Relevant bibliographies by topics / Neuroblastoma

Academic literature on the topic 'Neuroblastoma'

Author: Grafiati
Published: 4 June 2021
Last updated: 30 July 2024

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Journal articles on the topic "Neuroblastoma"

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Stiborová, Marie, Jitka Poljaková, Tomáš Eckschlager, Rene Kizek, and Eva Frei. "DNA and histone deacetylases as targets for neuroblastoma treatment." Interdisciplinary Toxicology 3, no. 2 (June 1, 2010): 47–52. http://dx.doi.org/10.2478/v10102-010-0010-6.

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DNA and histone deacetylases as targets for neuroblastoma treatmentNeuroblastoma, a tumor of the peripheral sympathetic nervous system, is the most frequent solid extra cranial tumor in children and is a major cause of death from neoplasia in infancy. Still little improvement in therapeutic options has been made, requiring a need for the development of new therapies. In our laboratory, we address still unsettled questions, which of mechanisms of action of DNA-damaging drugs both currently use for treatment of human neuroblastomas (doxorubicin, cis-platin, cyclophosphamide and etoposide) and another anticancer agent decreasing growth of neuroblastomasin vitro, ellipticine, are predominant mechanism(s) responsible for their antitumor action in neuroblastoma cell linesin vitro.Because hypoxia frequently occurs in tumors and strongly correlates with advanced disease and poor outcome caused by chemoresistance, the effects of hypoxia on efficiencies and mechanisms of actions of these drugs in neuroblastomas are also investigated. Since the epigenetic structure of DNA and its lesions play a role in the origin of human neuroblastomas, pharmaceutical manipulation of the epigenome may offer other treatment options also for neuroblastomas. Therefore, the effects of histone deacetylase inhibitors on growth of neuroblastoma and combination of these compounds with doxorubicin, cis-platin, etoposide and ellipticine as well as mechanisms of such effects in human neuroblastona cell linesin vitroare also investigated. Such a study will increase our knowledge to explain the proper function of these drugs on the molecular level, which should be utilized for the development of new therapies for neuroblastomas.
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Wei, Qiang, Zhao Guo, Dong Chen, and Xinjian Jia. "MiR-542-3p suppresses neuroblastoma cell proliferation and invasion by downregulation of KDM1A and ZNF346." Open Life Sciences 15, no. 1 (April 10, 2020): 173–84. http://dx.doi.org/10.1515/biol-2020-0018.

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AbstractNeuroblastoma is one of the most common malignancies in infants and children. MicroRNAs (miRNAs) have been reported as significant regulators that play important roles in neuroblastoma development. This research aimed to analyze the functional mechanism of miR-542-3p in neuroblastoma. Here, we found that miR-542-3p was downregulated and KDM1A as well as ZNF346 were upregulated in neuroblastoma tissues and cells. Both overexpression of miR-542-3p and the knockdown of KDM1A suppressed cell proliferation and invasion in neuroblastomas. Moreover, miR-542-3p reduced the levels of KDM1A and ZNF346 through interaction. Both KDM1A overexpression and ZNF346 upregulation weakened the effect of miR-542-3p on neuroblastoma cells. Besides, miR-542-3p negatively regulated tumor growth in vivo. Our results suggested that miR-542-3p suppressed cell proliferation and invasion by targeting KDM1A and ZNF346 in neuroblastomas, providing a theoretical basis for the treatment of neuroblastoma.
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Ando, Kiyohiro, Yusuke Suenaga, and Takehiko Kamijo. "DNA Ligase 4 Contributes to Cell Proliferation against DNA-PK Inhibition in MYCN-Amplified Neuroblastoma IMR32 Cells." International Journal of Molecular Sciences 24, no. 10 (May 19, 2023): 9012. http://dx.doi.org/10.3390/ijms24109012.

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Identifying the vulnerability of altered DNA repair machinery that displays synthetic lethality with MYCN amplification is a therapeutic rationale in unfavourable neuroblastoma. However, none of the inhibitors for DNA repair proteins are established as standard therapy in neuroblastoma. Here, we investigated whether DNA-PK inhibitor (DNA-PKi) could inhibit the proliferation of spheroids derived from neuroblastomas of MYCN transgenic mice and MYCN-amplified neuroblastoma cell lines. DNA-PKi exhibited an inhibitory effect on the proliferation of MYCN-driven neuroblastoma spheroids, whereas variable sensitivity was observed in those cell lines. Among them, the accelerated proliferation of IMR32 cells was dependent on DNA ligase 4 (LIG4), which comprises the canonical non-homologous end-joining pathway of DNA repair. Notably, LIG4 was identified as one of the worst prognostic factors in patients with MYCN-amplified neuroblastomas. It may play complementary roles in DNA-PK deficiency, suggesting the therapeutic potential of LIG4 inhibition in combination with DNA-PKi for MYCN-amplified neuroblastomas to overcome resistance to multimodal therapy.
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Koneru, Balakrishna, Ahsan Farooqi, Thinh H. Nguyen, Wan Hsi Chen, Ashly Hindle, Cody Eslinger, Monish Ram Makena, et al. "ALT neuroblastoma chemoresistance due to telomere dysfunction–induced ATM activation is reversible with ATM inhibitor AZD0156." Science Translational Medicine 13, no. 607 (August 18, 2021): eabd5750. http://dx.doi.org/10.1126/scitranslmed.abd5750.

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Cancers overcome replicative immortality by activating either telomerase or an alternative lengthening of telomeres (ALT) mechanism. ALT occurs in ~25% of high-risk neuroblastomas, and progression in patients with ALT neuroblastoma during or after front-line therapy is frequent and often fatal. Temozolomide + irinotecan is commonly used as salvage therapy for neuroblastoma. Patient-derived cell lines and xenografts established from patients with relapsed ALT neuroblastoma demonstrated de novo resistance to temozolomide + irinotecan [SN-38 in vitro, P < 0.05; in vivo mouse event-free survival (EFS), P < 0.0001] vs. telomerase-positive neuroblastomas. We observed that ALT neuroblastoma cells manifested constitutive ataxia-telangiectasia mutated (ATM) activation due to spontaneous telomere dysfunction which was not observed in telomerase-positive neuroblastoma cells. We demonstrated that induction of telomere dysfunction resulted in ATM activation that, in turn, conferred resistance to temozolomide + SN-38 (4.2-fold change in IC50, P < 0.001). ATM knockdown (shRNA) or inhibition using a clinical-stage small-molecule inhibitor (AZD0156) reversed resistance to temozolomide + irinotecan in ALT neuroblastoma cell lines in vitro (P < 0.001) and in four ALT xenografts in vivo (EFS, P < 0.0001). AZD0156 showed modest to no enhancement of temozolomide + irinotecan activity in telomerase-positive neuroblastoma cell lines and xenografts. Ataxia telangiectasia and Rad3 related (ATR) inhibition using AZD6738 did not enhance temozolomide + SN-38 activity in ALT neuroblastoma cells. Thus, ALT neuroblastoma chemotherapy resistance occurs via ATM activation and is reversible with ATM inhibitor AZD0156. Combining AZD0156 with temozolomide + irinotecan warrants clinical testing for neuroblastoma.
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Moore, H. C., K. M. Wood, M. S. Jackson, M. A. Lastowska, D. Hall, H. Imrie, C. P. F. Redfern, et al. "Histological profile of tumours from MYCN transgenic mice." Journal of Clinical Pathology 61, no. 10 (August 4, 2008): 1098–103. http://dx.doi.org/10.1136/jcp.2007.054627.

