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Gpx2 is an overexpressed gene in rat breast cancers induced by three different chemical carcinogens.

Gpx2 is an overexpressed gene in rat breast cancers induced by three different chemical carcinogens. Research Abstract Details 

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  • Gpx2 is an overexpressed gene in rat breast cancers induced by three different chemical carcinogens. Abstract Text:

    aya naiki-itoAya Naiki-Ito,makoto asamotoMakoto Asamoto,naomi hokaiwadoNaomi Hokaiwado,satoru takahashiSatoru Takahashi,hiroko yamashitaHiroko Yamashita,hiroyuki tsudaHiroyuki Tsuda,kumiko ogawaKumiko Ogawa,tomoyuki shiraiTomoyuki Shirai,aya naiki-itoAya Naiki-Ito,makoto asamotoMakoto Asamoto,naomi hokaiwadoNaomi Hokaiwado,satoru takahashiSatoru Takahashi,hiroko yamashitaHiroko Yamashita,hiroyuki tsudaHiroyuki Tsuda,kumiko ogawaKumiko Ogawa,tomoyuki shiraiTomoyuki Shirai,

    Gene expression alterations are essential for the process of carcinogenesis. A carcinogen may have specific mechanisms for inducing tumors, which may involve inducing characteristic gene expression alterations. In this study, we attempted to identify genes crucial for mammary carcinogenesis. For this purpose, we used human c-Ha-ras proto-oncogene transgenic rats (Hras128), which are highly sensitive to mammary carcinogens including N-methyl-N-nitrosourea, 7,12-dimethyl benz[a]anthracene, and 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine. DNA microarray analysis revealed that glutathione peroxidase 2 (Gpx2) was commonly up-regulated in the mammary carcinomas induced by the three different carcinogens, and its up-regulation was confirmed by quantitative reverse transcriptase-PCR and Western blotting analysis. In addition, expression of GPX2 was recognized in all 41 immunohistochemically examined cases of human breast cancer. Forced suppression of GPX2 expression by siRNA resulted in significant growth inhibition in both rat and human mammary carcinoma cell lines with wild-type p53 cells. Thus, these data suggested that GPX2 may be involved in mammary carcinogenesis and cell proliferation in both rats and humans, indicating that GPX2 may be a novel target for the prevention and therapy of breast cancer.

    Gpx2 is an overexpressed gene in rat breast cancers induced by three different chemical carcinogens. Publishing Authors By Initials

    a naiki-itoA Naiki-Ito,m asamotoM Asamoto,n hokaiwadoN Hokaiwado,s takahashiS Takahashi,h yamashitaH Yamashita,h tsudaH Tsuda,k ogawaK Ogawa,t shiraiT Shirai,a naiki-itoA Naiki-Ito,m asamotoM Asamoto,n hokaiwadoN Hokaiwado,s takahashiS Takahashi,h yamashitaH Yamashita,h tsudaH Tsuda,k ogawaK Ogawa,t shiraiT Shirai,

    For similar proteins: dna-binding proteins: tumor suppressor protein p53 research abstracts see: proteins: dna-binding proteins: tumor suppressor protein p53 research

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    Gpx2 is an overexpressed gene in rat breast cancers induced by three different chemical carcinogens. Journal Published:

    PUBLICATION TYPE: Research Support, Non-U.S. Gov

    Journal: Cancer research

    VOLUME: 67

    Page Numbers: 11353-8

    Journal Abbreviation: Cancer Res.

    ISSN: 1538-7445

    DAY: 1

    MONTH: Dec

    YEAR: 2007

    Gpx2 is an overexpressed gene in rat breast cancers induced by three different chemical carcinogens. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 2984705

    Gpx2 is an overexpressed gene in rat breast cancers induced by three different chemical carcinogens. Keywords Mesh Terms:

    KEYWORDS: Tumor Suppressor Protein p53

    MESH TERMS: metabolism

    Chemical & Substance for Abstract: Gpx2 is an overexpressed gene in rat breast cancers induced by three different chemical carcinogens. Information

    Substance Name: Glutathione Peroxidase

    Registry Number: EC 1.11.1.9

    Grant and Affiliation Information for Gpx2 is an overexpressed gene in rat breast cancers induced by three different chemical carcinogens.

    AFFILIATION: Department of Experimental Pathology and Tumor Biology, Nagoya City University Graduate School of Medical Sciences, Mizuho-cho, Mizuho-ku, Nagoya, Japan.

    Country: United States

    United States Research PublicationUnited States Research Publication

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    MEDLINETA: Cancer Res

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