Publications by authors named "G Milazzo"
Article Synopsis
- MYCN oncogene amplification is linked to aggressive childhood neuroblastoma, but a study found a germline mutation in Runx1t1 that can prevent tumor development associated with MYCN.
- This mutation affects a conserved zinc finger domain and reduces the risk of neuroblastoma by inhibiting cell growth and reversing hyperplasia, which is a precursor to tumor formation.
- RUNX1T1 is part of a transcriptional repression complex that impacts chromatin accessibility without directly regulating MYCN, and its silencing affects other cancers, indicating its broader significance in tumor biology.
Neuroblastoma (NB) is one of the primary causes of death for pediatric malignancies. Given the high heterogeneity in NB's mutation landscape, optimizing individualized therapies is still challenging. In the context of genomic alterations, amplification is the most correlated event with poor outcomes.
View Article and Find Full Text PDFThe molecular mechanisms and gene regulatory networks sustaining cell proliferation in neuroblastoma (NBL) cells are still not fully understood. In this tumor context, it has been proposed that anti-proliferative drugs, such as the pan-HDAC inhibitor panobinostat, could be tested to mitigate tumor progression. Here, we set out to investigate the effects of panobinostat treatment at the unprecedented resolution offered by single-cell sequencing.
View Article and Find Full Text PDFNeuroblastoma (NB) is a childhood cancer arising from sympatho-adrenal neural crest cells. MYCN amplification is found in half of high-risk NB patients; however, no available therapies directly target MYCN. Using multi-dimensional metabolic profiling in MYCN expression systems and primary patient tumors, we comprehensively characterized the metabolic landscape driven by MYCN in NB.
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