Role of homologous recombination in carcinogenesis

Alexander J.R. Bishop, Robert H. Schiestl

Research output: Contribution to journalReview articlepeer-review

96 Scopus citations


Cancer develops when cells no longer follow their normal pattern of controlled growth. In the absence or disregard of such regulation, resulting from changes in their genetic makeup, these errant cells acquire a growth advantage, expanding into precancerous clones. Over the past decade many studies have revealed the relevance of genomic mutation in this process, be it by misreplication, environmental damage, or a deficiency in repairing endogenous and exogenous damage. Here we discuss the possibility of homologous recombination as an errant DNA repair mechanism that can result in loss of heterozygosity or genetic rearrangements. Some of these genetic alterations may play a primary role in carcinogenesis, but they are more likely to be involved in secondary and subsequent steps of carcinogenesis by which recessive oncogenic mutations are revealed. Patients, whose cells display an increased frequency of recombination, also have an elevated frequency of cancer, further supporting the link between recombination and carcinogenesis.

Original languageEnglish (US)
Pages (from-to)94-105
Number of pages12
JournalExperimental and Molecular Pathology
Issue number2
StatePublished - Apr 2003
Externally publishedYes


  • Cancer
  • Carcinogen-induced deletions
  • Genomic instability diseases
  • Homologous recombination
  • Loss of heterozygosity

ASJC Scopus subject areas

  • Molecular Biology
  • Clinical Biochemistry
  • Pathology and Forensic Medicine


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