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Peer-reviewedCC BY-NC-ND 4.0British Journal of Cancer

A functional landscape for chromosome 17q in neuroblastoma: balancing replication stress and genomic stability

  • Elien Hilgert1
  • Lisa Depestel1
  • Nadine Van Roy1
  • Stephen Roberts2
  • Kaat Durinck1
  • Frank Speleman1
  1. 1Department of Biomolecular Medicine, Faculty of Medicine & Health Sciences, Ghent University; Cancer Research Institute Ghent (CRIG), Ghent, Belgium
  2. 2Department of Pediatrics, Oregon Health & Science University, Portland, OR USA
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Abstract

Neuroblastoma is characterised by extensive genomic instability despite a marked paucity of recurrent somatic mutations. Instead, the disease is predominantly driven by chromosomal alterations, including segmental chromosomal imbalances, small structural variants, and oncogene amplification. A major unmet challenge is identifying key oncogenic drivers, beyond MYCN amplification, hidden within these recurrent DNA copy number alterations. Extra wild-type gene copies can alter expression levels and thus contribute to tumour development and affect survival. Increasing evidence suggests that these copy number-affected genes confer resistance to replication stress, a hallmark of high-risk neuroblastoma tumours. Among the most frequent and prognostically significant alterations is the gain of chromosome 17q. In this review, we discuss selected top-ranked candidate genes on 17q implicated in replication fork dynamics and DNA damage repair that we previously identified through an integrative functional genomics study. Improved understanding of the mechanisms by which 17q copy number-driven genes regulate replication stress responses and DNA damage repair may expose fundamental vulnerabilities in aggressive neuroblastoma and guide the development of novel targeted therapeutic strategies.

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Cite

BibTeXRIS
BibTeX
@article{hilgert2026functional,
  title = {{A functional landscape for chromosome 17q in neuroblastoma: balancing replication stress and genomic stability}},
  author = {Elien Hilgert and Lisa Depestel and Nadine Van Roy and Stephen Roberts and Kaat Durinck and Frank Speleman},
  journal = {British Journal of Cancer},
  year = {2026},
  month = aug,
  doi = {10.1038/s41416-026-03569-w},
  url = {https://doi.org/10.1038/s41416-026-03569-w},
  note = {CC BY-NC-ND 4.0},
}
RIS
TY  - JOUR
TI  - A functional landscape for chromosome 17q in neuroblastoma: balancing replication stress and genomic stability
AU  - Elien Hilgert
AU  - Lisa Depestel
AU  - Nadine Van Roy
AU  - Stephen Roberts
AU  - Kaat Durinck
AU  - Frank Speleman
PY  - 2026
DA  - 2026/08/07
JO  - British Journal of Cancer
DO  - 10.1038/s41416-026-03569-w
UR  - https://doi.org/10.1038/s41416-026-03569-w
AB  - Neuroblastoma is characterised by extensive genomic instability despite a marked paucity of recurrent somatic mutations. Instead, the disease is predominantly driven by chromosomal alterations, including segmental chromosomal imbalances, small structural variants, and oncogene amplification. A major unmet challenge is identifying key oncogenic drivers, beyond MYCN amplification, hidden within these recurrent DNA copy number alterations. Extra wild-type gene copies can alter expression levels and thus contribute to tumour development and affect survival. Increasing evidence suggests that these copy number-affected genes confer resistance to replication stress, a hallmark of high-risk neuroblastoma tumours. Among the most frequent and prognostically significant alterations is the gain of chromosome 17q. In this review, we discuss selected top-ranked candidate genes on 17q implicated in replication fork dynamics and DNA damage repair that we previously identified through an integrative functional genomics study. Improved understanding of the mechanisms by which 17q copy number-driven genes regulate replication stress responses and DNA damage repair may expose fundamental vulnerabilities in aggressive neuroblastoma and guide the development of novel targeted therapeutic strategies.
SN  - 0007-0920
SN  - 1532-1827
ER  -