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(TNF-) in Tumor Promotion as Revealed by TNF--deficient Mice1
Saitama Cancer Center Research Institute, Saitama 362-0806, Japan [M. S., S. O., E. S., H. F.]; Ludwig Institute for Cancer Research, New York Branch at Memorial Sloan-Kettering Cancer Center, New York, New York 10021 [M. W. M.]; and National Institute of Health Sciences, Tokyo 158-8501, Japan [A. S.]
To examine the hypothesis that tumor necrosis factor (TNF) 
is an essential cytokine in carcinogenesis, we conducted two-stage carcinogenesis experiments with an initiator, 7,12-dimethylbenz(a)anthracene (DMBA), plus either of two tumor promoters, okadaic acid and 12-O-tetradecanoylphorbol-13-acetate (TPA), on the skin of TNF--deficient (TNF-/-) mice. TNF-/- mice treated with DMBA plus okadaic acid developed no tumors for up to 19 weeks, and at 20 weeks, the percentage of tumor-bearing TNF-/- mice was 10%, whereas the percentage of tumor-bearing TNF+/+ mice was 100%. In TNF-/- mice treated with DMBA plus TPA, tumor onset was delayed 4 weeks, and the time to development of small tumors in 100% of mice was 9 weeks later than that seen in TNF+/+ CD-1 mice. The average number of tumors in TPA-treated TNF-/- mice was 2.8, compared with 11.8 for TNF+/+ CD-1 mice. To understand the residual tumor-promoting activity in TNF-/- mice, we also investigated the possible significance of interleukin (IL) 1 as an additional cytokine in tumor promotion. A single application of TPA and okadaic acid increased IL-1 and IL-1ß gene expression in TNF-/- mice. All of our results demonstrate that TNF- is the key cytokine for tumor promotion in mouse skin and, very possibly, for carcinogenesis in humans as well.
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