Distinct Pattern of Allelic Loss and Inactivation of Cadherin 1 and 5 Genes in Mammary Carcinomas Arising in p53^<+/-> Mice

スポンサーリンク

概要

• 論文の詳細を見る

• Mammary carcinoma/Loss of heterozygosity/p53^<+/-> mice/Cadherin gene/Tumor suppressor gene. p53 is one of the most frequently mutated genes in mammary carcinomas (MCs). To detect tumor suppressor genes cooperating with a hetero-deficient p53 gene in mammary carcinogenesis, we first examined allelotypes in MCs from (BALB/cHeA x MSM/Ms) F_<1-> p53^<+/-> and (BALB/cHeA x 129/SvEv) F_<-1> p53^<+/-> female mice, and then surveyed down-regulated genes in the allelic loss regions. Genome-wide screening at 42 loci identified frequent (more than 30%) loss of heterozygosity (LOH) on chromosomes 5, 8, 11, 12, 14 and 18 in the MCs from either of the F_1 mice. The MCs in the p53^<+/-> mice indicated highly frequent LOH, especially on chromosomes 8, 11 and 12, distinct from other mouse tumors. More than 60% of the 38 MCs from (BALB/cHeA x MSM/Ms) F_1- p53^<+/-> mice showed LOH in a region ranging from D8Mit85 (105.0 Mb from centromere) to D8Mit113 (111.8 Mb) on chromosome 8, a region syntenic to human chromosome 16q22.1, on which LOH has been found in breast cancers. RT-PCR analyses revealed that the LOH of chromosome 8 was associated with the reduced and/or complete loss of expression of Cdhl and Cdh5 genes in 15 (58%) and 8 (31%) of 26 MCs derived from the F_1 mice, respectively. Thus, inactivation of Cdh1 and Cdh5 is likely to cooperate with the loss of p53, suggesting a possible tumor suppressive function of these genes in mammary carcinogenesis.

• 日本放射線影響学会の論文
• 2007-03-20

著者

• Song C‐w

  Korea Institute Of Toxicology Korea Research Institute Of Chemical Technology

• Song Chang-woo

  大阪府立大学 生命環境科学研究科

• Hong Doo-pyo

  大阪府立大学 生命環境科学研究科

• Hong Doo-pyo

  Graduate School Of Agriculture And Biological Sciences Osaka Prefecture University

• UMESAKO Seiichi

  Graduate School of Agriculture and Biological Sciences, Osaka Prefecture University

• IIGA Sayoko

  Graduate School of Agriculture and Biological Sciences, Osaka Prefecture University

• TAKAHASHI Masahiro

  Graduate School of Agriculture and Biological Sciences, Osaka Prefecture University

• IMURA Kae

  Research Institute of New Medicines, Shionogi Pharmaceutical Co.

• MORI Nobuko

  Graduate School of Agriculture and Biological Sciences, Osaka Prefecture University

• SONG Chang-Woo

  Korea Institute of Toxicology, Korea Research Institute of Chemical Technology

• NIWA Otsura

  Radiation Biology Center, Kyoto University

• OKUMOTO Masaaki

  Graduate School of Agriculture and Biological Sciences, Osaka Prefecture University

• Niwa Otsura

  Radiation Biology Center Kyoto University

• Niwa Otsura

  Radiat. Biol. Ctr. Kyoto Univ.

• Okamoto Mieko

  Experimental Radiobiology For Children's Health Research Group Research Center For Radiation Pr

• Okumoto M

  Graduate School Of Agriculture And Biological Sciences Osaka Prefecture University:research Institut

• Okumoto Masaaki

  大阪府立大学 生命環境科学研究科

• Okumoto Masaaki

  Res. Inst. Advan. Sci. Technol. Osaka Prefecture Univ.

• Okumoto Masaaki

  Graduate School Of Agriculture And Biological Sciences Osaka Prefecture University

• Imura Kae

  Research Institute Of New Medicines Shionogi Pharmaceutical Co.

