Relevant bibliographies by topics / MYCN

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'MYCN'

Author: Grafiati
Published: 4 June 2021
Last updated: 26 July 2025

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Journal articles on the topic "MYCN"

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Chen, Monica F., Allison Richards, Patrick Evans, et al. "Abstract 1394: Comprehensive clinical and genomic analysis for patients with MYC, MYCN, and MYCL amplified solid tumors." Cancer Research 83, no. 7_Supplement (2023): 1394. http://dx.doi.org/10.1158/1538-7445.am2023-1394.

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Abstract Introduction: The MYC gene family (MYCf), which includes MYC, MYCN, and MYCL, is deregulated in ~70% of cancers and is associated with treatment resistance. Whereas older investigational therapies for MYC amplified tumors were unsuccessful, promising novel targeted therapies are in early phase clinical trials. Unfortunately, it remains unclear how to select patients whose cancers may harbor true MYC addiction. We thus sought to characterize factors such as amplification level, focality, and clonality that may correlate with increased MYC dependence. Methods: Utilizing a center-wide ne
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Aldosari, Naji, Sandra H. Bigner, Peter C. Burger, et al. "MYCC and MYCN Oncogene Amplification in Medulloblastoma." Archives of Pathology & Laboratory Medicine 126, no. 5 (2002): 540–44. http://dx.doi.org/10.5858/2002-126-0540-mamoai.

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Abstract Context.—Brain tumors are the most common solid tumor in childhood, and medulloblastoma is the most common malignant brain tumor in this age group. Cytogenetic abnormalities that have been described in childhood medulloblastoma include loss of 17p, amplification of MYCC (c-myc), amplification of MYCN (N-myc), and isochromosome 17q. Data on these tumors indicate that the frequency of MYCC amplification is 5% to 10%. Fluorescence in situ hybridization is a powerful tool for investigating these features on archival material. Objectives.—To determine if intratumoral heterogeneity exists f
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Valle, Kenya Pleitez, Miriam Velez, Yang Zhao, et al. "Abstract 3941: CRISPR screen of human stem cell derived MYC-driven medulloblastoma tumors reveal the mitochondria as a vulnerability." Cancer Research 85, no. 8_Supplement_1 (2025): 3941. https://doi.org/10.1158/1538-7445.am2025-3941.

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Abstract Background: Medulloblastoma (MB) is the most common malignant pediatric brain tumor and is derived from neuroepithelial stem cells (NESC). Amplification of each member of the MYC family of oncogenes (MYCN, CMYC, MYCL) has been found in MB tumors and amplified-MYCN or CMYC correlates with poor prognosis. Since transcription factors such as MYC are difficult to drug with small molecules, more druggable targets need to be identified. While genetic screens can be performed on human MB cell lines, there is a lack of a proper isogenic control to distinguish targets that also negatively affe
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Raut, Pawan Kumar, Bishwanath Chatterjee, Hana Kim, and Frederic G. Barr. "Abstract 7042: Role of Myc family proteins in the growth and oncogenic transformation of fusion-positive rhabdomyosarcoma." Cancer Research 85, no. 8_Supplement_1 (2025): 7042. https://doi.org/10.1158/1538-7445.am2025-7042.

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Abstract Fusion-positive rhabdomyosarcoma (FP RMS) is a pediatric soft tissue cancer associated with the myogenic lineage and characterized by a PAX::FOXO1 fusion gene, either PAX3::FOXO1 or PAX7::FOXO1. Our previous studies demonstrated that a human myoblast model of FP RMS requires MYCN as well as PAX3::FOXO1 for oncogenic transformation. The MYC family proteins including MYC, MYCN or MYCL are often amplified or overexpressed in different cancers, and contribute to regulation of oncogenic properties. This study aims to investigate the expression of these Myc family proteins in FP RMS cell li
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Liu, Zhiliang, Tiantian Han, Rongrong Kong, et al. "Clinical characterization of MYC family proto-oncogene amplification in solid tumors from Chinese patients." Journal of Clinical Oncology 41, no. 16_suppl (2023): e15140-e15140. http://dx.doi.org/10.1200/jco.2023.41.16_suppl.e15140.