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Background:MYCN is the most commonly amplified gene in human neuroblastomas. This proto-oncogene has been overexpressed in a mouse model of the disease in order to explore the role of MYCN in this tumour.Aims:To report the histopathological features of neuroblastomas from MYCN transgenic mice.Methods:27 neuroblastomas from hemizygous transgenic mice and four tumours from homozygous mice were examined histologically; Ki67 and MYCN immunocytochemistry was performed in 24 tumours.Results:Tumours obtained from MYCN transgenic mice resembled human neuroblastomas, displaying many of the features associated with stroma-poor neuroblastoma, including heterogeneity of differentiation (but no overt ganglionic differentiation was seen), low levels of Schwannian stroma and a high mitosis karyorrhexis index. The tumours had a median Ki67 labelling index of 70%; all tumours expressed MYCN with a median labelling index of 68%. The most striking difference between the murine and human neuroblastomas was the presence of tingible body macrophages in the transgenic mouse tumours reflecting high levels of apoptosis. This has not previously been described in human or other murine neuroblastoma models.Conclusions:These studies highlight the histological similarities between tumours from MYCN transgenic mice and human neuroblastomas, and reaffirm their role as a valuable model to study the biology of aggressive human neuroblastoma.
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Secomandi, Eleonora, Amreen Salwa, Chiara Vidoni, Alessandra Ferraresi, Carlo Follo, and Ciro Isidoro. "High Expression of the Lysosomal Protease Cathepsin D Confers Better Prognosis in Neuroblastoma Patients by Contrasting EGF-Induced Neuroblastoma Cell Growth." International Journal of Molecular Sciences 23, no. 9 (April 26, 2022): 4782. http://dx.doi.org/10.3390/ijms23094782.

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Neuroblastoma is a malignant extracranial solid tumor arising from the sympathoadrenal lineage of the neural crest and is often associated with N-MYC amplification. Cathepsin D has been associated with chemoresistance in N-MYC-overexpressing neuroblastomas. Increased EGFR expression also has been associated with the aggressive behavior of neuroblastomas. This work aimed to understand the mechanisms linking EGFR stimulation and cathepsin D expression with neuroblastoma progression and prognosis. Gene correlation analysis in pediatric neuroblastoma patients revealed that individuals bearing a high EGFR transcript level have a good prognosis only when CTSD (the gene coding for the lysosomal protease Cathepsin D, CD) is highly expressed. Low CTSD expression was associated with poor clinical outcome. CTSD expression was negatively correlated with CCNB2, CCNA2, CDK1 and CDK6 genes involved in cell cycle division. We investigated the biochemical pathways downstream to EGFR stimulation in human SH-SY5Y neuroblastoma cells engineered for overexpressing or silencing of CD expression. Cathepsin D overexpression decreased the proliferative potential of neuroblastoma cells through downregulation of the pro-oncogenic MAPK signaling pathway. EGFR stimulation downregulated cathepsin D expression, thus favoring cell cycle division. Our data suggest that chemotherapeutics that inhibit the EGFR pathway, along with stimulators of cathepsin D synthesis and activity, could benefit neuroblastoma prognosis.
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Secomandi, Eleonora, Amreen Salwa, Chiara Vidoni, Alessandra Ferraresi, Carlo Follo, and Ciro Isidoro. "High Expression of the Lysosomal Protease Cathepsin D Confers Better Prognosis in Neuroblastoma Patients by Contrasting EGF-Induced Neuroblastoma Cell Growth." International Journal of Molecular Sciences 23, no. 9 (April 26, 2022): 4782. http://dx.doi.org/10.3390/ijms23094782.

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Neuroblastoma is a malignant extracranial solid tumor arising from the sympathoadrenal lineage of the neural crest and is often associated with N-MYC amplification. Cathepsin D has been associated with chemoresistance in N-MYC-overexpressing neuroblastomas. Increased EGFR expression also has been associated with the aggressive behavior of neuroblastomas. This work aimed to understand the mechanisms linking EGFR stimulation and cathepsin D expression with neuroblastoma progression and prognosis. Gene correlation analysis in pediatric neuroblastoma patients revealed that individuals bearing a high EGFR transcript level have a good prognosis only when CTSD (the gene coding for the lysosomal protease Cathepsin D, CD) is highly expressed. Low CTSD expression was associated with poor clinical outcome. CTSD expression was negatively correlated with CCNB2, CCNA2, CDK1 and CDK6 genes involved in cell cycle division. We investigated the biochemical pathways downstream to EGFR stimulation in human SH-SY5Y neuroblastoma cells engineered for overexpressing or silencing of CD expression. Cathepsin D overexpression decreased the proliferative potential of neuroblastoma cells through downregulation of the pro-oncogenic MAPK signaling pathway. EGFR stimulation downregulated cathepsin D expression, thus favoring cell cycle division. Our data suggest that chemotherapeutics that inhibit the EGFR pathway, along with stimulators of cathepsin D synthesis and activity, could benefit neuroblastoma prognosis.
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Secomandi, Eleonora, Amreen Salwa, Chiara Vidoni, Alessandra Ferraresi, Carlo Follo, and Ciro Isidoro. "High Expression of the Lysosomal Protease Cathepsin D Confers Better Prognosis in Neuroblastoma Patients by Contrasting EGF-Induced Neuroblastoma Cell Growth." International Journal of Molecular Sciences 23, no. 9 (April 26, 2022): 4782. http://dx.doi.org/10.3390/ijms23094782.

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Neuroblastoma is a malignant extracranial solid tumor arising from the sympathoadrenal lineage of the neural crest and is often associated with N-MYC amplification. Cathepsin D has been associated with chemoresistance in N-MYC-overexpressing neuroblastomas. Increased EGFR expression also has been associated with the aggressive behavior of neuroblastomas. This work aimed to understand the mechanisms linking EGFR stimulation and cathepsin D expression with neuroblastoma progression and prognosis. Gene correlation analysis in pediatric neuroblastoma patients revealed that individuals bearing a high EGFR transcript level have a good prognosis only when CTSD (the gene coding for the lysosomal protease Cathepsin D, CD) is highly expressed. Low CTSD expression was associated with poor clinical outcome. CTSD expression was negatively correlated with CCNB2, CCNA2, CDK1 and CDK6 genes involved in cell cycle division. We investigated the biochemical pathways downstream to EGFR stimulation in human SH-SY5Y neuroblastoma cells engineered for overexpressing or silencing of CD expression. Cathepsin D overexpression decreased the proliferative potential of neuroblastoma cells through downregulation of the pro-oncogenic MAPK signaling pathway. EGFR stimulation downregulated cathepsin D expression, thus favoring cell cycle division. Our data suggest that chemotherapeutics that inhibit the EGFR pathway, along with stimulators of cathepsin D synthesis and activity, could benefit neuroblastoma prognosis.
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Keyel, Michelle E., Kathryn L. Furr, Min H. Kang, and C. Patrick Reynolds. "A Multi-Color Flow Cytometric Assay for Quantifying Dinutuximab Binding to Neuroblastoma Cells in Tumor, Bone Marrow, and Blood." Journal of Clinical Medicine 12, no. 19 (September 27, 2023): 6223. http://dx.doi.org/10.3390/jcm12196223.

