Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA222324 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:scRNAseq in Dbh-iCre LSL-MYCN mouse model of neuroblasoma
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Project description:Expression profiling of murine MYCN-driven neuroendocrine tumor from LSL-MYCN hGFAP-Cre mice.
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Project description:Neuroblastoma is an embryonal tumor arising from the neural crest. It can be mimicked in mice by neural crest-specific overepxression of oncogenes such as MYCN or mutated ALK. Expression profiling of murine neuroblastoma driven by MYCN were compared to those driven by mutated ALK and to mouse normal adrenal tissue.
2012-03-31 | E-GEOD-32386 | biostudies-arrayexpress
Project description:Analysis of differential gene expression. The influence of a constitutively activated mutant Kit receptor on gene expression in fetal hematopoietic cells was analyzed. Results provide information of genes and cellular processes that are influenced by Kit signaling. Total RNA obtained from embryonic day E13.5 fetal liver of double transgenic R26-LSL-KITD816V:Vav-iCre mice compared to single transgenic controls. R26-LSL-KITD816V mice have been registered with the mouse genome database (MGI:5516508, allele named Gt(ROSA)26sorTM1(GFP-cKIT*)Hsc). Vav-iCre mice have been described by De Boer et al. in 2003.
2014-10-17 | E-GEOD-53581 | biostudies-arrayexpress
Project description:The ALK^F1174L mutation is associated with intrinsic and acquired resistance to crizotinib and cosegregates with MYCN in neuroblastoma. In this study, we generated a mouse model overexpressing ALK^F1174L in the neural crest. Comapred to mice expressing ALK^F1174L or MYCN alone, combined expression of the two aberrations led to development of neuroblastoma with a shorter latency and higher penetrance. Here, we evaluated the transcriptional profiles of MYCN-driven neuroblastomas with or without the expression of ALK^F1174L to determine the pathogenic consequences of the ALK^F1174L/MYCN interaction in neuroblastoma. 10 mice were analysed in this study. Five ALK^F1174L/MYCN tumors were compared with five MYCN tumors. Total RNA was extracted, samples were labeled and processed using the Agilent Low Input Quick Amp two color Cy3(sample) and Cy5 (mouse reference) labeling kit and hybridized to Agilent SurePrint G3 Mouse Gene Expression arrays.
2012-07-04 | E-GEOD-35560 | biostudies-arrayexpress
Project description:The ALK^F1174L mutation is associated with intrinsic and acquired resistance to crizotinib and cosegregates with MYCN in neuroblastoma. In this study, we generated a mouse model overexpressing ALK^F1174L in the neural crest. Comapred to mice expressing ALK^F1174L or MYCN alone, combined expression of the two aberrations led to development of neuroblastoma with a shorter latency and higher penetrance. Here, we evaluated the transcriptional profiles of MYCN-driven neuroblastomas with or without the expression of ALK^F1174L to determine the pathogenic consequences of the ALK^F1174L/MYCN interaction in neuroblastoma.
2012-07-05 | GSE35560 | GEO
Project description:Amplification of MYCN is the most prominent genetic marker of high-stage neuroblastoma, a childhood tumor originating from the neural crest. We generated a transgenic mouse with Cre-conditional induction of MYCN in dopamine beta hydroxylase expressing cells that develops murine neuroblastomas.
2014-09-01 | GSE51297 | GEO
Project description:MYCN amplification in neuroblastoma leads to aberrant expression of MYCN oncoprotein, which binds active genes promoting transcriptional amplification. Yet how MYCN coordinates transcription elongation to meet productive transcriptional amplification and which elongation machinery represents MYCN-driven vulnerability remain to be identified. We conducted a targeted screen of transcription elongation factors and identified the super elongation complex (SEC) as a unique vulnerability in MYCN-amplified neuroblastomas. MYCN directly binds EAF1 and recruits SEC to enhance processive transcription elongation. Depletion of EAF1 or AFF1/AFF4, another core subunit of SEC, leads to a global reduction in transcription elongation and elicits selective apoptosis of MYCN-amplified neuroblastoma cells. A combination screen reveals SEC inhibition synergistically potentiates the therapeutic efficacies of FDA-approved BCL2 antagonist ABT-199, in part due to suppression of MCL1 expression, both in MYCN-amplified neuroblastoma cells and in patient-derived xenografts. These findings identify disruption of the MYCN-SEC regulatory axis as a promising therapeutic strategy in neuroblastoma.
2023-05-10 | PXD039332 | Pride
Project description:Amplification of MYCN is the most prominent genetic marker of high-stage neuroblastoma, a childhood tumor originating from the neural crest. We generated a transgenic mouse with Cre-conditional induction of MYCN in dopamine beta hydroxylase expressing cells that develops murine neuroblastomas. The expression profiles of six tumors from adrenals and two tumors from superial cervical gangliae were compared to three non-malignant adrenals from wildtype mice. These profiles of adrenals have been previously described (Molenaar et al., Nature Genetics 2012). Wild type samples are accessible at the AMC webpage: http://hgserver1.amc.nl/cgi-bin/r2/main.cgi, and accessible for registered users.
2014-09-01 | E-GEOD-51297 | biostudies-arrayexpress
Project description:To confirm the neuroblastomas (NB) identity of human neuroblastomas from mouse-human neural crest chimeric mice model (CHNBs) we characterized their gene expression profiles by RNA-Seq (CHNBs MYCN+ALKF1174L; n=8). For a global comparison of gene expression profiles of CHNBs with other NB models, we further collected RNA-seq data from patient derived xenografts of neuroblastoma (PDX NBs ; MYCNamp+ALKwt PDX; n=2, and MYCNamp+ALKF1174L PDX; n=3), neuroblastomas from genetically engineered mouse model (GEMM NBs; Th-MYCN+ALKF1174L; n=3), neuroblastoma established cell lines (n=2; Kelly, MYCNamp+ALKF1174L; SH-SY5Y, MYCNwt+ ALKF1174L), human pluripotent derived human neural crest cells (hNCCs; wt hNCCs; n=2, and MYCN+ALKF1174L hNCCs, with Dox; n=2) and from hNCC xenografts (MYCN+ALKF1174L; n=5).
2020-01-29 | GSE144366 | GEO