Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA295019 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Expression data from neuroblastoma of TH-MYCN/KI Alk mice
| PRJNA201043 | ENA
Project description:The RET gene has been identified previously as a target of activated ALK at the mRNA level in both human neuroblastoma cell lines and primary tumors as well as in murine tumors driven by mutated Alk and MYCN. Moreover, it has been shown that tumor growth of murine TH-MYCN/KI Alkmut tumors was impaired upon Ret inhibition by the vandetanib inhibitor, suggesting RET as a therapeutic target in ALK mutated neuroblastoma. To further demonstrate the crucial role of RET in ALK mutated driven neuroblastoma oncogenesis, transgenic TH-MYCN mice were bred with KI RetM919T tumors. We document an oncogenic cooperation between activated Ret and MYCN overexpression in neuroblastoma formation. We used microarrays to analyze the global programme of gene expression of MYCN/RetM919T tumors and compare these profiles with profiles of MYCN/Alkmut tumors (GSE46583). Altogether, our data show that MYCN/RetM919T tumors present with expression profiles close to MYCN/Alkmut tumors.
2017-09-15 | GSE72678 | GEO
Project description:It has been already reported that there are undifferentiated/proliferating neuroblasts in the postnatal sympathetic ganglia in TH-MYCN mice, a neuroblastoma model. We established suitable spheroid culture condition that selectively isolates undifferentiated neuroblasts from superior mesenteric ganligon (SMG) of TH-MYCN mice. In order to investigate the chromosomal alterations (gains or losses) of spheres derived from TH-MYCN mice, we carried out array comparative genomic hybridization. We investigated whether chromosomal alterations occured during early neuroblastoma tumorigenesis in TH-MYCN mice.
2017-04-01 | GSE89740 | GEO
Project description:Regulation of mRNA splicing is a critical and tightly regulated cellular function, underlying the majority of proteomic diversity in our genomes. While disruption of this process is common in disease, the basic genetic complexity of alternative splicing in vivo remains poorly understood. To delineate the splicing landscape in disease, we used an integrative genomics approach and combined both genome and exon level transcriptome data in two somatic tissues (cerebella and peripheral ganglia) from a transgenic mouse model of neuroblastoma, a tumor that arises from peripheral ganglia. These data identify splicing quantitative trait loci (sQTL) that modulate differential splicing across the genome. Among these, an sQTL at FUBP1 revealed a splicing event that modulated levels of the MYC oncoprotein in human neuroblastoma-derived cell lines and correlated with outcome in neuroblastoma. Through this unbiased sQTL analysis, we also define de novo splicing motifs that serve as sites for recurrent mutations in cancer and lead to functional changes in exon expression, enhancing our understanding of the cancer genome. Exon expression from Superior Cervical Ganglia and Cerebellum from 102 backcrossed mice (TH-MYCN, FVB/NJ and 129/SvJ) were correlated with 349 genotyping markers to identify putative sQTL The mice were the N1 generation of a backcross between TH-MYCN (FVB/NJ background) and wild-type 129/SvJ: TH-MYCN (FVB/NJ) + 129/SvJ -> F1 (TH-MYCN FVB/NJ,129/SVJ) F1 (TH-MYCN FVB/NJ,129/SVJ) + 129/SvJ -> N1
2015-04-03 | E-GEOD-55248 | biostudies-arrayexpress
Project description:In order to investigate the chromosomal alterations (gains or losses) of tumor tissuees developed in TH-MYCN mice, a neuroblastoma model, we carried out array comparative genomic hybridization. We investigated whether chromosomal alterations occured in the tumor tissues developed in the abdomen of TH-MYCN hemizygote mice.
2017-04-01 | GSE89739 | GEO
Project description:It has been already reported that there are undifferentiated/proliferating neuroblasts in the postnatal sympathetic ganglia in TH-MYCN mice. We established suitable spheroid culture condition that selectively isolates undifferentiated neuroblasts from superior mesenteric ganligon (SMG) of TH-MYCN mice. In the present study, in order to investigate the transcriptomic differences between embryonic day 13.5 (E13.5) WT derived primary spheres and E13.5 TH-MYCN derived passageable spheres, we carried out microarray gene expression analysis. We investigated critical molecular events in MYCN-transformed neuroblastoma cells in TH-MYCN mice.
2017-04-01 | GSE87783 | GEO
Project description:Enhancer invasion shapes MYCN dependent transcriptional amplification in neuroblastoma [ChIP-seq Th-MYCN]
| PRJNA392062 | ENA
Project description:TH-MYCN Mice with Caspase-8 Deficiency Develop Advanced Neuroblastoma with Bone Marrow Metastasis
| PRJNA182245 | ENA
Project description:TH-MYCN Mice with Caspase-8 Deficiency Develop Advanced Neuroblastoma with Bone Marrow Metastasis
| PRJNA179446 | ENA
Project description:Changes in epigenetic regulation are believed to be a major contributing factor to neuroblastoma development. Using a large-scale in vivo mutagenesis screen in Th-MYCN transgenic mice, we identified a single point mutation in the transcriptional corepressor Runx1t1, that can block N-myc-driven neuroblastoma tumorigenesis. The loss of function mutation disrupts a highly conserved zinc finger domain (NHR4) within Runx1t1. Crossing an independent Runx1t1 knockout model with Th-MYCN mice, demonstrated that Runx1t1 haploinsufficiency is enough to prevent neuroblastoma development and reverse ganglia hyperplasia. Silencing RUNX1T1 in human neuroblastoma cells resulted in decreased colony formation in vitro, and significant inhibition of tumor growth in vivo. Our results show that RUNX1T1 forms part of a transcriptional LSD1-CoREST3-HDAC repressive complex that regulates the epigenomic landscape and chromatin accessibility, to control neuron-specific pathway genes and maintain an undifferentiated state. Runx1t1 thus represents an entirely novel and highly promising target not previously described in neuroblastoma.
2024-08-10 | PXD050375 | Pride