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GD2, a disialoganglioside, is present on the surface of most neuroblastomas, as well as on some other cancers, such as melanoma and osteogenic sarcoma. The anti-GD2 antibody ch14.18 (dinutuximab) has an FDA-registered indication for use as maintenance therapy for high-risk neuroblastoma with cytokines and 13-cis-retinoic acid after myeloablative therapy. Recent studies using immunohistochemistry of tumor or tumor cells in marrow have shown that some neuroblastomas are negative for GD2. Dinutuximab and other anti-GD2 antibodies are increasingly used in combination with cytotoxic chemotherapy for treating relapsed neuroblastoma, so it is important to be able to identify patients with tumor cells with low GD2 expression, as such patients may experience toxicity but not benefit from the antibody therapy. As the most common clinical samples available for relapsed neuroblastoma are bone marrow aspirates, we developed a method to quantify dinutuximab binding density and the frequency of neuroblastoma cells positive for the antibody in bone marrow aspirates. Here, we describe a multi-color flow cytometry assay that employs non-GD2 antibodies to identify neuroblastoma cells in a mixed population (tumor, bone marrow, or blood) and an anti-GD2 antibody to quantify both the frequency and density of GD2 expression on neuroblastoma cells.
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Ramsay, Hans A., Kalevi J. A. Kairemo, and Antti P. Jekunen. "Somatostatin receptor imaging of olfactory neuroblastoma." Journal of Laryngology & Otology 110, no. 12 (December 1996): 1161–63. http://dx.doi.org/10.1017/s0022215100136023.

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AbstractNeural-crest tumours, including neuroblastomas, express somatostatin receptors. This can be shown by radionuclide labelling of octreotide, a somatostatin analogue. Studies on imaging with this substance have dealt with childhood neuroblastomas. Olfactory neuroblastoma (aesthesioneuroblastoma) is a rare tumour in which somatostatin receptor content has not been analysed, nor have radionuclide methods for diagnostic purposes been described. We report a case of olfactory neuroblastoma, in which scanning with m In-labelled octreotide was performed. A strong uptake was seen at the base of the skull. This was confirmed as a recurrent tumour by magnetic resonance (MR) imaging. Uptake was also observed in the neck and chest, indicating extensive spread of the disease.Somatostatin receptor expression has been shown to correlate with prognosis in childhood neuroblastoma. The accuracy of labelled octreotide in the diagnosis of olfactory neuroblastoma indicates that it might be useful in radionuclide therapy of patients with advanced disease, when no other treatment modalities are available.
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Dissertations / Theses on the topic "Neuroblastoma"

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Schulze, Franziska. "Die Telomerlänge als Prognosefaktor in MYCN nicht-amplifizierten Neuroblastomen." Doctoral thesis, Universitätsbibliothek Leipzig, 2016. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-200943.

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Eines der charakteristischen Merkmale des Neuroblastoms stellt seine einzigartige biologische Heterogenität dar, die eine genaue Ausage des weiteren klinischen Verlaufes stark erschwert. Bestimmte prognostisch wirksame klinische, molekularbiologische und genetische Faktoren, wie zum Beispiel Alter bei Erstdiagnose, Tumorstadium, MYCN-Amplifikation und 1p Deletion, werden seit längerem zur Risikostratifizierung genutzt. Bereits in anderen Tumorerkrankungen konnte nun der Einfluß einer Telomerlängenveränderung auf das Gesamtüberleben von Patienten nachgewiesen werden. Telomere sichern die genomische Integrität und bestimmen maßgeblich die proliferative Kapazität jeder somatischen Zelle. Aktuelle Forschungsergebnisse legen die Vermutung nahe, dass Veränderungen der Telomerlänge auch in Neuroblastomen einen prognostischen Effekt auf das Gesamtüberleben haben. In diesem Kontext untersucht die vorliegende Arbeit den Zusammenhang zwischen Telomerlänge und Gesamtüberleben in 420 MYCN nicht-amplifizierten primären Neuroblastomen mit Erstdiagnosen von 1983-2001. Hierfür wurden die relativen Telomerlängen mithilfe einer neu etablierten monochromen multiplex q-RT-PCR ermittelt. Anschließend wurden diese sowohl mit ausgesuchten klinischen Variablen (Alter bei Erstdiagnose, Tumorstadium, Primärlokalisation des Tumors, Histologie, Geschlecht und Rezidivauftreten) korreliert als auch auf ihren Einfluß auf das Gesamt- und ereignisfreie Überleben untersucht. In Korrelation mit den klinischen Parametern konnte zwischen Alter bei Erstdiagnose und Telomerlänge ein eindeutiger Zusammenhang nachgewiesen werden. Je älter die Patienten bei Erstdiagnose, desto höher war sowohl der Anteil verlängerter Telomere als auch der extremer Telomerlängenveränderungen. Neuroblastome mit verlängerten Telomeren zeigten in der gleichen Altersgruppe ein verringertes Gesamtüberleben der betroffenen Patienten verglichen mit Neuroblastomen mit verkürzten Telomeren. Somit könnte eine Telomerlängenveränderung, insbesondere verlängerte Telomere, im klinischen Alltag als Hinweis auf einen prognostisch ungünstigen Verlauf genutzt werden.
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Deveau, Paul. "Evolution sous-clonale dans le neuroblastome." Thesis, Université Paris-Saclay (ComUE), 2017. http://www.theses.fr/2017SACLS140/document.

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Le neuroblastome est le cancer solide extra-cranial le plus fréquent chez l’enfant. Il est caractérisé par une très grande hétérogénéité tant au niveau clinique que moléculaire. Alors que certains patients rentrent spontanément en rémission, on peut se demander quels facteurs permettent la réémergence du cancer chez d’autres malgré traitement. Pour répondre à cette question, il convient d’identifier chez les patients ayant rechuté, les différentes populations clonales coexistant au diagnostic et/ou à la rechute. Cela permet, entre autre, d’étudier les voies différemment altérées entre ces deux temps. Dans cette optique, nous présentons ici QuantumClone, un algorithme de reconstruction clonal à partir de données de séquençage, ainsi que son application à une cohorte de patients souffrant d’un neuroblastome. Sur ces données, l’application de notre méthode a permis d’identifier des différences dans le ratio de variants prédits fonctionnels par rapport à ceux prédits passagers entre les populations ancestrales, enrichies à la rechute ou appauvries à la rechute
Neuroblastoma is the most frequent solid extra-cranial cancer of childhood. This cancer displays a high heterogeneity both at clinical and molecular levels. Even though in some patients spontaneous remission can be observed, some others relapse despite treatment and surgical resection. It may be wondered which are the factors that distinguish these two cases. In order to answer this question, identification of populations coexisting at diagnosis and/or relapse in the patients which have relapsed is a prerequisite. This would allow, between other things, to study the pathways differently altered in clones that are specific to each time point. With this in mind, we hereby present QuantumClone, a clonal reconstruction algorithm from sequencing data. In addition, we applied this method to a cohort of patients suffering from neuroblastoma. On these data, our method identified differences in the functional mutation rate, i.e. the number of putative functional variants by total number of variants, between the ancestral clones, clones expanding at relapse, and clones shrinking at relapse
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Delisle, Lucille. "Role of the mutated ALK oncogene in neuroblastoma oncogenesis and in development." Thesis, Paris 11, 2015. http://www.theses.fr/2015PA11T036.

