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Cancer testis antigens and genomic instability: More than immunology

Ash Jay1, Diedre Reitz1, Satoshi H Namekawa1

  • 1Department of Microbiology and Molecular Genetics, University of California, Davis, Davis, CA, 95616-8665, USA.

DNA Repair
|September 4, 2021
PubMed

Insights

Cancer testis antigens (CTA/CTG) misexpressed in cancers can cause genomic instability by disrupting DNA repair. This suggests CTAs could serve as biomarkers for homologous recombination deficiency in tumors.

Area of Science:

  • Oncology
  • Genetics
  • Molecular Biology

Background:

  • Cancer testis antigens (CTA/CTGs) are typically expressed in testes but aberrantly found in various human cancers.
  • Concerted CTA/CTG misexpression challenges the germ cell theory of cancer.
  • Many CTA/CTGs are implicated in meiotic chromosome metabolism and recombination.

Purpose of the Study:

  • To review the role of CTA/CTGs in meiotic chromosome metabolism.
  • To explore the link between CTA/CTG misexpression and genomic instability.
  • To assess CTA/CTGs as potential biomarkers for homologous recombination (HR) status in cancer.

Main Methods:

  • Interrogation of cancer databases to identify CTA/CTGs involved in meiotic processes.
  • Review of recent scientific literature on CTA/CTG function and cancer biology.
  • Analysis of the impact of CTA/CTG misexpression on DNA repair pathways.

Main Results:

  • A subset of CTA/CTGs is involved in meiotic chromosome metabolism, including recombination.
  • Misexpression of certain CTA/CTGs in somatic cells leads to genomic instability.
  • Interference with homologous recombination (HR) by CTA/CTGs is a key mechanism of genomic instability.

Conclusions:

  • CTA/CTG misexpression can induce an HR-deficient phenotype in cancer cells.
  • HR-deficient tumors exhibit synthetic lethality with PARP inhibitors.
  • CTA/CTG expression patterns may serve as novel biomarkers for predicting HR status and guiding cancer therapy.
Keywords:
BRCAnessHomologous recombinationMeiosisPoly (ADP-ribose) polymerase inhibitionReplication fork protection

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