• Iiga Sayoko

  Graduate School Of Agriculture And Biological Sciences Osaka Prefecture University

• Umesako Seiichi

  Graduate School Of Agriculture And Biological Sciences Osaka Prefecture University

• Umesako Sei-ichi

  Res. Inst. Advan. Sci. Technol. Osaka Prefecture Univ.

• Song Chang-woo

  Korea Institute Of Toxicology

• Mori N

  Graduate School Of Agriculture And Biological Sciences Osaka Prefecture University:research Institut

• Mori Nobuko

  大阪府立大学 生命環境科学研究科

• Mori Nobuko

  Department Of Applied Bioscience Research Institute Of Advanced Science & Technology University

• Mori Nobuko

  Graduate School Of Agriculture And Biological Sciences Osaka Prefecture University:research Institut

• Takahashi Masahiro

  Graduate School Of Agriculture And Biological Sciences Osaka Prefecture University

• Mori Nobuko

  Res. Inst. For Advan. Sci. &technol. Osaka Pre-fecture University.

関連論文

• 3P344 大腸菌再構成系内におけるMEKとMKPによるERKリン酸化・脱リン酸化反応の計測(その他,第48回日本生物物理学会年会)
• Fasヘテロ欠損マウスにおけるヘテロ接合性消失の解析
• 2-II-10 ビタミンB_欠乏ラットにおけるグルコーストランスポーターの発現 : 第48回大会研究発表要旨 : 一般研究発表要旨
• 2-II-6 ビタミンB_欠乏ラットにおけるアミノ酸の代謝 : 第48回大会研究発表要旨 : 一般研究発表要旨
• Genetic Control of the Radiosensitivity of Lymphoid Cells for Antibody Formation Ability in Mice
• Analysis for Tumor Suppressor Regions Involved in Radiation Lymiphomagenesis (I) Allelic Loss Regions in the Lymphomas from p53 Mice
• Distinct Pattern of Allelic Loss and Inactivation of Cadherin 1 and 5 Genes in Mammary Carcinomas Arising in p53^ Mice
• Preferential Induction of Mammary Tumors in p53 Hemizygous BALB/c Mice by Fractionated Irradiation of a Sub-lethal Dose of X-rays
• Analysis of Tumor Suppressor Gene Regions Involved in Radiation Tumorigenesis of p53 and Atm Heterozygous Deficient Mice
• Generation of Large Homozygous Chromosomal Segments by Mitotic Recombination during Lymphomagenesis in F1 Hybrid Mice
• Putative Tumor-suppressor Gene Regions Responsible for Radiation Lymphomagenesis in F_1 Mice with Different p53 Status
• Putative Tumor Suppressor Regions Responsible for Radiation Lymphomagenesis in F_1 Mice with DifferentGenetic Interactions
• Analysis of Tumor Suppressor Regions in Radiation-Induced Lymphomas of Fas Heterozygous Deficient Mice
• Analysis for Tumor Suppressor Regions Involved in Radiation Lymphomagenesis - Allelic Loss Regions on Chromosome 19 -
• Lymphomagenesis by Fractionated X-irradiation and LOH Analysis of the Lymphomas in Atm Haplo-insufficient Mice
• Radiation-Induced Mammary Carcinogenesis in Rodent Models : What's Different from Chemical Carcinogenesis?
• 43 Age dependency of X ray-induced mammary carcinogenesis in Apc^ mice(Radiation carcinogenesis, Abstracts of the 46th Annual Meeting of the Japan Radiation Research Society)
• Radiation-Induced Lymphomas in MSM, (BALB/cHeA x MSM) F_1 and (BALB/cHeA x STS/A) F_1 Hybrid Mice
• Mouse Mammary Tumor Virus Proviral Integration in the DD/Tbr Mice
• 222 X-ray-induced genomic instability in Atm knock-out mouse cells(Genetic instability, Abstracts of the 46th Annual Meeting of the Japan Radiation Research Society)
• Analysis for Tumor Suppressor Regions Involved in Radiation Lymphomagenesis (II) Analysis of Three Genes as a Caddidate in Frequent Allelic Loss Region on Chromosome 12
• Mapping of putative ether-anesthesia resistance gene using C57BL/6J and MSM/Ms mouse strains