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Le neuroblastome (NB) est une tumeur pédiatrique du système nerveux sympathique. Des mutations activatrices du gène ALK (Anaplastic Lymphoma Kinase) ont été identifiées dans 8 % des formes sporadiques et dans des formes familiales de NB. Le gène ALK code pour un récepteur tyrosine kinase appartenant à la famille des récepteurs à l’insuline, principalement exprimé dans le système nerveux central et périphérique. Le récepteur ALK représente une cible thérapeutique pertinente dans ce cancer. Des mutations de novo du gène ALK ont également été rapportées dans une forme syndromique associant NB congénital et encéphalopathie sévère avec dysmorphie du tronc cérébral, suggérant un rôle développemental du gène ALK en plus de son implication dans l’oncogenèse.Dans ce contexte, mon projet de thèse avait pour but de déterminer le rôle du récepteur ALK muté dans l’oncogenèse du NB et le développement, principalement à l’aide de modèles murins originaux obtenus au laboratoire. J’ai ainsi largement caractérisé deux lignées de souris KI (Knock-In) Alk pour les deux mutations les plus fréquemment observées dans le NB: F1174L et R1275Q chez l’homme, correspondant à F1178L et R1279Q chez la souris.Une analyse détaillée de ces deux lignées de souris n’a pas révélé de phénotype majeur chez les souris KI AlkR1279Q hétérozygotes et homozygotes ainsi que chez les hétérozygotes KI AlkF1178L. Par contre, nous avons documenté une forte létalité post-natale des animaux KI AlkF1178L homozygotes et montré que ces nouveaux-nés présentent des troubles majeurs d’alimentation. Les homozygotes KI AlkF1178L phénocopient donc partiellement les patients encéphalopathes. La différence d’effet observé entre les animaux hétérozygotes et homozygotes suggère fortement qu’il existe un seuil d’activation du récepteur Alk compatible avec la survie.Nous avons ensuite exploré le rôle du récepteur ALK muté dans le système nerveux sympathique des souris KI Alkmut. Cette analyse a montré que l’activation du récepteur induit un excès de prolifération des neurones sympathiques de E14.5 à la naissance. Néanmoins, nous n’avons pas observé de NB chez ces animaux. En croisant ces souris avec la lignée TH-MYCN, nous avons documenté une coopération des mutations Alk avec l’oncogène MYCN pour le développement de NB. La comparaison des profils transcriptomiques des tumeurs murines MYCN et MYCN/Alkmut a révélé que l’expression de l’oncogène Ret (codant également un récepteur à activité tyrosine kinase) était fortement induite par l’activation du récepteur Alk. Le traitement des souris par un inhibiteur de l’activité kinase du récepteur Ret a montré une diminution de la taille des tumeurs suggérant que le gène Ret joue un rôle majeur dans l’oncogenèse induite par le récepteur Alk muté. Par ailleurs, l’induction de l’expression du gène RET par le récepteur ALK muté dans les NB a été confirmée dans des lignées et des tumeurs humaines.Afin de déterminer le mécanisme par lequel l’activation du récepteur ALK aboutit à la régulation de l’expression du gène RET des expériences ont été effectuées sur des lignées humaines de NB dans lesquelles le récepteur ALK peut être activé ou inactivé. Ce travail a montré que l’expression du gène RET est dépendante de l’axe ALK-ERK-ETV5. En effet, la modulation de l’activité du récepteur ALK affecte l’expression des gènes ETV5 et RET. Cet effet est dépendant de l’activation de la voie MEK/ERK. Par ailleurs, ETV5 active l’expression du gène RET. Afin de confirmer le rôle de Ret dans l’oncogenèse dépendante du récepteur Alk, nous avons croisé des souris portant une mutation activatrice de Ret avec les souris TH-MYCN. Nous avons ainsi mis en évidence que le récepteur Ret activé coopère avec l’oncogène MYCN dans le développement de tumeurs et que ces tumeurs sont des NB présentant des caractéristiques très semblables à celles des tumeurs MYCN/Alkmut. Le gène Ret apparaît donc comme une cible essentielle du récepteur Alk muté dans l’oncogenèse du NB
Neuroblastoma (NB) is a pediatric tumor arising from the sympathetic nervous system. Activating mutations of the ALK gene have been observed in around 8 % of sporadic neuroblastoma as well as in familial cases. The ALK gene encodes a tyrosine kinase receptor of the insulin receptor super-family. It is mainly expressed in the central and peripheral nervous system. The ALK receptor represents a therapeutic target in this cancer. De novo ALK mutations have also been reported in a syndrome associating congenital NB and severe encephalopathy with abnormal shape of the brainstem, suggesting a developmental role for the ALK gene in addition to its implication in oncogenesis.In this context, my PhD project was to determine the role of the mutated ALK receptor in NB oncogenesis and in development, mainly with original mouse models obtained in the laboratory. I extensively characterized two knock-in (KI) Alk mouse lines with the two mutations that are most frequently observed in NB: F1174L and R1275Q in human and F1178L and R1279Q in mouse.A detailed analysis of these two mouse lines showed that the KI AlkR179Q heterozygous and homozygous mice as well as the KI AlkF1178L heterozygous mice do not show striking clinical signs. On the contrary, we documented a high postnatal lethality for KI AlkF1178L homozygous mice and showed that these pups presented with a dramatic reduced milk intake. Thus, the KI AlkF1178L homozygous mice partially phenocopy the human patients with encephalopathy. The difference of phenotype between the heterozygous and the homozygous KI AlkF1178L mice highly suggest a threshold of activity of the Alk receptor compatible with survival.We then explored the role of the mutated ALK receptor in the sympathetic nervous system of the KI Alkmut mice. This analysis showed that the activation of the receptor induces an excess of proliferation in sympathetic neurons from E14.5 to birth. However, we could not observe NB in these animals. We next bread these mice with the transgenic TH-MYCN line. We documented cooperation between Alk mutations and the MYCN oncogene to induce NB. Comparison of transcriptomic profiles of MYCN vs MYCN/Alkmut tumors revealed that the expression of the Ret oncogene (encoding a tyrosine kinase receptor) was strongly induced by the activation of the Alk receptor. Besides, the induction of the expression of the RET gene by the mutated ALK receptor in NB was confirmed in human cell lines and tumors.In order to determine the mechanism by which the activation of the ALK receptor regulates RET gene expression, experiments were done on human NB cell lines in which the ALK receptor can be activated or inactivated. This work showed that RET gene expression is dependent of the ALK-ERK-ETV5 axis. Indeed, the modulation of the ALK receptor activity affects gene expression of ETV5 and RET. This effect is dependent of the activation of the MEK/ERK pathway. Besides, ETV5 increases RET gene expression. In order to confirm the role of the Ret receptor in oncogenesis driven by the mutated Alk receptor, we bread mice bearing an activating mutation of the Ret gene with the TH-MYCN mice. We showed that the activated Ret receptor cooperates with the MYCN oncogene in tumor formation and that these tumors are NB presenting with characteristics very close to MYCN/Alkmut tumors. Thus, the Ret gene appears to be an essential target of the mutated Alk receptor in NB oncogenesis
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Peirsis, Pages Maria. "Anti-Angiogenesis in neuroblastoma." Thesis, University of Bristol, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.529877.

