Do alterations in mitochondrial DNA play a role in breast carcinogenesis?

Thomas E. Rohan, Lee Jun Wong, Tao Wang, Jonathan Haines, Geoffrey C. Kabat

Research output: Contribution to journalArticle

22 Citations (Scopus)

Abstract

A considerable body of evidence supports a role for oxidative stress in breast carcinogenesis. Due to their role in producing energy via oxidative phosphorylation, the mitochondria are a major source of production of reactive oxygen species, which may damage DNA. The mitochondrial genome may be particularly susceptible to oxidative damage leading to mitochondrial dysfunction. Genetic variants in mtDNA and nuclear DNA may also contribute to mitochondrial dysfunction. In this review, we address the role of alterations in mtDNA in the etiology of breast cancer. Several studies have shown a relatively high frequency of mtDNA mutations in breast tumor tissue in comparison with mutations in normal breast tissue. To date, several studies have examined the association of genetic variants in mtDNA and breast cancer risk. The G10398A mtDNA polymorphism has received the most attention and has been shown to be associated with increased risk in some studies. Other variants have generally been examined in only one or two studies. Genome-wide association studies may help identify new mtDNA variants which modify breast cancer risk. In addition to assessing the main effects of specific variants, gene-gene and gene-environment interactions are likely to explain a greater proportion of the variability in breast cancer risk.

Original languageEnglish (US)
Article number604304
JournalJournal of Oncology
DOIs
StatePublished - 2010

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Mitochondrial DNA
Carcinogenesis
Breast
Breast Neoplasms
Gene-Environment Interaction
Mitochondrial Genome
Genome-Wide Association Study
Oxidative Phosphorylation
Mutation Rate
Genes
DNA Damage
Reactive Oxygen Species
Mitochondria
Oxidative Stress
Mutation
DNA

ASJC Scopus subject areas

  • Oncology

Cite this

Do alterations in mitochondrial DNA play a role in breast carcinogenesis? / Rohan, Thomas E.; Wong, Lee Jun; Wang, Tao; Haines, Jonathan; Kabat, Geoffrey C.

In: Journal of Oncology, 2010.

Research output: Contribution to journalArticle

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