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Neuroblastoma

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"Neuroblastoma: Molecular Mechanisms and Therapeutic Interventions comprehensively reviews current concepts in molecular and histopathological mechanisms that influence the growth of human malignant neuroblastoma, along with exciting therapeutic interventions. This book features a broad collection of contributions from leading investigators in histopathology, molecular mechanisms, genetics, epigenetics, microRNAs, proteomics, and metabolism in controlling growth and death in neuroblastoma. Recent developments in therapeutic interventions for neuroblastoma are also covered extensively, including chapters on surgery, chemotherapy, targeted therapy and immunotherapy. This book is ideal for advanced undergraduate students, graduate students, medical students, postdoctoral fellows, and investigators with an interest in current molecular concepts and therapeutic interventions"--Publisher's description.

Neuroblastoma. --- Neuroblastoma --- Treatment.

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Alzheimer’s disease (AD) is described as being the most common cause of dementia among older people. This neurodegenerative illness is characterized by the progressive loss of neurons in the central nervous system in particular at the level of the hippocampus.This neuronal loss which ends up preading to all the cortical areas is responsible, inter alia, for the appearance of serious behavioural problems as well as cognitive disorders.
Histologically, Alzheimer disease is characterized by the presence of senile plaques in the brain. These extracellular lesions contain a core made up mainly of amyloid B peptide (AB). Amyloid B peptide, whose accumulation is at the root of neuronal death, is produced by the cleavage of its precursor: the amyloid precursor protein (APP). APP is a transmembrane protein whose function remains unknown to date. However, several possible functions of APP have been highlighted. Indeed it seems that APP plays an important role in the mechanisms of neuronal plasticity, the regulation of neuronal excitability and cellular adhesion.
In the course of the present work, we have attempted to analyse the physiological functions of APP. To this end, we silenced expression of the gene coding APP in two cells by plasmid ransfection. Initially, we transfected in a stable way a recombinant plasmid mU6pro into cells from hamster ovaries expressing human APP (CHO APP695) thus inducing important morphological modifications. On the other hand, the stable transfection of cell lines of mouse neuroblastoma (N1E 115) with the recombinant mU6pro shows that the partial silencing of the local expression of endogenous mouse APP inhibits the differentiation of N1E 115 cells induced by DMSO. Thus we show that the inhibition of the expression of APP protein alters neuronal plasticity and cellular adhesion both in neuronal and non-neuronal cell lines La maladie d’Alzheimer (MA) est décrite comme étant la première cause de démence chez le sujet âgé. Cette maladie neurodégénérative se caractérise par la perte progressive des neurones du système nerveux central notamment au niveau de l’hippocampe. Cette perte neuronale qui finit par s’étendre à l’ensemble des aires corticales est responsable, entre autres, de l’apparition d’importants troubles du comportement ainsi que des troubles cognitifs.
Histologiquement, la maladie d’Alzheimer se caractérise par la présence dans le cerveau de plaques séniles. Ces lésions extracellulaires contiennent un noyau constitué majoritairement de peptides amyloïde AB. Le peptide amyloïde AB, dont l’accumulation est à l’origine de la mort des cellules neuronale, est produit par le clivage de son précurseur : le précurseur du peptide amyloïde (APP). L’APP est une protéine transmembranaire dont la fonction reste à ce jour inconnue. Cependant, plusieurs fonctions possibles de l’APP ont été mises en évidence. En effet, l’APP jouerait un rôle important dans les mécanismes de plasticité neuronale, de régulation de l’excitabilité neuronale et d’adhésion cellulaire.
Au cours de ce travail, nous avons tenté d’analyser les fonctions physiologiques de l’APP. Pour cela, nous avons éteint l’expression du gène codant l’APP dans deux modèles cellulaires par la technique d’ARN interférent (RNAi). Les ARN interférents ont été exprimés dans les cellules par transfection de plasmide. Dans un premier temps, nous avons transfecté de manière stable un plasmide mU6pro recombinant dans des cellules d’ovaire d’hamster exprimant l’APP humain (CHO APP695) ce qui induit d’importantes modifications morphologiques. D’autre part, la transfection stables des lignées de neuroblastes de souris (N E 115) avec le mU6pro recombinant montre que l’extinction partielle de l’expression de l’APP endogène de souris inhibe la différenciation de l’expression de la protéine APP altère la plasticité neuronale et l’adhésion cellulaire à la fois dans des lignées de cellules neuronales et non-neuronales

CHO Cells --- Neuroblastoma

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Pheochromocytoma, paraganglioma and neuroblastoma are the most common neural crest-derived tumors in adults and children, respectively. These neoplasms are associated with significant morbidity and mortality. Some international studies currently underway are researching and evaluating the presence of any similarities and differences between these tumors. Hopefully, future results will reveal several potential novel genes and pathways that might have major roles in the pathogenesis and progression of these neoplasms. This book discusses epidemiology, genetics, and treatment of these malignancies.

Neuroblastoma. --- Nonchromaffin paraganglioma. --- Pheochromocytoma.

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Adolescent. --- Child. --- Infant. --- Kind. --- Kind. --- Kinderen. --- Neuroblastom. --- Neuroblastom. --- Neuroblastoma. --- Neuroblastoma.