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Almutair, Bader Obaid Shreid. "Hypomethylated genes in neuroblastoma." Thesis, University of Bristol, 2017. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.743008.

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Medeiros, Helouise Richardt. "Efeito da estimulação magnética estática em linhagem celular de neuroblastoma e neuroblastoma diferenciado." Universidade Federal do Rio Grande do Sul, 2017. http://hdl.handle.net/10183/179044.

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Estimulação Magnética vem sendo utilizada no tratamento de várias patologias do sistema nervoso central, mas a compreensão de sua ação em nível celular precisa ser melhor investigada. Sendo assim, o objetivo principal desta dissertação foi estabelecer, em cultura celular, um método de Estimulação Magnética Estática (E- ME) e avaliar seu efeito em diferentes tipos celulares. Para tanto, foi desenvolvido um suporte de placa de cultura com ímãs NeFeB (neodímio-ferro-boro) com a forma cilíndrica de 12mm de diâmetro por 6mm de altura. Cada suporte apresenta seis ímãs espaçados, de modo que os campos magnéticos não interajam entre si. As células de neuroblastoma humano SH-SY5Y foram plaqueadas 1x106 células por poço e cultivadas em placas de 24 poços. A análise microscópica das placas demonstrou que as células adaptaram-se ao novo ambiente, demonstrando aderência e crescimento adequados à superfície da placa. Após este primeiro passo, as células SH-SY5Y foram estimuladas utilizando 0,1 T, 0,2 T e 0,3 T por 60 minutos, buscando determinar a melhor intensidade de EME. Após, este período de estimulação, para avaliar a viabilidade celular, foi realizado o ensaio de MTT (brometo de [3- (4,5-dimetiltiazol-2yl)-2,5-difenil tetrazolium) nos grupos de células estimuladas e não estimuladas. Não tendo sido observada diferença estatisticamente significativa entre os grupos avaliados. A partir da obtenção destes dados, foram definidos os parâmetros de intensidade e período de estimulação da EME. Os experimentos foram, então, realizados aplicando 24 horas de estimulação com intensidade de 0,3T em culturas de diferentes tipos celulares. Optamos por utilizar, além de células de neuroblastoma humano SH-SY5Y, outro tipo de células tumoral, células de melanoma vaginal; e células de neuroblastoma diferenciado em células neuronais e células mesenquimais derivadas de adipócitos. Com estas escolhas objetivamos determinar a resposta de diferentes tipos celulares a EME. Para tanto, cada tipo celular foi dividido em 4 grupos, 2 grupos não estimulados (controles) avaliadas imediatamente (CI) e 24h após o final do experimento (C24), e 2 grupos estimulados por 24h, que foram avaliados imediatamente (EI) e 24h após o final da exposição a EME (E24). Para verificar a resposta celular a EME foram avaliados parâmetros de toxicidade (MTT, PI (Iodeto de propídeo) e HO (Hoechst), de neuroplasticidade (expressão do gene do receptor de BDNF (PCR em tempo real)) e ciclo celular (citometria de fluxo). Os resultados obtidos demonstram que imediatamente após a EME, houve uma diminuição significativa na viabilidade celular das células SH-SY5Y indiferenciadas (Kruskal Wallis, P<0,05). Já no grupo 24h, não houve diferença estatisticamente significativa em nenhum dos gru 9 pos avaliados (Kruskal Wallis, P>0,05). Visto que, houve uma diminuição da viabili- dade celular nas células SH-SY5Y, imediatamente após a estimulação, na busca de encontrar o mecanismo de ação pelo qual estas células apresentavam uma diminui- ção celular, utilizamos as técnicas de PI e de HO para avaliar apoptose e necrose celular, respectivamente. Adicionalmente avaliamos o ciclo celular. Desta forma e, considerando que apenas as células de neuroblastoma humano SH-SY5Y apresen- taram diminuição significativa na viabilidade celular, somente neste tipo celular foi feito esta avaliação. Não foi encontrada diferença estatisticamente significativa entre os grupos. No entanto, a análise descritiva demonstrou que, 24h após o estímulo, as células SH-SY5Y não diferenciadas apresentaram uma redução de duplicação celular (Kruskal Wallis, P >0,05). Outro fator avaliado nas células SH-SY5Y diferenciadas e não diferenciadas, como parâmetro de neuroplasticidade, foi expressão do gene do receptor Trk-β. Não foi encontrada diferença significativa, no entanto na análise descritiva, as células SH-SY5Y não diferenciadas avaliadas 24h após a aplicação de EME, apresentaram um aumento na expressão deste gene, sugerindo um aumento da neuroplasticidade. Estes resultados demonstram um efeito de longa duração da EME, por pelo menos até 24h após o final da EME, corroborando com dados prévios de nosso grupo de pesquisa, utilizando modelos animais e ETCC (estimulação transcraniana por corrente contínua), outra técnica neuromodulatoria, que mostraram efeito por até 7 dias após o termino da tratamento. Interessantemente, não foram observadas diferenças na viabilidade celular nas de- mais culturas celulares analisadas. Estes resultados são muito relevantes, pois demonstram que, em relação aos parâmetros de viabilidade celular analisados, a EME é uma técnica segura no protocolo utilizado (24h de 0,3T de EME). Os dados desta dissertação demonstram que a EME apresenta diferentes efeitos em relação à toxicidade em células de tumores neuronais, tumores não neuronais e células com morfologia normal. A diminuição da viabilidade celular nas células SH-SY5Y indiferenciadas é um resultado surpreendente e favorável considerando ser linhagem celular tumoral. Desta forma estes resultados avaliados em conjunto sugerem que a EME é uma técnica segura que, em células normais não provocou alterações importantes nos parâmetros avaliados e em tumores de células não neuronais não alterou o crescimento celular. No entanto, ainda se faz necessário aumentar o numero amostral da avaliação das fases do ciclo celular a expressão do gene Trk-β, assim como mais estudos para avaliar outros parâmetros de toxicidade e também diferentes protocolos de estimulação celular utilizando a EME.
Magnetic stimulation has been used in the treatment of various pathologies of the central nervous system, but the understanding of its action at the cellular level needs to be investigated. Thus, the main objective of this dissertation was to establish, in cell culture, a method of Static Magnetic Stimulation (SMS). For this purpose, a cul- ture plate holder with NeFeB (neodymium-iron-boron) magnets with a cylindrical shape of 12mm in diameter by 6mm in height was developed. Cells were plated 1x106 cells per well and cultured in 24-well plates. Microscopic analysis of plaques demonstrated that the cells adapted to the new environment, demonstrating ade- quate adhesion and growth to the plaque surface. This was extremely important to the development of this article. After this first step, human neuroblastoma cells (SH- SY5Y) were stimulated using 0.1 T, 0.2 T and 0.3 T for 60 minutes, in order to de- termine the best intensity of static magnetic stimulation. After this stimulation period, to evaluate cell viability, the MTT [3-(4,5-dimethylthiazol-2-yl)-2,5- diphenyltetrazolium] assay was performed on stimulated (stimulated group) and non- stimulated (control group) cells. No significant difference was observed between the groups evaluated. From the data obtained, it was defined the use of the highest in- tensity tested, an increase in the period of stimulation and application in other cell types. The experiments were then performed applying 24 hours of stimulation with 0.3T intensity in cultures of different cell types. Considering that the cells initially used were of neuronal tumor, we chose to use, in addition to human neuroblastoma cells, another type of tumor cells (vaginal melanoma cells), and cells with normal character- istics in their morphology, such as SH-SY5Y differentiated into neuronal cells and mesenchymal adipocyte-derived cells. With these choices we aimed to determine if different cell types would respond in the same way to SMS. In order to do so, each cell type was divided into 4 groups, 2 non-stimulated groups (controls) evaluated im- mediately (CI) and 24h at the end of the experiment (C24), 2 groups stimulated for 24h, which were evaluated immediately (SI) and 24h after the end of exposure to SMS (S24). To assess the cellular response to EME, toxicity parameters [MTT, PI (Propidium iodide) and HO (Hoechst)] and cell cycle (flow cytometry) were done. The results obtained demonstrate that immediately after SMS, a significant decrease in cell viability of undifferentiated SH-SY5Y cells was found (Kruskal Wallis, P <0.05). In the 24h group, there was no statistically significant difference in any of the groups evaluated (Kruskal Wallis, P> 0.05). Since there was a decrease in cell viability in SH-SY5Y cells, immediately after stimulation, in the search to find the mechanism of action by which these cells had a cellular decrease, we used the PI and HO tech- niques to evaluate apoptosis and death cell and respectively. Additionally, we evalu- ated the cell cycle. In this way, and considering that only SH-SY5Y human neuroblastoma cells showed a significant decrease in cell viability, only this cell type was evaluated. There were no statistically significant differences between groups. 11 However, the descriptive analysis demonstrated that, 24 h after the stimulus, undif- ferentiated SH-SY5Y cells present a decrease in cytoplasm division in the G1 phase and, in G2 phase, a decrease in nuclear division, leading to a reduction of cell dupli- cation (Kruskal Wallis, P> 0.05). Another factor evaluated in differentiated and undif- ferentiated SH-SY5Y cells as a parameter of neuroplasticity was expression of the Trk-β gene. No significant difference was found, however in the descriptive analysis, the undifferentiated SH-SY5Y cells evaluated 24h after the application of SMS showed an increase in the expression of this gene, suggesting an increase in neuro- plasticity. These results demonstrate a long-term effect of SMS for at least 24 hours after the end of the SMS, supporting previous data from our research group, using animal models and TDCs (transcranial direct current stimulation), and another neuromodulatory technique, which showed effect for up to 7 days after the end of treatment. Interestingly, no differences in cell viability were observed in the other cell cultures analyzed. These results are very relevant because they demonstrate that, in relation to the cell viability parameters analyzed; SMS is a safe technique in the pro- tocol used (24h of 0.3T of SMS). The data from this dissertation demonstrate that SMS has different effects in relation to toxicity in cells of neuronal tumors, non- neuronal tumors and cells with normal morphology. Decreased cell viability in undif- ferentiated SH-SY5Y cells is a surprising and favorable finding considering that it is a tumor cell line. Thus, these results evaluated together suggest that SMS is a safe technique that in normal cells did not induce important changes in the evaluated pa- rameters and in non-neuronal cell tumors did not alter the cell growth. However, it is still necessary to increase the sample number of the evaluation of the phases of the cell cycle and the expression of the Trk-β gene, as well as more studies to evaluate other parameters of toxicity and also different protocols of cellular stimulation using SMS.
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Semeraro, Michaela. "Neuroblastoma and gastrointestinal stromal tumor as a target for natural killer lymphocytes : the role of ncr3/nkp30." Thesis, Paris 11, 2013. http://www.theses.fr/2013PA11T045/document.

