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Defining chromosomal translocation risks in cancer.

Marc A Hogenbirk1, Marinus R Heideman2, Iris de Rink3

  • 1Division of Biological Stress Response, Netherlands Cancer Institute, 1066 CX Amsterdam, The Netherlands; m.hogenbirk@bluebee.com h.jacobs@nki.nl.

Proceedings of the National Academy of Sciences of the United States of America
|June 16, 2016
PubMed
Summary

Chromosomal translocations in cancer are not caused by promoter activity but by open chromatin. Gene size also correlates with translocation risk, suggesting broader mechanisms beyond promoter-specific factors.

Keywords:
activation-induced cytidine deaminasecancerchromosomal translocationmultiomicspaired integrative analysis

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Area of Science:

  • Genetics
  • Cancer Biology
  • Molecular Biology

Background:

  • Chromosomal translocations are key events in cancer development.
  • Distinguishing causative factors from mere correlations is crucial for understanding their origin.
  • Previous studies suggested various molecular mechanisms, including promoter-related activities.

Purpose of the Study:

  • To investigate the molecular determinants of chromosomal translocation risk.
  • To clarify the role of promoter-specific activities versus broader genomic features.
  • To identify novel insights into the initiation of translocations in cancer.

Main Methods:

  • In-depth analysis of publicly available genome-wide datasets.
  • Statistical correlation analysis between translocation risk and genomic features.
  • Comparison of findings with existing literature and hypotheses.

Main Results:

  • Chromosomal translocation risk is causally unrelated to promoter stalling (Spt5), transcriptional activity, or activation-induced cytidine deaminase off-targeting.
  • Open chromatin configuration, not specific to promoters, is linked to elevated translocation risk in promoter regions.
  • Gene size directly correlates with translocation risk in both mice and human cancers.
  • A subset of translocations may originate from double-strand breaks induced by an access-independent process.

Conclusions:

  • Promoter-specific activities are generally irrelevant to chromosomal translocation risk.
  • Open chromatin and gene size are significant factors influencing translocation occurrence.
  • Novel insights into translocation origins provide a foundation for understanding cancer development.