Radiation-induced chromatid breaks and deficient DNA repair in cancer predisposition

This publication has 71 references indexed in Scilit:

• Targeting Double-Strand Breaks to Replicating DNA Identifies a Subpathway of DSB Repair That Is Defective in Ataxia-Telangiectasia Cells
  Biochemical and Biophysical Research Communications, 1999
• Repair of oxidative DNA base lesions induced by fluorescent light is defective in xeroderma pigmentosum group A cells
  Nucleic Acids Research, 1999
• The fidelity of double strand breaks processing is impaired in complementation groups B and D of Fanconi anemia, a genetic instability syndrome.
  Somatic Cell and Molecular Genetics, 1997
• p53, the Cellular Gatekeeper for Growth and Division
  Cell, 1997
• On the Role of DNA Double-Strand Breaks in Toxicity and Carcinogenesis
  Critical Reviews in Toxicology, 1997
• Hypersensitivity of ataxia telangiectasia fibroblasts to ionizing radiation is associated with a repair deficiency of DNA double-strand breaks
  International Journal of Radiation Biology, 1997
• Fluorescent light-induced chromatid breaks distinguish Alzheimer disease cells from normal cells in tissue culture.
  Proceedings of the National Academy of Sciences, 1996
• Abnormal Chromosome Repair and Risk of Developing Cancer
  Environmental Health Perspectives, 1993
• DNA excision-repair defect of xeroderma pigmentosum prevents removal of a class of oxygen free radical-induced base lesions.
  Proceedings of the National Academy of Sciences, 1993
• Germ-line transmission of a mutated p53 gene in a cancer-prone family with Li–Fraumeni syndrome
  Nature, 1990