Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0027819 (neuroblastoma)
 27,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

MYEOV and NEGR1 are novel candidate gene targets in neuroblastoma that were identified by chromosomal gain in 11q13 and loss in 1p31, respectively, through single nucleotide polymorphism array analysis. In the present study, to assess the involvement of MYEOV and NEGR1 in the pathogenesis of neuroblastoma, we analyzed their mutation status and/or expression profiles in a panel of 55 neuroblastoma samples, including 25 cell lines, followed by additional functional studies. No tumor-specific mutations of MYEOV or NEGR1 were identified in our case series. Expression of MYEOV was upregulated in 11 of 25 cell lines (44%) and in seven of 20 fresh tumors (35%). The siRNA-mediated knockdown of MYEOV in NB-19 cells, which exhibit high expression of MYEOV, resulted in a significant decrease in cell proliferation (P = 0.0027). Conversely, expression studies of NEGR1 revealed significantly lower expression of this gene in neuroblastomas at an advanced stage of the disease. Exogenous NEGR1 expression in neuroblastoma cells induced significant inhibition of cell growth (P = 0.019). The results of these studies provide supporting evidence for MYEOV and NEGR1 as gene targets of 11q13 gains and 1p31 deletions in a neuroblastoma subset. In addition, the findings suggest a possible prognostic value for NEGR1 in neuroblastoma.
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PMID:Aberrations of NEGR1 on 1p31 and MYEOV on 11q13 in neuroblastoma. 2162 8

Neuroblastoma (NB) is the most common extracranial malignant tumor of childhood and is characterized by a broad heterogeneity in clinical presentation and evolution. Recent advances in pangenomic analysis of NB have revealed different recurrent chromosomal aberrations. Indeed, it is now well established that the overall genomic profile is important for treatment stratification. In previous studies, 11 genes were shown to be recurrently amplified (ODC1, ALK, GREB1, NTSR2, LIN28B, MDM2, CDK4, MYEOV, CCND1, TERT, and MYC) besides MYCN, with poor survival of NB patients harboring these amplifications being suggested. 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. Clinical data were retrospectively collected. We additionally evaluated the association of FRS2 gene expression with NB patient outcome using the public R2 Platform. We found eight NB samples with high grade amplification of one or two loci on chromosome arm 12q. The regional amplifications were located on bands 12q13.3-q14.1 and 12q15-q21.1 involving the genes CDK4, MDM2, and the potential oncogenic gene FRS2. The CDK4, MDM2, and FRS2 loci were coamplified in 8/8 samples. The 12q amplifications were associated with very poor prognosis and atypical clinical features of NB patients. Further functional and clinical investigations are needed to confirm or refute these associations.
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PMID:Genomic coamplification of CDK4/MDM2/FRS2 is associated with very poor prognosis and atypical clinical features in neuroblastoma patients. 3175 73

Neuroblastoma (NB) is the most common extracranial solid tumor derived from neural crest in children. Recently, the role of miRNA has been studied extensively in the development of NB. Here, we investigated the clinical significance of microRNA-490-5p (miR-490-5p) in NB. A total of 72 pairs of NB tumor tissues and matched adjacent normal nerve tissues were collected from NB patients. The expression of miR-490-5p was significantly down-regulated in NB tissues and cell lines using quantitative real-time PCR. Using Pearson Chi-square test and Kaplan-Meier analysis, we found that significantly decreased miR-490-5p levels were correlated with INSS stage, lymph-node metastasis, and poor survival prognosis in NB patients. MiR-490-5p overexpression significantly suppressed cell proliferation migration, invasion, and induced cell cycle G0/G1 arrest and cell apoptosis in NB cell lines (SH-SY5Y and SK-N-SH) using CCK-8, flow cytometry, and transwell assays. Mechanistically, MYEOV was confirmed as a target gene of miR-490-5p by luciferase reporter assay. Furthermore, MYEOV knockdown imitated, while overexpression rescued the changes in the biological features of miR-490-5p on NB cells. Our results demonstrated for the first time that miR-490-5p functions as a tumor suppressor in NB by targeting MYEOV, which might provide novel approaches for the treatment of NB.
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PMID:MiR-490-5p functions as tumor suppressor in childhood neuroblastoma by targeting MYEOV. 3189 78