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e15140 Background: The dysregulation of the MYC family oncogenes ( c-MYC, MYCN and MYCL) play critical roles in tumorigenesis, prognosis and immune escape. MYC inactivation can result in sustained tumour regression and many therapeutic agents that directly target MYC are under development. MYC signaling is associated with tumor cell PD-L1, overall immune cell infiltration. Herein, we explore MYC family proto-oncogene amplification profiles and clinical characterization in chinese solid tumors. Methods: This research comprehensively characterized gene mutations by next-generation sequencing (NG
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Yuan, Ye, Mohammad Alzrigat, Aida Rodriguez-Garcia, et al. "Target Genes of c-MYC and MYCN with Prognostic Power in Neuroblastoma Exhibit Different Expressions during Sympathoadrenal Development." Cancers 15, no. 18 (2023): 4599. http://dx.doi.org/10.3390/cancers15184599.

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Deregulation of the MYC family of transcription factors c-MYC (encoded by MYC), MYCN, and MYCL is prevalent in most human cancers, with an impact on tumor initiation and progression, as well as response to therapy. In neuroblastoma (NB), amplification of the MYCN oncogene and over-expression of MYC characterize approximately 40% and 10% of all high-risk NB cases, respectively. However, the mechanism and stage of neural crest development in which MYCN and c-MYC contribute to the onset and/or progression of NB are not yet fully understood. Here, we hypothesized that subtle differences in the exp
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Chernov, A. N. "The impact of the nerve growth factor on the number of MYCC, MYCN oncogene copies in human medulloblastoma cells." Malignant tumours 9, no. 1 (2019): 22–28. http://dx.doi.org/10.18027/2224-5057-2019-9-1-22-28.

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Introduction: The search for new molecular targets for chemotherapy of malignancies, particularly pediatric brain tumors, is a relevant issue of modern oncology. MYC expression and amplification is often observed in brain tumors, which is an unfavorable prognostic factor. Many oncogenic processes are regulated by some growth factors including the nerve growth factor (NGF).Purpose: To study the changes in the number of MYCCand MYCN‑gene copies in MB cells exposed to the NGF.Material and methods: The impact of the NGF on the number of MYCC‑, MYCN oncogene copies in the primary human medulloblast
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von Bueren, André O., Rolf-Dieter Kortmann, Katja von Hoff, et al. "Treatment of Children and Adolescents With Metastatic Medulloblastoma and Prognostic Relevance of Clinical and Biologic Parameters." Journal of Clinical Oncology 34, no. 34 (2016): 4151–60. http://dx.doi.org/10.1200/jco.2016.67.2428.

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Purpose To assess an intensified treatment in the context of clinical and biologic risk factors in metastatic medulloblastoma. Patients and Methods Patients (4 to 21 years old, diagnosed between 2001 and 2007) received induction chemotherapy, dose-escalated hyperfractionated craniospinal radiotherapy, and maintenance chemotherapy. Subgroup status and other biologic parameters were assessed. Results In 123 eligible patients (median age, 8.2 years old; median follow-up, 5.38 years), 5-year event-free survival (EFS) and overall survival (OS) were 62% (95% CI, 52 to 72) and 74% (95% CI, 66 to 82),
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Chico, Jose Manuel, Esther Lechner, Gemma Fernandez-Barbero, et al. "CUL3BPME3 ubiquitin ligases regulate MYC2, MYC3, and MYC4 stability and JA responses." Proceedings of the National Academy of Sciences 117, no. 11 (2020): 6205–15. http://dx.doi.org/10.1073/pnas.1912199117.

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The jasmonate (JA)-pathway regulators MYC2, MYC3, and MYC4 are central nodes in plant signaling networks integrating environmental and developmental signals to fine-tune JA defenses and plant growth. Continuous activation of MYC activity is potentially lethal. Hence, MYCs need to be tightly regulated in order to optimize plant fitness. Among the increasing number of mechanisms regulating MYC activity, protein stability is arising as a major player. However, how the levels of MYC proteins are modulated is still poorly understood. Here, we report that MYC2, MYC3, and MYC4 are targets of BPM (BTB
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Szemes, Marianna, Zsombor Melegh, Jacob Bellamy, et al. "Transcriptomic Analyses of MYCN-Regulated Genes in Anaplastic Wilms’ Tumour Cell Lines Reveals Oncogenic Pathways and Potential Therapeutic Vulnerabilities." Cancers 13, no. 4 (2021): 656. http://dx.doi.org/10.3390/cancers13040656.

