ArticleProceedings of the National Academy of Sciences of the United States of America2016
Defining chromosomal translocation risks in cancer.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 25 citations in OpenAlex.
- ESR1 fusion proteins in breast cancer: distinguishing oncogenic drivers from passenger events.Oncogene · 2026Review
- Heterogeneity-preserving discriminative feature selection for disease-specific subtype discovery.Nature communications · 2025Article
- Chromothripsis.Methods in molecular biology (Clifton, N.J.) · 2025Review
- Two-Dimensional-PAGE Coupled with nLC-MS/MS-Based Identification of Differentially Expressed Proteins and Tumorigenic Pathways in MCF7 Breast Cancer Cells Transfected for JTB Protein Silencing.Molecules (Basel, Switzerland) · 2023Article
- Generalizations of the genomic rank distance to indels.Bioinformatics (Oxford, England) · 2023Article
- Chromosomal Rearrangements and Chromothripsis: The Alternative End Generation Model.International journal of molecular sciences · 2023Review
- Different Tumor Types Share a Common Nuclear Map of Chromosome Territories.Cancer informatics · 2023Article
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- DECO: decompose heterogeneous population cohorts for patient stratification and discovery of sample biomarkers using omic data profiling.Bioinformatics (Oxford, England) · 2019Article
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Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chromosomal translocations are a hallmark of cancer. Unraveling the molecular mechanism of these rare genetic events requires a clear distinction between correlative and causative risk-determinants, where technical and analytical issues can be excluded. To meet this goal, we performed in-depth analyses of publicly available genome-wide datasets. In contrast to several recent reports, we demonstrate that chromosomal translocation risk is causally unrelated to promoter stalling (Spt5), transcriptional activity, or off-targeting activity of the activation-induced cytidine deaminase. Rather, an open chromatin configuration, which is not promoter-specific, explained the elevated translocation risk of promoter regions. Furthermore, the fact that gene size directly correlates with the translocation risk in mice and human cancers further demonstrated the general irrelevance of promoter-specific activities. Interestingly, a subset of translocations observed in cancer patients likely initiates from double-strand breaks induced by an access-independent process. Together, these unexpected and novel insights are fundamental in understanding the origin of chromosome translocations and, consequently, cancer.
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Registered trials
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