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Both cell autonomous and non-autonomous processes modulate the association between replication timing and mutation

Oriya Vardi-Yaacov1, Adar Yaacov1,2,3, Shai Rosenberg2,3

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Cancer somatic mutations are influenced by DNA replication timing. Some tumors show a weak link between replication timing and mutation rate, indicating unique mutational processes and potential immune system involvement.

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Area of Science:

  • Genomics
  • Cancer Biology
  • Molecular Oncology

Background:

  • Cancer somatic mutations arise from various DNA mutational and repair processes.
  • Mutation rates (MR) are generally higher in late replication timing (RT) regions.
  • However, other biological processes can modulate the association between RT and MR.

Purpose of the Study:

  • To systematically analyze the mutational landscape across diverse cancer types.
  • To investigate the factors influencing the association between replication timing and mutation rate.
  • To identify unique characteristics of tumors exhibiting a weak RT-MR association.

Main Methods:

  • Analysis of somatic mutations in 2787 tumors from 32 distinct tumor types.
  • Systematic examination of the mutational landscape and its correlation with replication timing.
  • Comparative analysis of mutational signatures, gene mutations, and gene expression profiles.

Main Results:

  • Approximately one-third of analyzed tumor samples displayed a weak association between replication timing and mutation rate.
  • These weak association samples exhibited distinct mutational signatures.
  • Enrichment of mutations in DNA replication, DNA repair, and chromatin structure genes was observed in weak association tumors.
  • Differentially expressed genes in weak association tumors were linked to cell-cell communication and immune system pathways.

Conclusions:

  • A subset of tumors deviates from the expected RT-MR association, driven by unique mutational processes.
  • Tumors with weak RT-MR association show distinct genetic alterations and gene expression patterns.
  • The enrichment of immune and cell-cell communication genes suggests a non-autonomous DNA damage response in these tumors.