Autor: |
Pelling JC, Ernst SM, Strawhecker JM, Johnson JA, Nairn RS, Slaga TJ |
Jazyk: |
angličtina |
Zdroj: |
Carcinogenesis [Carcinogenesis] 1986 Sep; Vol. 7 (9), pp. 1599-602. |
DOI: |
10.1093/carcin/7.9.1599 |
Abstrakt: |
Alterations in the expression of the Ha-ras oncogene were investigated in SENCAR mice epidermis at various stages of initiation and promotion during two-stage skin carcinogenesis in SENCAR mice. Adult SENCAR mice were treated with 200 nmol of the (+) enantiomer of benzo[a]pyrene 7,8-diol 9,10-epoxide-anti (BPDE-anti), a potent initiating agent, followed by repetitive treatments with the tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA). Other mice were 'sham'-initiated with the (-) enantiomer of BPDE-anti, which is inactive as a tumor initiator. Polyadenylated RNA was isolated from pre-tumor epidermis and tumors at eight different stages of tumorigenesis and analyzed for changes in Ha-ras expression using Northern blot hybridization. Significantly enhanced levels of Ha-ras RNA were observed in TPA-promoted papillomas as early as 7 weeks after initiation. Only trace amounts of Ha-ras RNA were present in untreated epidermis or epidermis treated with the (+) or (-) enantiomer followed by 2-12 treatments with TPA (pre-papilloma stage). Southern blot hybridization of tumor DNA indicated that the increased expression of the Ha-ras oncogene was not due to gene amplification. We conclude that elevated levels of Ha-ras expression can occur at an early stage of tumor development in mouse epidermis in vivo and may play a role in tumorigenesis. |
Databáze: |
MEDLINE |
Externí odkaz: |
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