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The MYCN proto-oncogene is deregulated in many cancers, most notably in neuroblastoma, where MYCN gene amplification identifies a clinical subset with very poor prognosis. Gene expression and DNA analyses have also demonstrated overexpression of MYCN mRNA, as well as focal amplifications, copy number gains and presumptive change of function mutations of MYCN in Wilms’ tumours with poorer outcomes, including tumours with diffuse anaplasia. Surprisingly, however, the expression and functions of the MYCN protein in Wilms’ tumours still remain obscure. In this study, we assessed MYCN protein expre
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Dissertations / Theses on the topic "MYCN"

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Vulcani-Freitas, Tânia Maria [UNIFESP]. "Perfil de expressão dos genes MYC, MYCN, TERT, ASPM e PRAME em Meduloblastoma." Universidade Federal de São Paulo (UNIFESP), 2010. http://repositorio.unifesp.br/handle/11600/9928.

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Made available in DSpace on 2015-07-22T20:50:35Z (GMT). No. of bitstreams: 0 Previous issue date: 2010-04-28<br>Meduloblastoma (MB) é o tumor maligno de sistema nervoso central (SNC) mais comum em criança, compreendendo 20% dos tumores primários de SNC e 40% dos tumores cerebelares da infância. Devido sua forte tendência metastática, o tratamento padrão pós-operatório inclui radio e quimioterapia, cujo impacto causa distúrbios endócrinos e de crescimento, e disfunção neurocognitiva a longo prazo. Frente a esses efeitos negativos, muitas pesquisas em meduloblastoma têm sido realizadas com in
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Östergren, Tiolina. "Identification of MYCN and SOX9 target genes and a study of drug treatment effects in medulloblastoma." Thesis, Uppsala universitet, Institutionen för biologisk grundutbildning, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-262085.

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Medulloblastoma (MB) is the most common malignant brain tumor affecting children. The transcription factors MYCN and SOX9 are associated with initiation, maintenance and recurrence of MB and are also connected to more aggressive tumors. In this study, a ChIP was performed to isolate DNA from genes that are transcriptionally regulated by these proteins. Identification of these target genes will reveal new potential drug targets and help us better understand the functions of MYCN and SOX9. The ChIP was not fully optimized during this project and the target genes were not sent for sequencing and
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George, Rani Elizabeth. "Gene co-amplification with MYCN in neuroblastoma." Thesis, University of Newcastle Upon Tyne, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.363879.

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Kenyon, Rebecca Margaret. "Analysis of the MYCN amplicon in neuroblastoma." Thesis, University of Newcastle Upon Tyne, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.321261.

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Stermann, Alexander. "MYCN-DNA-Vakzine zur Behandlung des Neuroblastoms." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2014. http://dx.doi.org/10.18452/16888.

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Das Neuroblastom (NB) zählt zu den therapieresistentesten Tumoren des Kleinkindalters. Besonders NB-Patienten mit MYCN-Amplifikation sind mit einer schlechten Prognose konfrontiert. Neuere Studien legen nahe, dass eine spezifische aktive Immuntherapie gegen MYCN ein vielversprechender Ansatz zur Bekämpfung dieser malignen Erkrankung darstellen könnte. Zur Untersuchung dieser Hypothese wurde ein sogenanntes Minigen-Vakzin, welches für drei ausgewählte Epitope aus der MYCN-AS-Sequenz kodiert, generiert. Die Auswahl der Minigen-Epitope erfolgte mit dem MHC-Liganden-Vorhersageprogramm syfpeithi, w
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Duarte, Alexandra. "The interplay between MYCN and the DNA damage response : modulation of MYCN expression, its interactions with components of the DNA damage response and cellular responses to N-myc following genotoxic stress." Thesis, Imperial College London, 2012. http://hdl.handle.net/10044/1/9832.

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The DNA damage response (DDR) forms a signaling cascade rapidly activated upon exposure to genotoxic stress. The DDR safeguards genomic integrity by halting cell cycle progression to allow repair of damaged DNA or by inducing cell death. Myc proteins are key regulators of cell proliferation that transcriptionally control the cell cycle machinery. Amplification of N-myc in neuroblastomas (MNA-NB) is associated with abrogation of the regulatory mechanisms that normally prevent aberrant cell proliferation and the interplay between N-myc and the DDR was here analysed. Initially, an association bet
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Ottaviani, Daniela. "In-Depth Characterization of Human Retinoblastoma Subtype 2 and Preclinical Models." Thesis, Université Paris-Saclay (ComUE), 2019. http://www.theses.fr/2019SACLS001.