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Depuis la formulation de la théorie de l’immuno-surveillance en 1957 par Burnet et Thomas, le monde scientifique s’est efforcé d’identifier les cellules immunitaires impliquées dans ce processus. Les lymphocytes Natural Killer (NK) constituent une composant majeure de l’immuno-surveillance innée dans plusieurs cancers hématologiques et solides. L’activité des lymphocytes NK passe principalement par une grande variété de récepteurs avec un rôle activateur ou inhibiteur. Parmi les récepteurs activateurs présents à la surface des lymphocytes NK, le récepteur NCR3/NKp30 a un rôle majeur dans la toxicité directe contre la cellule cible et dans l’activation des cellules dendritiques.Les tumeurs stromales gastrointestinales (GIST) et le Neuroblastome (NB) sont deux tumeurs sensibles à l’immuno-surveillance par les lymphocytes NK. Dans une étude récente notre équipe a démontré que l’épissage alternatif du gène NCR3/NKp30 peut être déterminant dans la fonction NK et dans la survie des patients atteints de GIST.Afin de caractériser les lymphocytes infiltrant le GIST, nous avons effectué une recherche visant à analyser l’infiltrat des lymphocytes CD3+, des lymphocytes T régulateurs (Treg) et des lymphocytes NK dans des tumeurs GIST localisés, et corréler ces résultats à la survie des patients. Nous avons mis en évidence que, avant traitement, les lymphocytes NK sont surtout localisés au niveau des fibres trabéculaires qui entourent la tumeur, alors que les lymphocytes T sont localisé à l’intérieur de la tumeur en contact avec les cellules tumorales qui expriment HLA-I.Nous avons aussi observé que les cellules NK ont un phénotype plutôt CD56bright et migrent à l’intérieur de la tumeur après traitement par Imatinib. L’analyse de survie a mis en évidence que les lymphocytes NK et T peuvent prédire la survie sans progression (PFS). Ces résultats mettent en évidence l’importance de l’infiltrat immunitaire dans la prédiction du risque de rechute dans le GIST et surlignent l’importance de viser une réponse immunitaire dans les protocoles thérapeutiques.Nous avons ensuite déterminé la proportion de lymphocytes NK dans le sang périphérique et dans la moelle dans une cohorte de Neuroblastome (NB) localisé et métastatique : une infiltration plus important par les NK CD56bright a été observé chez les patients présentant une maladie métastatique et chez les patients avec une réponse mineure au traitement d’induction. De plus, les NK présents dans les échantillons de moelle osseuse infiltrés par les neuroblastes, présentaient une expression plus basse du récepteur NKp30. L’expression du ligand de NKp30, B7-H6, a été mise en évidence sur les neuroblastes infiltrant la moelle osseuse, et sa forme soluble, sB7-H6, a été retrouvée être positivement corrélée à l’extension de maladie et inversement à la réponse au traitement d’induction. L’analyse de l’épissage alternatif du gène NCR3/NKp30 a permis de mettre en évidence l’impact des isoformes NKp30 sur la survie sans progression chez les patients atteints de NB de haut risque en maladie minimale résiduelle après chimiothérapie d’induction. En particulier, les patients présentant un taux élevé de l’isoforme pro-inflammatoire (NKp30b) par rapport à l’isoforme immunosuppressive (NKp30c), présentent une meilleure survie sans évènement. Nous avons aussi démontré le rôle des monocytes dans l’amplification de la réponse NKp30 dépendant. Les résultats de notre recherche dans le GIST et dans le NB, deux maladies différentes mais toutes les deux sensibles aux lymphocytes NK, surlignent l’importance d’intégrer de nouvelles options thérapeutiques aptes à cibler le système immunitaire
Since Burnet and Thomas formulated in 1957 the cancer immunosurveillance theory, the scientific world has made tremendous progress to identify the immune cells involved in this process. Natural Killer (NK) cells have emerged as a major component of the innate immunosurveillance of several hematological and solid malignancies. The activity of NK-cells is mainly mediated through their wide variety of receptors with activating and inhibitory functions. Among the versatile receptors present on NK cells, the activating receptor NCR3/NKp30 is a major receptor involved in both direct killing of target cells and mutual NK and dendritic cell activation.Gastrointestinal stromal tumors (GIST) and Neuroblastoma (NB) are known to be tumors sensitive to NK immunosurveillance. In a recent study we showed that alternative splicing of NCR3/NKp30 gene can affect NK cell function and GIST patient’s outcome.In order to better characterize the GIST tumor-infiltrating lymphocytes, we analyzed the CD3+, T regulatory (Treg) and NK lymphocytes infiltration within primary localized GIST tumors and we determined their prognostic value. We described that, before treatment, NK cells are mainly localized in fibrous trabeculae while T lymphocytes are in the tumor nests in HLA-I positive tumor cells contact. Moreover infiltrating NK cells displayed a secreting CD56bright phenotype, and accumulate in tumor nests after Imatinib (IM) treatment. Importantly CD3+ and NK lymphocytes independently predicted progression free survival (PFS). These results highlight the importance of the immune infiltrate in re-define the GIST risk stratification and allow enhancing the immune response in the therapeutic decisions.We next investigated the proportions of NK cells in blood and bone marrow (BM) in a cohort of localized and metastatic NB; a high proportion of CD56bright NK cells was associated with metastatic NB and with poor response to induction treatment within the metastatic NB. Moreover, infiltrated BM presented NKp30 down regulation. The expression of the NKp30 ligand, B7-H6, was found on BM neuroblasts, while the soluble protein, sB7-H6 correlated with resistance to treatment. Furthermore the transcriptional status of NKp30/NCR3 dictated the event-free survival rates of HR-NBs with minimal residual disease post-induction chemotherapy: in particular patients presenting a high proportion of the immunosuppressive isoform (NKp30c) compared to the pro-inflammatory isoform (NKp30b), presented a worse outcome. We further demonstrated the significant role of monocytes to amplify the NKp30 activation response.These researches in GIST and NB, two different but at the meantime NK-sensitive diseases support the effort to define new immunological therapeutic approaches and to determine their optimal use
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Ponthan, Frida. "Retinoids in experimental neuroblastoma therapy /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-427-5/.

