction. 3. Myeloablative therapy. 3.1. Bone marrow purging. 3.2. New myeloablative regimens. 4. Minimal residual disease. 5. Treatment of relapse. 6. Future plans. References.

    Chapter 34. Treatment of Advanced Neuroblastoma: The European Experience

    (O. Hartmann, F. Berthold). Introduction. 1. Methods. 1.1. Bone marrow involvement. 1.2. Skeletal extension. 1.3. Other assessment. 2. Results: Stage 3. 2.1. Induction therapy. 2.2. Surgical procedure. 2.3. Post-surgical therapy. 2.4. Prognostic factors. 3. Results: Stage 4. 3.1. Induction therapy. 3.2. Surgical resection of the primary tumor. 3.3. Post-induction therapy. 3.4. Consolidation therapy. 3.5. Maintenance therapy. 4. Discussion. 4.1. What is the best induction chemotherapy?. 4.2. What is the role of surgical resection of the primary tumor in the treatment of stage 4 disease? 4.3. What is the role of consolidation therapy? 4.4. Is there a place for maintenance chemotherapy? 4.5. What is the role of post-consolidation therapy? 4.6. What are the prognostic factors in stage 4 neuroblastoma? 5. Future prospects. 5.1. For patients with stage 3 disease. 5.2. For patients with stage 4 disease. Acknowledgment. References.

    Chapter 35. Treatment of Advanced Neuroblastoma: The Japanese Experience

    (Y. Tsuchida, M. Kaneko). Introduction. 1. Basic studies on the effectiveness of chemotherapeutic agents. 2. Essential tumor markers in the protocol study. 3. Protocol 1985. 3.1. Results in patients older than 12 months of age. 3.2. Results in patients younger than 12 months of age. 4. Protocol 1991 with stratification of treatment based on N-myc amplification status. 4.1. Outline of protocol 1991. 4.2. Results with protocol 1991 with stratification of treatment. 5. Long-term survivors of advanced neuroblastoma with N-myc amplification. 6. Protocol 1998. 7. Lessons from the Japanese experience. Acknowledgments. References.

    Chapter 36. Radionuclide Therapy of Neuroblastoma:131I-Meta-iodobenzylguanidine (MIBG)

    (P. A. Voűte). Introduction. 1. Treatment procedure. 1.1. MIBG in patients as first-line treatment. 1.2. 131I-MIBG treatment in patients with stage 4 neuroblastoma with curative and palliative intent. 1.3. Patients with recurrent neuroblastoma with curative intent. 2. Side effects of treatment. Conclusion. References.

    Chapter 37. Radiotherapy in neuroblastoma

    (J.L. Habrand, G.J. DAngio). Introduction. 1. Radiosensitivity. 1.1. Radiobiological evidence. 1.2. Clinical evidences. 2. Radiotherapy techniques. 2.1 Total dose and dose fractionation. 2.2 Target volume and protection of organs at risk. 3. Indications. 4. Radiotherapeutical innovations. 5. Disseminated neuroblastoma. 6. Palliative irradiation. 6.1. Skull. 6.2. Soft tissue. 7. Other indications. 8. Late effects of therapy. 8.1. Restricted fields. 8.2. Growth and development. 8.3. Specific organ damage. 8.4. Summary. 9. Total body irradiation (TBI). 9.1. Growth and development. 9.2. Heart and lungs. 9.3. Endocrine function. 9.4. Thyroid. 9.5. Growth hormone (GH). 9.6. Gonads. 9.7. Cataracts. 10. Second malignant neoplasms (SMNs). References.

    Chapter 38. Surgery for Neuroblastoma

    (Y. Tsuchida, M.P. La Quaglia). Introduction. 1. Determination of high-risk and low-risk neuroblastoma. 2. Surgery for high-risk neuroblastoma. 2.1. Background. 2.2. Surgical techniques for advanced (high-risk) neuroblastoma. 3. Complications of surgery for advanced neuroblastoma. 4. Chemotherapy preceding radical surgery in advanced neuroblastoma. 5. Clinical results. 5.1. Stage 3 patients. 5.2. Stage 4 patients. 6. Surgery for low-risk neuroblastoma. 6.1. Introduction. 6.2. Surgery for INSS stage 1, 2A, 2B, and favorable biology stage 3 neuroblastoma. 6.3. Surgery for INSS stage 4S neuroblastoma. 7. The role of the surgeon in initial diagnosis, staging, and supportive care. Summary. Acknowledgment. References.

    Chapter 39. Retinoid Therapy of Neuroblastoma

    (C.P. Reynolds, S.O. Lie). 1. Maturation of cancer cells. 2. Maturation of neuroblastoma. 3. Retinoic acid. 4. Retinoic acid receptors. 5. 13-cis-retinoic acid. 5.1. High-dose, pulse, 13-cis-RA. 5.2. Low-dose, continuous 13-cis-RA in neuroblastoma. 5.3. 13-cis-RA versus all-trans-retinoic acid. 5.4. Phase III trial of high-dose, pulse, 13-cis-RA in neuroblastoma. 5.5. Toxicity of 13-cis-RA. 5.6. Administration of 13-cis-RA. 6. Fenretinide. 6.1. Mechanism of action of fenretinide. 6.2. Clinical experience with fenretinide. Summary. References.

    Chapter 40. Immunotherapy of Neuroblastoma

    (N.-K.V. Cheung, A.L. Yu). Introduction. 1. Immunotherapy. 2. Sensitivity of neuroblastoma to immune destruction. 3. Monoclonal antibodies and clinical trials. 4. Cell-mediated immunity against neuroblastoma. References.

    Chapter 41. Prognosis of Low-Risk and High-Risk Neuroblastoma

    (A.D.J. Pearson, T. Philip). Introduction. 1. Classification system based upon patient age and tumor stage. 2. Therapeutic classification based upon age, stage, and MYCN amplification. 3. Current Paediatric Oncology Group (POG) and Childrens Cancer Group (CCG) risk classification. 4. Other variables to be included in risk classification. 5. Appropriate therapy for risk groups. 6. Refinements of clinical risk groups. 7. The value of molecular versus histological and biochemical markers on an international basis. 8. Long-term cure. Conclusion. References.

    Chapter 42. Late Effects of Treatment for Neuroblastoma

    (A.T. Meadows, Y. Tsunematsu). Introduction. 1. Growth and development. 1.1. Linear growth. 1.2. Thyroid function. 1.3. Gonadal function. 1.4. Ototoxicity. 2. Vital organ function. 2.1. Cardiac function. 2.2. Pulmonary function. 2.3. Renal and urinary tract function. 3. Second neoplasms. 4. Childhood cancer survivor study. Summary and conclusion. References.

    Index.
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