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  Adult craniopharyngiomas : differences and lessons from paediatrics

  Emmanuel Jouanneau, Gérald Raverot, editors.

  Summary: This volume focuses on adult craniopharyngiomas, offering various perspectives. The first part of the book provides an up-to-date overview of the pathogenesis and management of adult craniopharyngiomas, helping readers understand the pathogenesis and molecular pathways. It highlights the importance of animal models for addressing molecular keys and for developing targeted therapies. The second part deals with clinical management, detailing the latest results in the era of endoscopic surgery, including the major contribution of the extended nasal endoscopic approaches for suprasellar and retrochiasmatic tumors. The book also discusses the key aspects of these tumors and how to manage them. The last part of the book addresses the future therapies and recurrences after surgery and radiotherapy. This volume is of interest to neurosurgeons, endocrinologists, paediatricians, radiologists and oncologists.
  
  Contents:
  Intro
  Foreword 1
  Foreword 2
  Acknowledgement
  Contents
  1: Histopathology and Molecular Pathology of Craniopharyngioma in Adults
  1.1 Introduction
  1.2 Adamantinomatous Craniopharyngioma
  1.2.1 Histopathology
  1.2.1.1 Histopathological Features
  1.2.1.2 Regressive Changes and Surrounding Nervous Tissue
  1.2.2 Molecular Pathology
  1.2.3 ACP and Odontogenesis
  1.3 Papillary Craniopharyngioma
  1.3.1 Histopathology
  1.3.2 Molecular Pathology
  1.3.3 Origin of PCP
  1.4 Mixed and Collision Tumors
  1.5 Malignant Transformation in Craniopharyngiomas 1.6 Differential Diagnosis
  1.6.1 ACP and Pilocytic Astrocytoma
  1.6.2 PCP and Rathke's Cleft Cyst with Squamous Metaplasia
  1.6.3 ACP and Sellar Xanthogranuloma
  1.6.4 ACP Versus PCP
  1.6.5 Cystic ACP and Rathke's Cleft Cysts
  1.7 Conclusion
  References
  2: Mouse Models of Craniopharyngioma
  2.1 Genetically Engineered Mouse Models (GEMMS) of Craniopharyngioma
  2.1.1 Adamantinomatous Craniopharyngioma
  2.1.2 Embryonic Model of Human ACP
  2.1.3 Inducible Model of Human ACP 2.2 Stem Cell Paracrine Tumourigenesis: A Novel Mechanism of Somatic Stem Cells Contribution to Tumour Formation
  2.3 Childhood-Onset Craniopharyngioma is a Developmental Disorder
  2.4 Cluster Cells Are Molecularly Similar and Share a Signature of Cellular Senescence
  2.5 Papillary Craniopharyngioma and Adamantinomatous Craniopharyngioma are Distinct Tumour Entities
  2.6 Patient-Derived Xenografts (PDXs) Models of Human Craniopharyngioma
  2.7 Therapeutic Lessons from Mouse Models
  2.8 Conclusion
  References 3: Epidemiology, Clinical Presentation, and Prognosis of Adult-Onset Craniopharyngioma
  3.1 History
  3.2 Epidemiology of Adult-Onset CP
  3.3 Clinical Presentation of Adult-Onset Craniopharyngioma
  3.3.1 Our series (Table 3.1)
  3.3.1.1 Ophthalmology
  3.3.1.2 Endocrine Symptoms
  3.3.1.3 Non-specific Symptoms
  3.3.1.4 Hypothalamic and Limbic Symptoms
  3.3.1.5 Radiology and Histology
  3.3.2 Literature
  3.3.2.1 Ophthalmology
  3.3.2.2 Endocrine
  3.3.2.3 Hypothalamic and Limbic Symptoms
  3.3.2.4 Other Symptoms 3.4 Long-Term Morbidity and Mortality in Treated Adult-Onset CP
  3.4.1 Morbidity
  3.4.1.1 Endocrine Morbidity
  3.4.1.2 Ophthalmologic Morbidity
  3.4.1.3 Hypothalamic Morbidity
  3.4.2 Mortality
  3.5 Modern Management of CP Improves Prognosis?
  3.6 Conclusion
  References
  4: Craniopharyngioma Diagnosis: A Rationale for Accurate MRI Assessment of Tumor Topography and Adhesion to the Hypothalamus
  4.1 Introduction. MRI Assessment of Craniopharyngiomas: What Essential Information Should a Neurosurgeon Obtain from It?

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• Article

  Modulations of myelopoiesis in vivo by chemically pure preparations of cell wall components from gram-negative bacteria: effects at different stages.

  Staber FG, Tarcsay L, Dukor P.

  Infect Immun. 1978 Apr;20(1):40-9.

  Modulation of myelopoiesis by chemically pure preparations of different cell wall components from gram-negative bacteria was investigated in vivo. The effects of lipid A, outer membrane lipoprotein, and murein were evaluated at several distinct stages: induction of colony-stimulating activity (CSA) in the serum, increase in the number of committed splenic precursor cells (CFU-C) forming granulocyte-macrophage colonies in vitro, and triggering into the cell cycle of noncommitted hemopoietic stem cells (CFU-S) from bone marrow. The results reveal different patterns of activity of the bacterial cell wall components (BCWC) tested. (i) In C57Bl/6 mice and C3H/Bom mice, all three preparations were potent inducers of CSA. In C3H/HeJ mice, CSA was only induced by lipoprotein and murein and not by lipid A. After injection of lipid A or lipoprotein, but not murein, the number of CFU-C in spleens of C57Bl/6 mice was increased up to 100-fold. In C3H/Bom and C3H/HeJ mice, not only murein but also lipoprotein were much less potent in this respect. (iii) In C57Bl/6 mice, both lipid A and lipoprotein, but not murein, were capable of inducing the proliferation of CFU-S, as demonstrated by a hot thymidine cytocide technique. Thus, induction of CSA and changes in the pool size of splenic CFU-C after administration of BCWC may be unrelated events. On the other hand, the increase of CFU-C might reflect the mitogenicity of BCWC for CFU-S.

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  PubMed