Repair analysis of mitomycin C-induced DNA crosslinking in ribosomal RNA genes in lymphoblastoid cells from Fanconi's anemia patients

Mutat Res. 1989 May;217(3):185-92. doi: 10.1016/0921-8777(89)90070-0.


The repair of mitomycin C (MMC)-induced DNA crosslinking was analyzed by denaturation-renaturation gel electrophoresis in ribosomal RNA genes in lymphoblastoid cell lines from 4 patients with Fanconi's anemia (FA). In comparison to normal lymphoblastoid cell lines, 2 lines of FA cells belonging to complementation group A clearly exhibited higher sensitivity to MMC and an almost identical deficiency in the removal of DNA crosslinking. A complementation group B cell line, HSC 62, exhibited a lower sensitivity than group A cells and a lesser deficiency in crosslink repair. Another 'non-A' group cell line, HSC 230, reproducibly exhibited even higher sensitivity to MMC than group A cells. The results on MMC crosslinkage removal at the molecular level correlated well with cell survival. The observed subtle differences of repair among the 4 FA cell lines might represent possible genetic differences in the respective FA complementation groups.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Anemia, Aplastic / genetics*
  • Cell Survival / drug effects
  • Cells, Cultured
  • Cross-Linking Reagents
  • DNA Damage*
  • DNA Repair*
  • DNA, Ribosomal / genetics*
  • Fanconi Anemia / genetics*
  • Humans
  • In Vitro Techniques
  • Lymphocytes
  • Mitomycin
  • Mitomycins / toxicity*
  • RNA, Ribosomal / genetics


  • Cross-Linking Reagents
  • DNA, Ribosomal
  • Mitomycins
  • RNA, Ribosomal
  • Mitomycin