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AID/APOBEC deaminases and cancer

Stefan Rebhandl1, Michael Huemer1, Richard Greil1

  • 1Department of internal Medicine III with Hematology, Medical Oncology, Hemostaseology, Infectious Diseases, Rheumatology, Oncologic Center, Laboratory for Immunological and Molecular Cancer Research, Paracelsus Medical University Salzburg, Austria ; Salzburg Cancer Research Institute, Salzburg, Austria.

Oncoscience
|June 23, 2015
PubMed

Insights

Mutations drive evolution and disease. Recent research shows cancer mutations aren't random, but linked to APOBEC enzymes, potentially driving cancer development.

Area of Science:

  • Genetics
  • Molecular Biology
  • Cancer Research

Background:

  • Mutations are fundamental to evolution and genetic diseases, including cancer.
  • Deep-sequencing reveals non-random mutation signatures in human cancers, challenging the notion of random DNA damage.
  • The AID/APOBEC family of DNA deaminases is increasingly implicated in these non-random mutations.

Purpose of the Study:

  • To review the role of mutagenic events caused by AID/APOBEC deaminases in cancer development.
  • To explore how these enzymes contribute to genomic instability and clonal evolution in cancer.

Main Methods:

  • Review of existing literature on DNA deaminases, mutation signatures, and cancer genomics.
  • Analysis of studies linking AID/APOBEC activity to specific mutation patterns in cancer genomes.

Main Results:

  • APOBEC enzymes, involved in immunity, can cause DNA deamination leading to mutations.
  • These mutations exhibit non-random patterns, including strand-bias and motif-specificity.
  • APOBEC-driven mutagenesis is proposed as a mechanism contributing to cancer development and evolution.

Conclusions:

  • AID/APOBEC deaminases are significant contributors to the mutagenic landscape of cancer.
  • Their activity can induce collateral genomic damage, promoting cancer progression.
  • Understanding APOBEC's role is crucial for cancer research and therapeutic strategies.
Keywords:
AIDAPOBEC3cancerdeaminationkataegismutation clustermutation signature

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