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Le rétinoblastome, un cancer pédiatrique de la rétine en développement, est la tumeur intraoculaire la plus fréquente chez l’enfant et représente environ 4 % de tous les cancers infantiles. Bien qu'il s'agisse d'une maladie rare, l'hôpital Curie (centre de référence pour le rétinoblastome en France) accueille environ 50 à 60 nouveaux patients chaque année. Notre groupe a précédemment caractérisé deux sous-types de rétinoblastomes. Les tumeurs de type « cone-like » ou sous-type 1 sont plutôt différenciées et homogènes, présentent une surexpression des gènes liés aux cellules cônes (photorécepte
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Maeshima, Ruhina. "MYCN silencing as therapeutics for neuroblastoma using RNA interference." Thesis, University College London (University of London), 2018. http://discovery.ucl.ac.uk/10043849/.

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Neuroblastoma (NB) is the most common solid tumour in childhood and accounts for 15% of childhood cancer deaths. It is known that high-risk NB is highly correlated with MYCN amplification. Overexpressed MYCN induces proliferation and cell growth and suppresses apoptosis and differentiation pathways in NB cells. Since RNA interference (RNAi) was first described, many research groups have investigated the application of RNAi with the use of short interfering RNA (siRNA). Our aim is to induce apoptosis and differentiation using RNAi as a novel therapeutic strategy for MYCN-amplified NB. Our hypot
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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 genomi
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Solari, Valeria. "MYCN-dependent expression of sulfatase-2 regulates neuroblastoma cells." Thesis, University of Liverpool, 2014. http://livrepository.liverpool.ac.uk/2003528/.

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Neuroblastoma (NBL) is the most common type of cancer diagnosed in the first year of life. It is a complex and heterogeneous disease that arises from the developing sympathetic nervous system. Despite numerous advances and the well-demonstrated role of MYCN in the pathogenesis of neuroblastoma, the mechanisms underlying its oncogenic function are not entirely understood and there is evidence that its function is, in part, dependent on the tumour microenvironment (TME). New and improved therapeutic targets are urgently required for this often lethal tumour. Heparan sulfate proteoglycans (HSPG)
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Books on the topic "MYCN"

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Zhang, Shuobo. Transcription factor activating protein 4 is synthetic lethal and a master regulator of MYCN amplified neuroblastoma. [publisher not identified], 2015.

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Asril, Sutan Zaili. Mimpi-mimpi Myan. Padang Ruang Kreatifitas, 2012.

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Wiwŏnhoe, Chinwi-myŏn Chi P'yŏch'an. Chinwi-myŏn chi. P'yŏngt'aek-si Munhwawŏn, 1999.

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Han'guk Munhwawŏn Yŏnhaphoe. Cheju T'ŭkpyŏl Chach'ido Chihoe. Ch'uja-myŏn yŏksa munhwaji. Han'guk Munhwawŏn Yŏnhaphoe Cheju T'ŭkpyŏl Chach'ido Chihoe, 2012.

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Jung-in, Choi, Lim Yeong-Hee 1960-, and Nagel Françoise 1951-, eds. Le rêve de Myun. Chan-Ok, 2009.

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Soucek, Laura, and Jonathan Whitfield, eds. The Myc Gene. Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1476-1.

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Soucek, Laura, and Nicole M. Sodir, eds. The Myc Gene. Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-429-6.

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Welsh Joint Education Committee, ed. Myn brain i! Y Lolfa, 2007.

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Ch'oe, Sŏ-myŏn. Chʻoe Sŏ-myŏn Monggol kihaeng. Samsŏng Chʻulpʻansa, 1990.

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Chin, Yong-sŏn. Chŏngsŏn Imgye-myŏn chimyŏng yurae. Chŏngsŏn-gun Imgye-myŏn, 2011.

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Book chapters on the topic "MYCN"

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Kamijo, Takehiko. "Neuroblastoma: Role of MYCN/Bmi1 Pathway in Neuroblastoma." In Pediatric Cancer. Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-2418-1_15.

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Liang, He. "Role of MYCN gene in high-risk neuroblastoma." In Biological Sciences and Environmental Health. CRC Press, 2024. http://dx.doi.org/10.1201/9781003587590-10.