• Analysis of Frequent Allelic Loss Regions in Radiation-Induced Lymphomas of Mice
• Frequent Loss of Heterozygosity in Radiation-Induced Lymphomas of Mice (V) Allelotype analysis in the Lymphomas from Intersubspesific crosses
• Fine mapping of LOH region in chromosome 11 and altered expression of Ikaros, Lif, Nf2, Osm and Egfr genes in X-ray-induced B6C3F1 thymic lymphomas
• Allelic Loss Analysis of Lymphomas Induced in Fas-Heterozygous Deficient Mice
• 51 Analysis of Allele Loss Regions in Chromosomes 9,10,12 in Radiation Mammary Carcinogenesis of Atm and p53 Heterozygous Deficient Mice(Radiation carcinogenesis, Abstracts of the 46th Annual Meeting of the Japan Radiation Research Society)
• 50 Analysis of Tumor Suppressor Gene Regions Involved in Radiation Mammary Carcinogenesis of p53 and Atm Heterozygous Deficient Mice(Radiation carcinogenesis, Abstracts of the 46th Annual Meeting of the Japan Radiation Research Society)
• 48 Resistance to radiation-induced mammary tumors in p53 hemizygous (BALB/c x C57BL/6)F_1 mice(Radiation carcinogenesis, Abstracts of the 46th Annual Meeting of the Japan Radiation Research Society)
• Prevalence of mammary tumors in p53 hemizygous BALB/c mice exposed repeatedly to a low dose of X-rays
• Allelic Variation in Mouse Prkdc and Susceptibility to Radiation Lymphomagenesis
• Linkage of susceptibility to radiation lymphomagenesis to the mouse chromosome 16 segment containing Rapopl - an analysis with congenic mice
• A Susceptibility Locus for Radiation Lymphomagenesis on Mouse Chromosome 16
• Susceptibility to Glucocorticoid-Induced Apoptosis Is Linked to p53 and Rapopl (chromosome 16), Genes Controlling Radiation-Induced Apoptosis
• Participation of ATM function in X-ray-induced delayed chromosomal instability
• Frequent Loss of Heterozygocity in Specific Chromo-somal Regions of Radiation-Induced Lymphomas in Mice
• Fine Localization of Nef1 and Nef3 and its Exclusion as Candidate Gene for Lens Rupture 2(Ir2)
• Candidate Signatures of Radiation Carcinogenesis
• Frequent Loss of Heterozygosity in Radiation-induced Lymphomas of Mice (IV) Mapping of the Gene(s) Related to Lymphomagenesis
• Frequent Loss of Heterozygosity in Radiation-Induced Lymphomas of Mice (III) Genomic Alterations in the Lymphomas of F1 Mice (BALB/cHeA X MSM/ Ms)
• Frequent Loss of Heterozygosity in Radiation- Induced Lymphonias of Mice
• Complete Nucleotide Sequence of Mouse Mammary Tumor Virus from JYG Chinese Wild Mice: Absence of Bacterial Insertion Sequences in the Cloned Viral gag Gene
• Genetic Dissection of Susceptibility to Radiation-Induced Death of Thymocytes and Mapping of a Suscep-tibility Gene in Mice
• Mouse strain difference in susceptibility to glucooortiooid-induoed apoptos is of thymocytes
• Fine mapping of the apoptosis susceptibility gene Rapop3 and the test of mcll as a likely candidate gene
• 1P-298 二重リン酸化ERKの細胞サイズ依存的な平衡状態の安定性評価(数理生物学,第46回日本生物物理学会年会)
• Radiation-Induced Mammary Carcinogenesis in Rodent Models: Whats Different from Chemical Carcinogenesis?
• Two loci affecting susceptibility to radiation-induced apoptosis of colonic crypt cells near Rapop2 (chromosome 9) and Rapop1 (chromosome 16)
• Mapping of the genes implicated in susceptibility to radiation-induced apoptosis of thymocytes to mouse chromosome 9 and chromosome 3
• Allelic Loss Analysis of Lymphomas Induced in Fas-Heterozygous Deficient Mice

もっと見る 閉じる

スポンサーリンク