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The latter approach is most likely to be useful in neuroblastoma with mutant p53.
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Together our data suggest that targeting glycolysis-metabolism in neuroblastoma with 17q amplification might be a useful, non-genotoxic strategy to overcome chemotherapy resistance in patients with high-stage disease.
Another report showed a decreased expression level of ACCN1 in neuroblastomas with high telomerase activity [41].
RASSF1A methylation in serum could have useful clinical applications in neuroblastoma management, if our results are confirmed in larger studies.
PolySia-NCAM appears to be a new clinically significant molecular marker in neuroblastoma, hopefully with additional value in neuroblastoma risk stratification.
Background.MYCN (N-myc) amplification in neuroblastoma is associated with poor clinical outcome.
Naslavsky, N. et al. Sphingolipid depletion increases formation of the scrapie prion protein in neuroblastoma cells infected with prions.
Chen, Y. & Stallings, R. L. Differential patterns of microRNA expression in neuroblastoma are correlated with prognosis, differentiation, and apoptosis.
However, encouraging results from early phase trials have been only obtained in neuroblastoma patients treated with anti-GD2 CAR-T cells, and in ErbB2-positive sarcomas treatment24.
PRKCDBP methylation in neuroblastoma was associated with unfavourable outcome [ 80].
As described previously [7], LMO3 has an oncogenic potential in collaboration with HEN2 in neuroblastoma cells.
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