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Specific Genomic Alterations in Rat Renal Cell Carcinomas Induced by N-Ethyl-N-hydroxyethylnitrosamine
Noboru Konishi
Second Department of Pathology, Nara Medical University, 840 Shijo-cho, Kashihara, Nara 634-8521, nkonishi{at}naramed-u.ac.jp
Mitsutoshi Nakamura
Second Department of Pathology, Nara Medical University, 840 Shijo-cho, Kashihara, Nara 634-8521
Eiwa Ishida
Second Department of Pathology, Nara Medical University, 840 Shijo-cho, Kashihara, Nara 634-8521
Yoichi Kawada
Second Department of Pathology, Nara Medical University, 840 Shijo-cho, Kashihara, Nara 634-8521
Masayoshi Nishimine
Second Department of Pathology, Nara Medical University, 840 Shijo-cho, Kashihara, Nara 634-8521
Hisaki Nagai
Department of Molecular Biology, Institute of Gerontology, Nippon Medical School 1-396, Kosugi, Nakahara-ku, Kawasaki, 211-8533, Japan
Mitsuru Emi
Department of Molecular Biology, Institute of Gerontology, Nippon Medical School 1-396, Kosugi, Nakahara-ku, Kawasaki, 211-8533, Japan
To characterize genetic alterations occurring in renal tumorigenesis, EHEN-induced renal cell tumors were examined using restriction landmark genomic scanning (RLGS) analysis, an electrophoretic separation technique that detects gene amplifi cations and deletions. Comparison of DNAs from tumor against those from corresponding nontumorous kidney and /or EHEN-treated kidney without development of renal tumors yielded specific alterations in terms of both amplifi ed and reduced DNA spots. Two amplifi ed spots were detected only in renal cell tumors and an additional four spots were frequent in EHEN-treated kidneys. One reduced spot was common to all tumor samples, and another was frequently detected in the tumors analyzed but not in EHEN-treated kidneys. A subset of the altered spots thus appeared to be specific for EHEN-induced renal tumorigenesis.
Key Words: N-ethyl-N-hydroxyethylnitrosamine rat renal cell tumor restriction landmark genomic scanning.
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Toxicologic Pathology, Vol. 29, No. 2,
232-236 (2001)
DOI: 10.1080/019262301317052503

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