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Italia, Matteo, and Fabio Dercole. "In Silico Modelling, Analysis, and Control of Complex Diseases: Addressing Clinical Questions, Personalized Treatments, and Healthcare Management." In SpringerBriefs in Applied Sciences and Technology. Springer Nature Switzerland, 2025. https://doi.org/10.1007/978-3-031-80268-3_8.

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Abstract Human diseases are complex and dynamic. Understanding and controlling diseases require interdisciplinary approaches, aided by advances in digital technology, data analysis, and computational power. Specifically, in his Ph.D. Thesis, Matteo Italia has developed in silico models to study cancers, Restless Legs Syndrome (RLS), and Covid-19. The goals are to answer clinical questions, optimize treatments, and manage healthcare. For cancers, the developed models suggest that dynamic and personalized protocols can overcome drug resistance more effectively than static protocols. For neurobla
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Xiang, Xiang, Zihan Zhang, Xuehua Peng, and Jianbo Shao. "Learning-Based Detection of MYCN Amplification in Clinical Neuroblastoma Patients: A Pilot Study." In Multiscale Multimodal Medical Imaging. Springer Nature Switzerland, 2022. http://dx.doi.org/10.1007/978-3-031-18814-5_9.

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Hatzi, Elissavet, Theodore Fotsis, Carol Murphy, et al. "MYCN Oncogene and Angiogenesis: Down-Regulation of Endothelial Growth Inhibitors in Human Neuroblastoma Cells." In Advances in Experimental Medicine and Biology. Springer US, 2000. http://dx.doi.org/10.1007/978-1-4615-4221-6_19.

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Yagyu, Shigeki, and Tomoko Iehara. "MYCN Nonamplified Neuroblastoma: Detection of Tumor-Derived Cell-Free DNA in Serum for Predicting Prognosis of Neuroblastoma." In Pediatric Cancer, Volume 4. Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-6591-7_2.

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Surace, Cecilia. "Medulloblastoma: Role of MYCN Gene Amplification Using Fluorescence In Situ Hybridization and Real Time Quantitative PCR Methods." In Pediatric Cancer, Volume 3. Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-4528-5_15.

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Schnupp, Peter, and Ute Leibrandt. "Mycin." In Expertensysteme. Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-662-00752-5_3.

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Schnupp, Peter, and Ute Leibrandt. "Mycin." In Expertensysteme. Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-95565-5_3.

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Ruiz-Pérez, María Victoria, Anna Frenzel, and Marie Arsenian Henriksson. "MYC." In Encyclopedia of Signaling Molecules. Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_319.

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Conference papers on the topic "MYCN"

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Aifantis, Iannis. "Abstract IA09: Dynamic regulation of MYC and MYCN ubiquitination." In Abstracts: AACR Special Conference on Myc: From Biology to Therapy; January 7-10, 2015; La Jolla, CA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1557-3125.myc15-ia09.

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Stermann, Alexander, Nicole Huebener, Diana Seidel, et al. "Abstract 4758: A new syngeneic MYCN-overexpressing neuroblastoma mouse model and MYCN-DNA vaccine." 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.am10-4758.

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Ikegaki, Naohiko, and Xao Tang. "Abstract 1218: A biological crosstalk between p53 and MYCN/MYC in neuroblastoma." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-1218.

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Tran, Hung N., Donglai Qi, and David Cobrinik. "Abstract 3703: MDM2 regulation of MYC and MYCN in pediatric neural cancers." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-3703.

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Stermann, Alexander, Nicole Huebener, and Holger N. Lode. "Abstract LB-155: A new syngeneic MYCN-overexpressing neuroblastoma mouse model and MYCN-DNA vaccine." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-lb-155.

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Kawauchi, Daisuke, Giles Robinson, Tamar Uziel, et al. "Abstract 3444: Enforced expression of MycN and C-Myc induces different medulloblastoma subtypes." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-3444.

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Wang, Larry L., Risa Teshiba, Naohiko Ikegaki, et al. "Abstract A37: Immunohistochemical detection of MYCN protein and MYC protein identifies highly aggressive neuroblastomas." In Abstracts: AACR Special Conference on Myc: From Biology to Therapy; January 7-10, 2015; La Jolla, CA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1557-3125.myc15-a37.