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Gaze, Mark Nicholas. "The targeted radioterapy of neuroblastoma." Thesis, Queen Mary, University of London, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.398207.

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Charlet, Jessica. "Genetic-epigenetic interactions in neuroblastoma." Thesis, University of Bristol, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.560496.

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The solid childhood cancer neuroblastoma arises from cells of the sympathetic nervous system. Neuroblastoma is the most common childhood cancer in children younger than one year old worldwide and accounts for 28% of all cancers diagnosed in Europe and the U.S. in infants. 25% of neuroblastomas bear an amplification of the proto-oncogene MYCN; in addition to this genetic alteration, epigenetic modifications such as transcriptional silencing of tumour suppressor genes by promoter DNA hypermethylation and histone modifications can occur. Previous studies have shown an interaction between MYC and DNA hypermethylation, through recruitment of de novo DNA methyltransferases to the promoter of MYC target genes, in order to repress their transcription. We hypothesised that MYCN might be similarly capable of repressing its target genes. Our results revealed that MYCN interacts with the maintenance and de novo methyltransferase DNMT1 and DNMT3A, respectively in MYCN amplified neuroblastoma cell lines and all three bind the promoter region of the hypermethylated gene RASSF1A. However, only minor changes in DNA methylation of RASSF1A were shown by pyrosequencing analysis upon MYCN knock-down. This probably indicates only a small involvement of MYCN in epigenetically-induced gene silencing by DNA hypermethylation. The important role of MYCN in gene activation was highlighted from DNA methylation microarray studies on neuroblastoma cell lines compared to human neural crest cells. 73% of all hit genes showed hypomethylation, which led to the conclusion that a more open chromatin configuration and thus increased gene expression is favoured in high stage neuroblastoma cell lines, where MYCN and MYC compensate each others protein levels. The same study also led to the discovery of a novel methylated gene MEGF10 in neuroblastoma. The importance of epigenetic silencing in neuroblastoma was also highlighted by the ability of DNA demethylating agent 5-Aza-2'-deoxycytidine to re-sensitise chemotherapeutic resistant neuroblastoma cells to commonly used cytotoxic drugs.
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Books on the topic "Neuroblastoma"

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Sarnacki, Sabine, and Luca Pio, eds. Neuroblastoma. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-18396-7.

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Hayat, M. A., ed. Neuroblastoma. Dordrecht: Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-2418-1.

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Moyes, Judy S. E., V. Ralph McCready, and Ann C. Fullbrook. Neuroblastoma. London: Springer London, 1989. http://dx.doi.org/10.1007/978-1-4471-1674-5.

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Cheung, Nai-Kong V., and Susan L. Cohn, eds. Neuroblastoma. Berlin, Heidelberg: Springer Berlin Heidelberg, 2005. http://dx.doi.org/10.1007/b137762.

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M, Brodeur Garrett, ed. Neuroblastoma. Amsterdam: Elsevier, 2000.

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Asgharzadeh, Shahab, and Frank Westermann, eds. Neuroblastoma. Cham: Springer International Publishing, 2024. http://dx.doi.org/10.1007/978-3-031-51292-6.

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H, Andre Lucas, and Roux Nathan E, eds. Neuroblastoma research trends. New York: Nova Science, 2008.

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Schor, Nina Felice. The neurology of neuroblastoma: Neuroblastoma as a neurobiological disease. Norwell, Mass: Kluwer Academic, 2002.

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Schor, Nina Felice. The Neurology of neuroblastoma: Neuroblastoma as a neurobiological disease. Norwell, Mass: Kluwer Academic, 2002.

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Schor, Nina Felice. The Neurology of Neuroblastoma. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-1057-4.

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Book chapters on the topic "Neuroblastoma"

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Clavel, Jacqueline, Brigitte Lacour, and Paula Rios. "Epidemiology." In Neuroblastoma, 3–15. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-18396-7_1.

