Loss of atm Radiosensitizes Multiple p53 Null Tissues

摘要: An unusual clinical finding in ataxia-telangiectasia, a human disorder caused by mutations atm , is exquisite sensitivity to γ irradiation. By contrast, homozygous deletion of p53 marked radiation resistance certain tissue compartments. Previous studies (A. J. Levine, Cell, 88: 323–331, 1997) have shown that, vitro, -deficient bone marrow cells are resistant Furthermore, the gastrointestinal radiosensitization engendered loss has recently been (C. H. Westphal et al. Nat. Genet., 16: 397–401, be independent . Expanding on previous work, we looked at vivo mice. Our results indicate that inbred FVB strain null mice survive lethal irradiation doses because resistance. Moreover, radiosensitizes even and mouse embryonic fibroblast cells. The presented here argue multiple tissues -independent manner. Hence, functional inhibition wild-type tumors may useful adjunct irradiation-based antitumor therapy.