Correction: Corrigendum: Selective targeting of HDAC1/2 elicits anticancer effects through Gli1 acetylation in preclinical models of SHH Medulloblastoma

Coni, Sonia; Mancuso, Anna Barbara; Magno, Laura Di; Sdruscia, Giulia; Manni, Simona; Serrao, Silvia Maria; Rotili, Dante; Spiombi, Eleonora; Bufalieri, Francesca; Petroni, Marialaura; Kusio-Kobiałka, Monika; Smaele, Enrico De; Ferretti, Elisabetta; Capalbo, Carlo; Mai, Antonello; Niewiadomski, Paweł; Screpanti, Isabella; Canettieri, Gianluca

doi:10.1038/srep46645

Cited by 7 publications

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“…HDACi further enhances the anticancer efficacy of other therapeutic regimens, such as ionizing radiation (IR) and can synergize with PI3K or MAPK/ERK inhibitors to impair tumour growth in vivo ( 150 – 152 ). Mechanistically, HDACi have been associated with different biological activities in MB, including the dissipation of mitochondrial membrane potential, changes in cell stemness, increased expression of the FOXO1 tumour suppressor gene, enhancing mitochondrial apoptosis in a p53-dependent manner and inhibition of the Hedgehog signalling ( 150 , 152 – 154 ). Taken together, these data provide strong support for clinical testing of HDACi in the treatment of paediatric brain cancer patients, particularly those with MB.…”

Section: Emerging Therapeutic Opportunitiesmentioning

confidence: 99%

Biological Role of MYCN in Medulloblastoma: Novel Therapeutic Opportunities and Challenges Ahead

et al. 2021

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The constitutive and dysregulated expression of the transcription factor MYCN has a central role in the pathogenesis of the paediatric brain tumour medulloblastoma, with an increased expression of this oncogene correlating with a worse prognosis. Consequently, the genomic and functional alterations of MYCN represent a major therapeutic target to attenuate tumour growth in medulloblastoma. This review will provide a comprehensive synopsis of the biological role of MYCN and its family components, their interaction with distinct signalling pathways, and the implications of this network in medulloblastoma development. We will then summarise the current toolbox for targeting MYCN and highlight novel therapeutic avenues that have the potential to results in better-tailored clinical treatments.

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Section: Emerging Therapeutic Opportunitiesmentioning

confidence: 99%

Biological Role of MYCN in Medulloblastoma: Novel Therapeutic Opportunities and Challenges Ahead

et al. 2021

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“…The prognoses of SHH-activated MBs are less favorable; SHH-MBs have an intact blood-brain barrier (BBB) and are less responsive to chemotherapy compared to WNT-MBs (22,26,27). Many SHH-MBs are age-dependent, with those aged ≥17 months more likely to harbor SMO and PTCH1 mutations (18,(28)(29)(30)(31)(32). Subgroup-driven clinical trials are currently underway to assess the efficacy of SHH pathway inhibitors such as vismodegib at diagnosis or in recurrent or refractory SHH-activated tumors.…”

Section: Introductionmentioning

confidence: 99%

Methylation Profiling of Medulloblastoma in a Clinical Setting Permits Sub-classification and Reveals New Outcome Predictions

et al. 2020

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Medulloblastoma (MB) is the most common childhood malignant brain tumor and is a leading cause of cancer-related death in children. DNA methylation profiling has rapidly advanced our understanding of MB pathogenesis at the molecular level, but assessments in Saudi Arabian (SA)-MB cases are sparse. MBs can be sub-grouped according to methylation patterns from FPPE samples into Wingless (WNT-MB), Sonic Hedgehog (SHH-MB), Group 3 (G3), and Group 4 (G4) tumors. The WNT-MB and SHH-MB subgroups are characterized by gain-of function mutations that activate oncogenic cell signaling, whilst G3/G4 tumors show recurrent chromosomal alterations. Given that each subgroup has distinct clinical outcomes, the ability to subgroup SA-FPPE samples holds significant prognostic and therapeutic value. Here, we performed the first assessment of MB-DNA methylation patterns in an SA cohort using archival biopsy material (FPPE n = 49). Of the 41 materials available for methylation assessments, 39 could be classified into the major DNA methylation subgroups (SHH, WNT, G3, and G4). Furthermore, methylation analysis was able to reclassify tumors that could not be sub-grouped through next-generation sequencing, highlighting its superior accuracy for MB molecular classifications. Independent assessments demonstrated known clinical relationships of the subgroups, exemplified by the high survival rates observed for WNT tumors. Surprisingly, the G4 subgroup did not conform to previously identified phenotypes, with a high prevalence in females, high metastatic rates, and a large number of tumor-associated deaths. Taking our results together, we demonstrate that DNA methylation profiling enables the robust sub-classification of four disease sub-groups in archival FFPE biopsy material from SA-MB patients. Moreover, we Alharbi et al. Clincal Methylation Profiling of Medulloblastomashow that the incorporation of DNA methylation biomarkers can significantly improve current disease-risk stratification schemes, particularly concerning the identification of aggressive G4 tumors. These findings have important implications for future clinical disease management in MB cases across the Arab world.

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Polymeric nanomedicine for overcoming resistance mechanisms in hedgehog and Myc-amplified medulloblastoma

et al. 2021

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Correction: Corrigendum: Selective targeting of HDAC1/2 elicits anticancer effects through Gli1 acetylation in preclinical models of SHH Medulloblastoma

Abstract: In this Article, Monika Kusio-Kobialka and Pawel Niewiadomski are incorrectly listed as being affiliated with

Cited by 7 publications

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Biological Role of MYCN in Medulloblastoma: Novel Therapeutic Opportunities and Challenges Ahead

Biological Role of MYCN in Medulloblastoma: Novel Therapeutic Opportunities and Challenges Ahead

Methylation Profiling of Medulloblastoma in a Clinical Setting Permits Sub-classification and Reveals New Outcome Predictions

Polymeric nanomedicine for overcoming resistance mechanisms in hedgehog and Myc-amplified medulloblastoma

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