Against Lung Cancer Cells: To Be, or Not to Be, That Is the Problem

We summarize the function of DNA repair molecules at a viewpoint of carcinogenic DNA damage and cancer therapy modulation involved in lung cancer

Naoko Okumura

2012

Scholarcy highlights

  • Lung cancer is the commonest fatal cancer whose risk is dependent on the number of cigarettes smoked per day as well as the duration years of the smoking
  • An imbalance between the mechanisms that generate and protect against reactive oxygen species results in oxidative damage including the DNA damage, which results in DNA strand breaks
  • ataxia telangiectasia-mutated is a checkpoint kinase that phosphorylates a large number of proteins in response to radiation-induced DNA damage, including p53, Chk2, and BRCA1
  • We summarize the function of DNA repair molecules at a viewpoint of carcinogenic DNA damage and cancer therapy modulation involved in lung cancer
  • The tumorigenic relevance of this DNA damage and instability is revealed by a series of studies, indicating that smokers with less efficient DNA repair capacities are at higher risk for developing lung cancer
  • When cells are exposed to genotoxic agents including irradiation, Rad51 protein is recruited to the sites of DNA damage and associated with nuclear matrix where it mediates the search for a homologous sequence during homologous recombination
  • Further studies on lung cancers will be necessary to determine the association of the DNA damage and the function of DNA repair-molecules with the relevant markers

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