ArticleNature communications2019
Proteogenomics and Hi-C reveal transcriptional dysregulation in high hyperdiploid childhood acute lymphoblastic leukemia.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 105 citations in OpenAlex.
- Trial
- An integrative molecular map of pediatric B-cell precursor acute lymphoblastic leukemia.Communications medicine · 2026Article
- A tissue-specific atlas of protein-protein associations enables prioritization of candidate disease genes.Nature biotechnology · 2026Article
- Is cancer the result of uncontrolled cellular growth? a glance into the tumorigenic process.Cancer cell international · 2026Review
- TP63 mediates the generation of tumour-specific chromatin loops that underlie MYC activation in radiation-induced tumorigenesis.Nature communications · 2025Article
- Estrogen-induced chromatin looping changes identify a subset of functional regulatory elements.Genome research · 2025Article
- A SIRT7-dependent acetylation switch regulates early B cell differentiation and lineage commitment through Pax5.Nature immunology · 2024Article
- Characterizing the allele-specific gene expression landscape in high hyperdiploid acute lymphoblastic leukemia with BASE.Scientific reports · 2024Article
- Oncogenic Enhancers in Leukemia.Blood cancer discovery · 2024Review
- The effect of trisomic chromosomes on spatial genome organization and global transcription in embryonic stem cells.Cell proliferation · 2024Article
- Proteogenomic profiling uncovers differential therapeutic vulnerabilities betweenHaematologica · 2024Article
- The Eμ-Ret mouse is a novel model of hyperdiploid B-cell acute lymphoblastic leukemia.Leukemia · 2024Article
- 3C methods in cancer research: recent advances and future prospects.Experimental & molecular medicine · 2024Review
- Extracellular matrix protein 1 (ECM1) is a potential biomarker in B cell acute lymphoblastic leukemia.Clinical and experimental medicine · 2024Article
- Characterisation of FLT3 alterations in childhood acute lymphoblastic leukaemia.British journal of cancer · 2024Article
- Mass Spectrometry-Based Proteogenomics: New Therapeutic Opportunities for Precision Medicine.Annual review of pharmacology and toxicology · 2024Review
- Cancer Evolution: A Multifaceted Affair.Cancer discovery · 2024Article
- Prevalence ofFrontiers in pediatrics · 2024Article
- Proteomics in Childhood Acute Lymphoblastic Leukemia: Challenges and Opportunities.Diagnostics (Basel, Switzerland) · 2023Review
- Optical Genome Mapping Identifies Novel Recurrent Structural Alterations in ChildhoodHemaSphere · 2023Article
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Authors and funding
15 authors at 4 institutions in 3 countries.
Funding
Abstract
Hyperdiploidy, i.e. gain of whole chromosomes, is one of the most common genetic features of childhood acute lymphoblastic leukemia (ALL), but its pathogenetic impact is poorly understood. Here, we report a proteogenomic analysis on matched datasets from genomic profiling, RNA-sequencing, and mass spectrometry-based analysis of >8,000 genes and proteins as well as Hi-C of primary patient samples from hyperdiploid and ETV6/RUNX1-positive pediatric ALL. We show that CTCF and cohesin, which are master regulators of chromatin architecture, display low expression in hyperdiploid ALL. In line with this, a general genome-wide dysregulation of gene expression in relation to topologically associating domain (TAD) borders were seen in the hyperdiploid group. Furthermore, Hi-C of a limited number of hyperdiploid childhood ALL cases revealed that 2/4 cases displayed a clear loss of TAD boundary strength and 3/4 showed reduced insulation at TAD borders, with putative leukemogenic effects.
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