ACTIVATED N-<i>ras</i> IN A HUMAN RECTAL CARCINOMA CELL LINE ASSOCIATED WITH CLONAL HOMOZYGOSITY IN <i>myb</i> LOCUS-RESTRICTION FRAGMENT POLYMORPHISM

• YUASA Yasuhito

  Department of Hygiene, Gunma University School of Medicine

• REDDY E. Premkumar

  Roche Institute of Molecular Biology

• RHIM Johng S.

  Laboratory of Cellular and Molecular Biology, National Cancer Institute

• TRONICK Steven R.

  Laboratory of Cellular and Molecular Biology, National Cancer Institute

• AARONSON Stuart A.

  Laboratory of Cellular and Molecular Biology, National Cancer Institute

抄録

An N-ras transforming gene was detected in human rectal carcinoma-derived cells (7060) and molecularly cloned. The genetic lesion responsible for the transforming activity of the 7060 oncogene was localized to a single nucleotide transition from A to T in codon 61 of the predicted protein. This lesion in the second exon results in substitution of histidine for glutamine at this position. We also found an EcoRI restriction fragment length polymorphism, consisting of two alleles, of the human c-myb gene. The 7060-transformed epithelial cells showed the homozygous phenotype, while normal fibroblasts of the same patient showed the heterozygous phenotype. This suggests a relationship between the phenotypic change in the c-myb locus and the induction of the 7060 tumor.

収録刊行物

• Ｊａｐａｎｅｓｅ　Ｊｏｕｒｎａｌ　ｏｆ　Ｃａｎｃｅｒ　Ｒｅｓｅａｒｃｈ　ＧＡＮＮ

  Ｊａｐａｎｅｓｅ　Ｊｏｕｒｎａｌ　ｏｆ　Ｃａｎｃｅｒ　Ｒｅｓｅａｒｃｈ　ＧＡＮＮ 77 (7), 639-647, 1986

  日本癌学会

キーワード

• Transforming gene
• <i>ras</i> gene
• Point mutation
• Restriction fragment length polymorphism
• Rectal carcinoma

詳細情報

• CRID: 1390282681282275328
• NII論文ID: 130007310196
• DOI: 10.20772/cancersci1985.77.7_639
• ISSN: 09105050
• 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