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Tanimoto, Terutaka, Hiroshi Tazawa, Hiroshi Noso, et al. "Abstract 5816: Ablation of oncogenic MYCN expression by hTERT-driven oncolytic adenovirus induces cell death in MYCN-amplified neuroblastoma." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-5816.

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Helmsauer, K., M. Valieva, S. Ali, et al. "Enhancer hijacking on the MYCN amplicon in neuroblastoma." In 33. Jahrestagung der Kind-Philipp-Stiftung für pädiatr. onkolog. Forschung. © Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1709775.

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Trajkovski, Marko, Metka Vivod, Mateus Webba da Silva, and Janez Plavec. "G-Quadruplex formation within proximal promoter of MYCN." In XVth Symposium on Chemistry of Nucleic Acid Components. Institute of Organic Chemistry and Biochemistry, Academy of Sciences of the Czech Republic, 2011. http://dx.doi.org/10.1135/css201112483.

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Reports on the topic "MYCN"

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George, Rani E. A Genetically Engineered Mouse Model of Neuroblastoma Driven by Mutated ALK and MYCN. Defense Technical Information Center, 2014. http://dx.doi.org/10.21236/ada613947.

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ธัญญะกิจไพศาล, พสุธา, та Bidwell, Joseph P. การศึกษาคุณสมบัติของสารซิมวาสเตติน ต่อการกระตุ้นการเพิ่มจำนวนเซลล์ และระดับอาร์เอ็นเอนำรหัสของ c-fos และ c-myc ในเซลล์สร้างกระดูก : รายงานวิจัยฉบับสมบูรณ์. จุฬาลงกรณ์มหาวิทยาลัย, 2003. https://doi.org/10.58837/chula.res.2003.9.

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งานวิจัยนี้มีวัตถุประสงค์เพื่อศึกษาผลของสารซิมวาสเตตินต่อการเพิ่มจำนวนเซลล์และระดับอาร์เอ็นนำรหัสของจีน c-fos และ c-myc ของเซลล์สร้างกระดูกที่แยกจากกระโหลกศีรษะของหนูแรกเกิดและเซลล์สร้างกระดูกที่แยกจากไขกระดูกของหนู โดยเซลล์จะถูกทดสอบด้วยสารซิมวาสเตตินในระดับความเข้มข้นที่กำหนดเป็นเวลา 24 ชั่วโมง จากนั้นเซลล์จะถูกวิเคราะห์ด้วยสารเอ็มทีที, [[superscript 3]H] thymidine incorporation assay และ Northern blot ตามลำดับ ผลการทดลองพบสารซิมวาสเตตินที่ระดับความเข้มข้น 2 ไมโครโมลาร์มีความเป็นพิษต่อเซลล์สร้างกระดูกที่แยกจากกระโหลกศีรษะและไขกระดูกของหนูอย่างมีนัยสำคัญทางสถิติเมื่อเปรียบเทียบกับกลุ่มควบคุม
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Dickson, Robert B. TGFa-myc Interactions in Mammary Tumorigenesis. Defense Technical Information Center, 1998. http://dx.doi.org/10.21236/ada360094.

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Dickson, Robert B. TGFa-myc Interactions in Mammary Tumorigenesis. Defense Technical Information Center, 1997. http://dx.doi.org/10.21236/ada334931.

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Dickson, Robert B. TGFa-myc Interactions in Mammary Tumorigenesis. Defense Technical Information Center, 1995. http://dx.doi.org/10.21236/ada301626.

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Erdmann, Martin. Lebensdauer des Farbigen Protons in der Myon-Proton-Streuung. Office of Scientific and Technical Information (OSTI), 1990. http://dx.doi.org/10.2172/1426711.

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Benaud, Christelle. Role in MYC in Anchorage-Dependent Growth. Defense Technical Information Center, 1999. http://dx.doi.org/10.21236/ada377816.

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Blume, Scott. Targeting mrtl to Reverse Myc in Breast Oncogenesis. Defense Technical Information Center, 2011. http://dx.doi.org/10.21236/ada552553.

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Prochownik, Edward. Evaluation of Molecular Inhibitors of the c-Myc Oncoprotein. Defense Technical Information Center, 2008. http://dx.doi.org/10.21236/ada502505.

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Jang, Joanne. The Role of RAs in Myc-Induced Mammary Tumorigenesis. Defense Technical Information Center, 2005. http://dx.doi.org/10.21236/ada446568.

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