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Potential mechanisms of endogenous retroviral-mediated genomic instability in human cancer

M T Romanish1, C J Cohen, D L Mager

  • 1Terry Fox Laboratory, British Columbia Cancer Agency, Vancouver, BC, Canada. mromanis@bccrc.ca

Seminars in Cancer Biology
|August 6, 2010
PubMed

Insights

Human endogenous retroviruses (HERVs) may contribute to cancer development through epigenetic changes that affect genome stability. Future high-throughput sequencing will clarify the role of HERVs and other transposable elements in malignancy.

Area of Science:

  • Genomics
  • Epigenetics
  • Retroviruses

Background:

  • Malignancy arises from complex genetic and epigenetic alterations.
  • Human endogenous retroviruses (HERVs) are remnants of ancient retroviral infections integrated into the human genome.
  • The precise roles of HERVs in cancer development are not fully understood.

Purpose of the Study:

  • To summarize current knowledge on HERV origin, activity, epigenetic state, and transcription.
  • To discuss the potential impact of HERV deregulation in cancer.
  • To highlight future research directions using high-throughput sequencing.

Main Methods:

  • Literature review and knowledge synthesis on HERVs.
  • Analysis of existing evidence linking epigenetic changes to HERV activity in cancer.
  • Discussion of potential mechanisms of HERV involvement in cancer pathogenesis.

Main Results:

  • Cancer-associated epigenetic changes may underlie HERV-mediated genome and transcriptome instability.
  • Deregulation of HERVs is suggested to play a role in malignancy.
  • Current understanding of HERV importance in cancer is limited.

Conclusions:

  • Epigenetic alterations in cancer may activate HERVs, contributing to genomic and transcriptomic instability.
  • HERVs represent a potential factor in cancer development that warrants further investigation.
  • Advancements in sequencing technologies will enable deeper exploration of HERV roles in cancer.

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