<I>Atm</I>-heterozygous deficiency enhances development of mammary carcinomas in <I>p53</I>-heterozygous knockout mice

• Okumoto Masaaki

  Res. Inst. Adv. Sci. Technol., Osaka Pref. Univ. Osaka Pref. Univ. Grad. Sch. Agric. Biol. Sci.

• Umesako Seiichi

  Osaka Pref. Univ. Grad. Sch. Agric. Biol. Sci.

• Iiga Sayoko

  Osaka Pref. Univ. Grad. Sch. Agric. Biol. Sci.

• Takahashi Masahiro

  Vet. Sci., Agric., Osaka Pref. Univ.

• Fujisawa Kae

  Shionogi Pharm. Co.

• Mori Nobuko

  Res. Inst. Adv. Sci. Technol., Osaka Pref. Univ. Osaka Pref. Univ. Grad. Sch. Agric. Biol. Sci.

• Niwa Otsura

  Radiat. Biol. Ctr., Kyoto Univ.

抄録

To investigate effects of heterozygous deficient p53 (p53^+/-) and/or Atm (Atm^+/-) genes in radiation-induced mammary tumorigenesis, we examined the tumor induction by X-irradiation in p53^+/- and/or Atm^+/-- (BALB/cHeA x MSM/Ms) F₁ female mice. Both p53^+/-Atm^+/- and p53^+/-Atm^+/+ mice efficiently developed mammary adenocarcinomas (MC) by X-irradiation of 5 Gy at 5 weeks of age and the incidences of the MC were 58% and 24%, respectively. Average number of MC per mouse in p53^+/-Atm^+/- group was significantly larger than that in p53^+/-Atm^+/+ mice. X-irradiation considerably shortened latent period of the MC development. These MC were observed early in irradiated group (during 25 to 43 weeks of age) compared with non-irradiated group (during 45 to 60 weeks of age). However, almost all irradiated p53^+/+ mice did not develop the MC in spite of Atm gene status. To analyze putative tumor suppressor genes in mammary carcinogenesis, we examined loss of heterozygosity (LOH) in the MC. Frequent LOH was observed on chromosomes 5, 8, 10, 11 and 12. Precise allelotype analyses on chromosomes 8, 10 and 12 have been performed. Examination of RNA expression of some candidate genes are in progress.

収録刊行物

• 日本放射線影響学会大会講演要旨集

  日本放射線影響学会大会講演要旨集 2004 (0), 68-68, 2004

  一般社団法人 日本放射線影響学会

詳細情報

• CRID: 1390001205644056576
• NII論文ID: 130005443074
• DOI: 10.11513/jrrsabst.2004.0_68_6
• 本文言語コード: en
• データソース種別:
  • JaLC
  • CiNii Articles
• 抄録ライセンスフラグ: 使用不可