Interleukin-1α (IL-1α), IL-1β, IL-1 receptor type I, IL-1 receptor antagonist, and TGF-β1 mRNAs in pediatric astrocytomas, ependymomas, and primitive neuroectodermal tumors

被引:21
|
作者
Ilyin, SE
Gonzalez-Gomez, I
Gilles, FH
Plata-Salaman, CR [1 ]
机构
[1] Univ Delaware, Sch Life & Hlth Sci, Div Mol Biol, Newark, DE 19716 USA
[2] Childrens Hosp, Dept Pathol, Los Angeles, CA 90027 USA
关键词
astrocyte; astrocytomas; brain tumor; cytokine; ependymomas; glia; growth factor; interleukins; nervous system; neuron; posterior fossa; RNase protection; TGF;
D O I
10.1007/BF02870186
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Interleukin-1 alpha (IL-1 alpha), IL-1 beta, interleukin-l receptor type I(IL-1RI, signaling receptor), and IL-1 receptor antagonist (IL-1Ra, endogenous inhibitor) are pivotal components of the IL-1 system. IL-1 and other cytokines induced by IL-1, such as TGF-beta 1, may participate in the growth of various tumor cells. In children, primary nervous system tumors represent the most common solid malignancy. We investigated the levels of IL-1 alpha, IL-1 beta, IL-1RI, IL-1Ra, and TGF-beta 1 mRNAs in pediatric astrocytomas (n = 19), ependymomas (n = 13), and primitive neuroectodermal tumors (n = 22) using sensitive and specific RNase protection assays. The data show a significant distinct cytokine mRNA profile among brain tumor types. Pilocytic, nonpilocytic, and anaplastic astrocytomas have significant increased levels of IL-1 beta, IL-1RI, and TGF-beta 1 mRNAs, but low levels of IL-1Ra mRNA; this may have implications for an IL-1 beta feedback system and IL-1 beta <-> TGF-beta 1 interactions in astrocytomas. Ependymomas show increased levels of IL-1 alpha and IL-1 beta mRNAs associated with low levels of IL-1Ra mRNA; primitive neuroectodermal tumors do not exhibit increased levels of any cytokine component examined. The data also suggest that a dysregulation of the balance between stimulatory and inhibitory cytokines may be involved in the growth and development of brain tumors via autocrine/paracrine mechanisms.
引用
收藏
页码:125 / 137
页数:13
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