In a murine model of breast cancer, IL-12 therapy exerts potent anti-angiogenic effects which contribute to tumor regression. After 7 days of treatment, levels of tumor VEGF protein decline markedly and are undetectable at 14 days. This decline is accompanied by a fall in MMP-9 and, as the tumors re
Murine interleukin-12 prevents the development of cancer cachexia in a murine model
โ Scribed by Kazushige Mori; Kaori Fujimoto-Ouchi; Tohru Ishikawa; Fumiko Sekiguchi; Hideo Ishitsuka; Yutaka Tanaka
- Publisher
- John Wiley and Sons
- Year
- 1996
- Tongue
- French
- Weight
- 744 KB
- Volume
- 67
- Category
- Article
- ISSN
- 0020-7136
No coin nor oath required. For personal study only.
โฆ Synopsis
Murine colon 26 carcinoma causes cachexia even when the tumor burden is small. In this tumor model, murine IL-I2 suppressed the induction of cancer cachexia and also inhibited tumor growth. IL-I2 reduced the serum levels of IL-6, a cachexia mediator in this model, and alleviated the body weight loss and other abnormalities associated with cachexia, such as adipose tissue wasting and hypoglycemia. The anticachectic activity was observed even at low doses of IL-12, insufficient to inhibit tumor growth. IL-I2 greatly increased levels of IFN-y in the tumor tissue and, to a lesser extent, in the circulation. IFN-y given intraperitoneally also prevented cancer cachexia, although it did not reduce IL-6 levels either in the tumor or in the circulation. In athymic mice bearing the same colon 26 tumor, IL-I2 was no longer anticachectic and did not induce IFN-y. These results indicate that the anticachectic activity of IL-I 2 is T-cell-dependent and results from at least 2 mechanisms, the down-regulation of IL-6 and the up-regulation of IFNy.
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