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Alternative lengthening of telomeres in childhood neuroblastoma from genome to proteome

Telomere maintenance by telomerase activation or alternative lengthening of telomeres (ALT) is a major determinant of poor outcome in neuroblastoma. Here, we screen for ALT in primary and relapsed neuroblastomas and characterize its features using multi-omics profiling. We aim to deepen the knowledge about the biology and clinical features of ALT-positive neuroblastomas by enriching ALT tumors in the study cohort independent of ATRX mutation status. Using a combination of genomic, transcriptomic and proteomic profiling, we provide evidence that this subgroup is clinically and molecularly distinct.

Click on a Dataset ID in the table below to learn more, and to find out who to contact about access to these data

Dataset ID Description Technology Samples
EGAD00001006587 HiSeq X Ten Illumina HiSeq 2000 Illumina HiSeq 2500 Illumina HiSeq 4000 715
EGAD00001006625 Illumina HiSeq 2000 Illumina HiSeq 2500 144
EGAD00001006626 HiSeq X Ten Illumina HiSeq 2000 Illumina HiSeq 2500 238
EGAD00001006637 Illumina HiSeq 2500 Illumina HiSeq 4000 89
EGAD00001006638 Illumina HiSeq 2500 Illumina HiSeq 4000 97
EGAD00001006639 HiSeq X Ten 63
EGAD00001006737 34
EGAD00001006739 HiSeq X Ten 17
EGAD00001006785 Illumina HiSeq 4000 9
Publications Citations
Alternative lengthening of telomeres in childhood neuroblastoma from genome to proteome.
Nat Commun 12: 2021 1269
34
The growing need for controlled data access models in clinical proteomics and metabolomics.
Nat Commun 12: 2021 5787
11
MYCN mediates cysteine addiction and sensitizes neuroblastoma to ferroptosis.
Nat Cancer 3: 2022 471-485
52
Inherited rare variants in homologous recombination and neurodevelopmental genes are associated with increased risk of neuroblastoma.
EBioMedicine 87: 2023 104395
6
Neuroblastoma arises in early fetal development and its evolutionary duration predicts outcome.
Nat Genet 55: 2023 619-630
7