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αβ-T Cells Engineered to Express γδ-T Cell Receptors Can Kill Neuroblastoma Organoids Independent of MHC-I Expression
Review

From DNA Copy Number Gains and Tumor Dependencies to Novel Therapeutic Targets for High-Risk Neuroblastoma

1
Department for Biomolecular Medicine, Ghent University, Medical Research Building (MRB1), Corneel Heymanslaan 10, B-9000 Ghent, Belgium
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Department of Internal Medicine and Pediatrics, Ghent University Hospital, Corneel Heymanslaan 10, B-9000 Ghent, Belgium
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Department of Pediatrics, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA
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Department of Biomedical Molecular Biology, Ghent University, Technologiepark 71, B-9052 Zwijnaarde, Belgium
*
Author to whom correspondence should be addressed.
Academic Editors: Walter Kolch and Cormac Owens
J. Pers. Med. 2021, 11(12), 1286; https://doi.org/10.3390/jpm11121286
Received: 11 October 2021 / Revised: 19 November 2021 / Accepted: 20 November 2021 / Published: 3 December 2021
(This article belongs to the Special Issue Precision Medicine for Neuroblastoma)
Neuroblastoma is a pediatric tumor arising from the sympatho-adrenal lineage and a worldwide leading cause of childhood cancer-related deaths. About half of high-risk patients die from the disease while survivors suffer from multiple therapy-related side-effects. While neuroblastomas present with a low mutational burden, focal and large segmental DNA copy number aberrations are highly recurrent and associated with poor survival. It can be assumed that the affected chromosomal regions contain critical genes implicated in neuroblastoma biology and behavior. More specifically, evidence has emerged that several of these genes are implicated in tumor dependencies thus potentially providing novel therapeutic entry points. In this review, we briefly review the current status of recurrent DNA copy number aberrations in neuroblastoma and provide an overview of the genes affected by these genomic variants for which a direct role in neuroblastoma has been established. Several of these genes are implicated in networks that positively regulate MYCN expression or stability as well as cell cycle control and apoptosis. Finally, we summarize alternative approaches to identify and prioritize candidate copy-number driven dependency genes for neuroblastoma offering novel therapeutic opportunities. View Full-Text
Keywords: neuroblastoma; DNA copy number gains; MYCN; dependency; drug targets neuroblastoma; DNA copy number gains; MYCN; dependency; drug targets
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MDPI and ACS Style

Decaesteker, B.; Durinck, K.; Van Roy, N.; De Wilde, B.; Van Neste, C.; Van Haver, S.; Roberts, S.; De Preter, K.; Vermeirssen, V.; Speleman, F. From DNA Copy Number Gains and Tumor Dependencies to Novel Therapeutic Targets for High-Risk Neuroblastoma. J. Pers. Med. 2021, 11, 1286. https://doi.org/10.3390/jpm11121286

AMA Style

Decaesteker B, Durinck K, Van Roy N, De Wilde B, Van Neste C, Van Haver S, Roberts S, De Preter K, Vermeirssen V, Speleman F. From DNA Copy Number Gains and Tumor Dependencies to Novel Therapeutic Targets for High-Risk Neuroblastoma. Journal of Personalized Medicine. 2021; 11(12):1286. https://doi.org/10.3390/jpm11121286

Chicago/Turabian Style

Decaesteker, Bieke, Kaat Durinck, Nadine Van Roy, Bram De Wilde, Christophe Van Neste, Stéphane Van Haver, Stephen Roberts, Katleen De Preter, Vanessa Vermeirssen, and Frank Speleman. 2021. "From DNA Copy Number Gains and Tumor Dependencies to Novel Therapeutic Targets for High-Risk Neuroblastoma" Journal of Personalized Medicine 11, no. 12: 1286. https://doi.org/10.3390/jpm11121286

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