Homologous recombination and its role in carcinogenesis

Alexander J.R. Bishop, Robert H. Schiestl

Producción científica: Review articlerevisión exhaustiva

48 Citas (Scopus)

Resumen

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 last 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 homologous recombination as another mechanism that can result in a 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.

Idioma originalEnglish (US)
Páginas (desde-hasta)75-85
Número de páginas11
PublicaciónJournal of Biomedicine and Biotechnology
Volumen2002
N.º2
DOI
EstadoPublished - 2002
Publicado de forma externa

ASJC Scopus subject areas

  • Biotechnology
  • Molecular Medicine
  • Molecular Biology
  • Genetics
  • Health, Toxicology and Mutagenesis

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