The only common CNV across all tumors was 17q gain, with differing chromosomal coordinates across samples but a common region of overlap distal to 17q21.31, suggesting this adverse prognostic biomarker may offer insight about additional drivers for multifocal neuroblastoma in patients with germline PHOX2B or NF1 aberrations.
C/EBPβ overexpression increases SNCA expression in neuroblastoma cells and putative C/EBPβ and δ binding sites are present in the SNCA genomic region suggesting that these proteins could regulate SNCA transcription.
The results also establish that LIN28B overexpression supports neuroblastoma onset and the metastatic potential of malignant cells through let-7a-dependent and let-7a-independent mechanisms.
We established the model system, OHC-NB1, from a bone marrow metastasis from a patient diagnosed with MYCN-amplified neuroblastoma and performed whole-exome sequencing on the source metastasis and the different models and passages during model development (monolayer cell line, 3D spheroid culture and subcutaneous xenograft tumors propagated in mice).
Here, we investigated the neuroprotective and restorative involvement of the DA DA-JC1 and liraglutide (Lg), a single GLP-1 receptor analogue, in vitro using human neuroblastoma (SH-SY5Y) against oxidative stress induced by oxygen peroxide (H<sub>2</sub>O<sub>2</sub>), and in vivo, in a mouse model of Alzheimer's disease (AD), APP/PS1.
In high-risk patients, CGH+SNP microarray analysis of primary neuroblastoma identifies SRCIN1 as frequently altered by hemizygous deletion, copy-neutral loss of heterozygosity, or disruption.
We showed that SESN2 and LC3II expressions were elevated, whereas SIRT1 and TPP1 expressions were decreased in the Aβ<sub>1-42</sub> -exposed human neuroblastoma cells (SH-SY5Y).
In summary, our meta-analysis is the first to provide clear evidence of an association between specific polymorphisms of LMO1 and susceptibility to NB.
To determine whether the therapeutic effect of trichostatin A on Alzheimer's disease is associated with the nuclear factor erythroid 2-related factor 2 (Nrf2) and Kelch-like epichlorohydrin-related protein-1 (Keap1) signaling pathway, amyloid β-peptide 25-35 (Aβ<sub>25-35</sub>) was used to induce Alzheimer's disease-like pathological changes in SH-SY5Y neuroblastoma cells.
To investigate the relations between anaplastic lymphoma kinase (<i>ALK</i>) and v-myc myelocytomatosis viral related oncogene neuroblastoma derived homolog (<i>MYCN</i>) protein expression and their prognostic roles in neuroblastoma tumours.
Genomic profiles of 628 NB samples analyzed by array-comparative genome hybridization (a-CGH) were re-examined to identify gene amplifications other them MYCN amplification.
Using biochemical, molecular, transmission electron microscopy, immunoblotting and immunofluorescence analyses, we studied the protective effects of ligand 1 against Aβ-induced synaptic and mitochondrial toxicities in mouse neuroblastoma (N2a) cells that express mutant APP.
In this study, neurotoxin-induced GDNF overexpression was detected for the first time in MES23.5 DA immortalized neuroblastoma (MES23.5 DA) cells soon after 6-hydroxydopamine (6-OHDA) treatment.
Since most cases are in children under the age of 2, understanding the role and regulation of ALK during neural crest development is an important goal in addressing neuroblastoma tumorigenesis.
Some of these shared susceptibility loci regulate the expression of relevant genes involved in NCC formation and developmental processes (such as <i>BARD1,</i><i>MSX1,</i> and <i>SHOX2</i>) and are enriched in several epigenetic markers from NB and fetal heart cell lines.