Deficient DNA repair capacity, a predisposing factor in breast cancer

Br J Cancer. 1996 Jul;74(1):1-5. doi: 10.1038/bjc.1996.307.

Abstract

Women with breast cancer and a family history of breast cancer and some with sporadic breast cancer are deficient in the repair of radiation-induced DNA damage compared with normal donors with no family history of breast cancer. DNA repair was measured indirectly by quantifying chromatid breaks in phytohaemagglutinin (PHA)-stimulated blood lymphocytes after either X-irradiation or UV-C exposure, with or without post treatment with the DNA repair inhibitor, 1-beta-D-arabinofuranosylcytosine (ara-C). We have correlated chromatid breaks with unrepaired DNA strand breaks using responses to X-irradiation of cells from xeroderma pigmentosum patients with well-characterised DNA repair defects or responses of repair-deficient mutant Chinese hamster ovary (CHO) cells with or without transfected human DNA repair genes. Deficient DNA repair appears to be a predisposing factor in familial breast cancer and in some sporadic breast cancers.

Publication types

  • Comparative Study

MeSH terms

  • Animals
  • Breast Neoplasms / blood
  • Breast Neoplasms / etiology*
  • Breast Neoplasms / genetics
  • CHO Cells / physiology
  • CHO Cells / radiation effects
  • Chromatids / radiation effects
  • Cricetinae
  • Cytarabine / pharmacology
  • DNA Damage
  • DNA Repair* / drug effects
  • DNA Repair* / genetics
  • DNA Repair* / radiation effects
  • DNA, Neoplasm / radiation effects
  • Female
  • Humans
  • Lymphocyte Activation / drug effects
  • Lymphocyte Activation / radiation effects
  • Lymphocytes / drug effects
  • Lymphocytes / radiation effects
  • Phytohemagglutinins / pharmacology
  • Risk Factors
  • Transfection
  • Ultraviolet Rays
  • X-Rays
  • Xeroderma Pigmentosum / metabolism
  • Xeroderma Pigmentosum / pathology
  • Xeroderma Pigmentosum / radiotherapy

Substances

  • DNA, Neoplasm
  • Phytohemagglutinins
  • Cytarabine