Hepatic tumors induced by carbon tetrachloride in transgenic mice carrying a human c‐H‐ras proto‐oncogene without mutations

Satoshi Tsunematsu, Hidetsugu Saito, Tatehiro Kagawa, Toshio Morizane, Jun‐Ichi ‐I Hata, Tatsuya Nakamura, Hiromasa Ishii, Masaharu Tsuchiya, Tatsuji Nomura, Motoya Katsuki

研究成果: Article査読

23 被引用数 (Scopus)

抄録

Hepatic tumors were generated in mice by repeated administration of carbon tetrachloride (CCI4). Eight transgenic (Tg) mice carrying a human c‐H‐ras proto‐oncogene (rasH2 line) and 9 non‐Tg mice were killed at 20 weeks. Tg mice developed more tumors than did non‐Tg littermates. Most tumors were neoplastic nodules, but I hepatocellular carcinoma (HCC) was found in a Tg mouse at 20 weeks. Three Tg and 2 non‐Tg mice were kept without further administration of CCI4. Two Tg mice died at 30 weeks of HCC with intra‐abdominal bleeding, and I Tg mouse developed HCC with a mesenteric metastasis at 32 weeks. No HCC was found in 2 non‐Tg mice at 32 weeks. Although mutations at codon 12, 13, and 61 of the H‐ras gene are often found in murine hepatocarcinogenesis, neither the tumors, including one HCC, nor the normal cells revealed any such mutations. These results showed that the unmutated human c‐H‐ras gene facilitates malignant transformation of hepatocytes when continuous liver‐cell death and regeneration is caused by repeated administration of CCI4. © 1994 Wiley‐Liss, Inc.

本文言語English
ページ(範囲)554-559
ページ数6
ジャーナルInternational Journal of Cancer
59
4
DOI
出版ステータスPublished - 1994 11 15
外部発表はい

ASJC Scopus subject areas

  • 腫瘍学
  • 癌研究

フィンガープリント

「Hepatic tumors induced by carbon tetrachloride in transgenic mice carrying a human c‐H‐ras proto‐oncogene without mutations」の研究トピックを掘り下げます。これらがまとまってユニークなフィンガープリントを構成します。

引用スタイル