Reactive oxygen species (ROS)--induced genetic and epigenetic alterations in human carcinogenesis

Dominique Ziech1, Rodrigo Franco, Aglaia Pappa

  • 1Department of Student Success Services, University of Nevada, Reno, NV 89557, USA.

Mutation Research
|March 23, 2011
PubMed

Insights

Oxidative stress, a state of excess reactive oxygen species (ROS), significantly impacts cancer development. This review explores how ROS-induced oxidative stress influences genetic and epigenetic alterations during human carcinogenesis.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Cancer is a complex, multistage disease driven by molecular alterations.
  • Gene expression changes, regulated by genetic and epigenetic factors, are crucial in cancer development.
  • Oxidative stress occurs when reactive oxygen species (ROS) overwhelm cellular antioxidant defenses.

Purpose of the Study:

  • To review the current understanding of reactive oxygen species (ROS)-induced oxidative stress.
  • To elucidate the role of oxidative stress in altering genetic and epigenetic mechanisms in human carcinogenesis.

Main Methods:

  • Literature review of existing research on oxidative stress and cancer.
  • Analysis of studies investigating the interplay between ROS, genetic alterations, and epigenetic modifications.
  • Synthesis of current knowledge on oxidative stress in cancer initiation, promotion, and progression.

Main Results:

  • Oxidative stress influences both genetic and epigenetic pathways involved in cancer.
  • ROS accumulation can trigger molecular cascades that promote carcinogenesis.
  • Altered gene expression due to oxidative stress is implicated across all stages of cancer development.

Conclusions:

  • Reactive oxygen species (ROS)-induced oxidative stress is a significant factor in human cancer development.
  • Understanding these molecular mechanisms is crucial for developing targeted cancer therapies.
  • Further research is needed to fully elucidate the complex interactions between oxidative stress and carcinogenesis.

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