Amplification of MYCN is the most prominent genetic marker of high-stage neuroblastoma, a childhood tumor originating from the neural crest. We generated a cell line (mNB-A1) from tumors developed in transgenic mouse and treated these cells with DMSO (n=6), the BRD4-inhibitor JQ1 (n=3) or the AURKA-inhibitor MLN8237 (n=3) for 24 h.
A Cre-conditional MYCN-driven neuroblastoma mouse model as an improved tool for preclinical studies.
Specimen part, Cell line, Treatment
View SamplesNeo/null loss of Tfap2a in E10.5 mouse facial prominences
Tfap2a-dependent changes in mouse facial morphology result in clefting that can be ameliorated by a reduction in Fgf8 gene dosage.
Specimen part
View SamplesThe goal of the experiment was to determine the transcriptional expression profile of zebrafish thrombocytes in order to enable comparison with mouse and human platelets. Overall design: Thrombocyte isolation from Tg(cd41:EGFP) zebrafish peripheral blood was performed using a novel monoclonal antibody (3H9) to Cd41
Sorting zebrafish thrombocyte lineage cells with a Cd41 monoclonal antibody enriches hematopoietic stem cell activity.
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View SamplesThe TP53 transcription factor is frequently mutated at later stages of epithelial cancers, indicating a possible role in their invasion and metastasis. Importantly, in most cases rather than a simple loss of function p53 mutation, point mutations of p53 accumulate at the protein level and may have dominant negative functions. This study analyses gene expression differences between mice harbouring p53 mutation who do and do not develop metastasis.
Targeting the LOX/hypoxia axis reverses many of the features that make pancreatic cancer deadly: inhibition of LOX abrogates metastasis and enhances drug efficacy.
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