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Structural variants drive context-dependent oncogene activation in cancer.

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Structural variants (SVs) altering 3D genome organization are common in cancer. Activity-by-contact models can predict oncogene activation by specific SVs, revealing distinct gene regulation modes.

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Area of Science:

  • Genomics
  • Cancer Biology
  • Epigenetics

Background:

  • Higher-order chromatin structure regulates gene expression via distal elements.
  • Structural variants (SVs) altering 3D genome organization can cause disease, especially cancer.
  • The reasons why only some SVs affect gene expression remain unclear.

Purpose of the Study:

  • To identify recurrent 3D genome structure alterations in cancer.
  • To determine the impact of specific SVs on oncogene activation.
  • To develop predictive models for SV consequences on gene expression.

Main Methods:

  • Analysis of Hi-C data from 92 cancer cell lines and patient samples.
  • CRISPR-Cas9 genome engineering to create de novo SVs.
  • Application of 'activity-by-contact' models.

Main Results:

  • Identified recurrent 3D genome structure alterations at oncogenes (MYC, TERT, CCND1).
  • Demonstrated that oncogene activity can be predicted by 'activity-by-contact' models.
  • Found that these models are only predictive for a subset of genes, indicating diverse regulatory mechanisms.

Conclusions:

  • SVs impacting 3D genome organization are prevalent in cancer.
  • Predictive rules for SVs' effects on oncogene activation are emerging.
  • Different gene classes utilize distinct regulatory modes involving distal elements.