Production of interleukin-1 beta and interleukin-6 in hepatoblastoma
Autor: | D von Schweinitz, Torsten Pietsch, Karl Welte, M R Hadam, H. Mildenberger |
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Rok vydání: | 1993 |
Předmět: |
Male
Cancer Research Hepatoblastoma medicine.medical_specialty Carcinoma Hepatocellular medicine.drug_class medicine.medical_treatment Alpha (ethology) Biology Internal medicine medicine Tumor Cells Cultured Humans Interleukin 6 Interleukin-6 Tumor Necrosis Factor-alpha Liver Neoplasms Interleukin Infant medicine.disease Receptor antagonist Cytokine Endocrinology Oncology Cell culture Child Preschool biology.protein Cancer research Tumor necrosis factor alpha Female Interleukin-1 |
Zdroj: | International journal of cancer. 53(5) |
ISSN: | 0020-7136 |
Popis: | Thrombocytosis and fever are frequent symptoms in children with hepatoblastoma. Interleukin-6 (IL-6) has been shown to mediate thrombocytosis and an acute-phase reaction including fever. We therefore investigated samples from 14 untreated patients with hepatoblastoma for this cytokine and in addition for interleukin-1 alpha (IL-1 alpha), interleukin-1 beta (IL-1 beta) and tumor necrosis factor-alpha (TNF-alpha), all of which are known to induce IL-6 production. High serum levels of IL-6 were only found in 3/14 patients; the other cytokines were not detectable. In contrast, 12/14 tumors produced substantial amounts of IL-6 in primary cell culture, while IL-1 beta was found in 3/14 supernatants; IL-1 alpha and TNF-alpha were always negative. Immunoenzymatic staining of fresh tumors revealed that IL-6 is not produced by the tumor cells, but rather by surrounding fibroblasts and endothelial cells. In tumor cells only IL-1 beta, but neither IL-1 alpha, TNF-alpha nor IL-6, could be detected. In co-culture experiments with fibroblasts and endothelial cells, addition of hepatoblastoma cells enhanced IL-6 production. Including an IL-1 receptor antagonist abolished this effect incompletely. Our results suggest that tumor cells in hepatoblastoma induce IL-6 production in surrounding fibroblasts and endothelial cells by virtue of their endogenous secretion of IL-1 beta and supposedly some other, as yet unidentified, mediator. |
Databáze: | OpenAIRE |
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