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Plantaz, Dominique, and Claire Freycon. "Neonatal Neuroblastoma." In Neuroblastoma, 191–203. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-18396-7_10.

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Segura, Vanessa, and Adela Cañete. "Low- and Intermediate-Risk Neuroblastoma." In Neuroblastoma, 205–12. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-18396-7_11.

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Matthay, Katherine K., and Dominique Valteau-Couanet. "High-Risk Neuroblastoma and Current Protocols." In Neuroblastoma, 213–35. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-18396-7_12.

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del Bufalo, Francesca, and Franco Locatelli. "Immunotherapy." In Neuroblastoma, 237–69. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-18396-7_13.

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Irwin, Meredith S. "Prognostic Factors and Risk Stratification." In Neuroblastoma, 271–92. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-18396-7_14.

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Mullassery, Dhanya, Laurence Abernethy, Rajeev Shukla, and Paul D. Losty. "Biopsy of Neuroblastoma." In Neuroblastoma, 295–311. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-18396-7_15.

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Saltsman, James A., Nicole J. Croteau, and Michael P. LaQuaglia. "Surgical Techniques." In Neuroblastoma, 313–25. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-18396-7_16.

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Vasudevan, Sanjeev A., and Jed G. Nuchtern. "Surgical Strategies for High Risk Neuroblastoma." In Neuroblastoma, 327–36. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-18396-7_17.

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Pio, Luca, Thomas Blanc, Christophe Glorion, Stephanie Puget, Michel Zerah, and Sabine Sarnacki. "Surgical Strategies for Neuroblastoma with Spinal Canal Involvement." In Neuroblastoma, 337–42. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-18396-7_18.

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Conference papers on the topic "Neuroblastoma"

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Danßmann, C., J. Toedling, F. Klironomos, A. Winkler, F. Hertwig, A. Eggert, JH Schulte, and S. Fuchs. "Circular RNAs in Neuroblastoma." In 31. Jahrestagung der Kind-Philipp-Stiftung für pädiatrisch onkologische Forschung. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1645000.

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Wang, David, and Dhruvil Oza. "Finding And Staging Neuroblastoma." In Radiopaedia 2024 Virtual Conference. Radiopaedia.org, 2024. http://dx.doi.org/10.53347/rposter-2450.

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Ferrandez, J. M., V. Lorente, D. de Santos, J. M. Cuadra, F. de la Paz, J. R. Alvarez, and E. Fernandez. "Human neuroblastoma cultures for biorobotics." In 2011 33rd Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2011. http://dx.doi.org/10.1109/iembs.2011.6091645.

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Melder, Katie, Garret Choby, Joao Almeida, Pierre-Olivier Champagne, Justin Cetas, Erik Chan, Jeremy Ciporen, et al. "Recurrence Morbidity of Olfactory Neuroblastoma." In 32nd Annual Meeting North American Skull Base Society. Georg Thieme Verlag KG, 2023. http://dx.doi.org/10.1055/s-0043-1762134.

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Palmieri, Daniel E., Kent S. Tadokoro, Ashok Muthukrishnan, Raja R. Seethala, Benita Valappil, and Carl H. Snyderman. "Lutathera Therapy for Olfactory Neuroblastoma." In 32nd Annual Meeting North American Skull Base Society. Georg Thieme Verlag KG, 2023. http://dx.doi.org/10.1055/s-0043-1762149.

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Attiyeh, Edward F., Michael D. Hogarty, Yaël P. Mossé, Sharon J. Diskin, Hakon Hakonarson, Shahab Asgharzadeh, Richard Sposto, et al. "Abstract 5258: Genomic characterization and targeted resequencing of high-risk neuroblastoma (the neuroblastoma TARGET)." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-5258.

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Ikegaki, Naohiko, Hiroyuki Shimada, and Xao X. Tang. "Abstract 2654: Induced stable neuroblastoma stem cells recapitulate in vivo highly aggressive large-cell neuroblastomas." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-2654.

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Huang, Chung-Hsuan, Yun-Ju Lai, Han-Yen Tu, and Chau-Jern Cheng. "Measurement and analysis of neuroblastoma cell death with holographic tomography." In Digital Holography and Three-Dimensional Imaging. Washington, D.C.: Optica Publishing Group, 2022. http://dx.doi.org/10.1364/dh.2022.m5a.7.

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This study presents a label-free approach for measurement and analysis of cell death using holographic tomography. Based on different cell sets, the neuroblastoma cell death with starving and apoptosis are demonstrated in three-demonstrational tomographic images.
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Disse, Gregory D., Matthew Bobinski, Mirna Lechpammer, Toby O. Steele, and Kiarash Shahlaie. "Ectopic Olfactory Neuroblastoma: A Case Report." In 30th Annual Meeting North American Skull Base Society. Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1702722.

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Mosse, Yael P. "Abstract SY14-02: ALK in neuroblastoma." In Proceedings: AACR 101st Annual Meeting 2010; Apr 17-21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-sy14-02.

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Reports on the topic "Neuroblastoma"

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Dotti, Gianpietro. Improve T Cell Therapy in Neuroblastoma. Fort Belvoir, VA: Defense Technical Information Center, July 2012. http://dx.doi.org/10.21236/ada610046.

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Dotti, Gianpietro. Improve T Cell Therapy in Neuroblastoma. Fort Belvoir, VA: Defense Technical Information Center, July 2014. http://dx.doi.org/10.21236/ada612327.

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Ding, Han-Fei. HOXC9-Induced Differentiation in Neuroblastoma Development. Fort Belvoir, VA: Defense Technical Information Center, October 2014. http://dx.doi.org/10.21236/ada613636.

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DeClerck, Yves A. Environment-Mediated Drug Resistance in Neuroblastoma. Fort Belvoir, VA: Defense Technical Information Center, October 2013. http://dx.doi.org/10.21236/ada591172.

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Dotti, Gianpietro. Improve T Cell Therapy in Neuroblastoma. Fort Belvoir, VA: Defense Technical Information Center, July 2013. http://dx.doi.org/10.21236/ada594698.

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Ding, Han-fei. HOXC9-Induced Differentiation in Neuroblastoma Development. Fort Belvoir, VA: Defense Technical Information Center, October 2013. http://dx.doi.org/10.21236/ada598450.

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Dotti, Gianpietro. Improve T Cell Therapy in Neuroblastoma. Fort Belvoir, VA: Defense Technical Information Center, July 2011. http://dx.doi.org/10.21236/ada550874.

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DeClerck, Yves A. Environment-Mediated Drug Resistance in Neuroblastoma. Fort Belvoir, VA: Defense Technical Information Center, October 2014. http://dx.doi.org/10.21236/ada616252.

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Marples, Brian. Overcoming the Mechanism of Radioresistance in Neuroblastoma. Fort Belvoir, VA: Defense Technical Information Center, June 2014. http://dx.doi.org/10.21236/ada609719.

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Du, Liqin, Zhenze Zhao, Alexander Pertsemlidis, and Xiuye Ma. Identifying microRNAs that Regulate Neuroblastoma Cell Differentiation. Fort Belvoir, VA: Defense Technical Information Center, September 2014. http://dx.doi.org/10.21236/ada611996.

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