4.7 Article

Interleukin-1 (IL-1α and IL-1β) and its receptors (IL-1RI, IL-1RII, and IL-1Ra) in prostate carcinoma

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CANCER
卷 100, 期 7, 页码 1388-1396

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WILEY
DOI: 10.1002/cncr.20142

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prostate carcinoma; interleukin-1; interleukin-1 transmembrane receptors; natural antagonist receptor

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BACKGROUND. The principal components of the interleukin-1 (IL-1) family are two secreted factors (IL-1alpha and IL-1beta), two transmembrane receptors (IL-1RI [biologically active] and IL-1RII [inert receptor]), and a natural antagonist receptor of IL-1 function (IL-1Ra). Changes in the expression pattern of these IL-1 members have been reported to be related to disease progression. The objective of the current study was to evaluate these changes in prostatic tissue by means of immunohistochemistry and Western blot analysis. METHODS. Immunohistochemical and Western blot analyses were performed in 20 normal samples, 35 samples of benign prostatic hyperplasia (BPH) and 27 samples 2 from patients with prostate carcinoma (PC). RESULTS. in normal prostate samples, immunoreactions to IL-1beta and IL-1RI were positive, whereas there were no immunoreactions observed to IL-1alpha, IL-1RII, or IL-1Ra. In BPH, in addition to immunoreactions to IL-Ibeta and IL-1RI, immunoreactions to IL-1alpha, IL-1RII, and IL-1Ra were observed in many samples. In samples of PC with low Gleason grade, most tumors had positive immunoreactions to IL-1alpha and IL-1RI. In samples of PC with high Gleason grade, immunoreactions were seen only to IL-1alpha, IL-1RI, and IL-1RII. CONCLUSIONS. The current results suggested that high expression levels of IL-1alpha and IL1-RI in epithelial cells in BPH and PC samples were involved in cell proliferation and that the loss of immunoexpression of IL-1beta and IL-1Ra was a characteristic feature of PC compared with normal prostate samples and BPH. Because this loss is progressive up to a complete absence of immunoexpression in PC of high Gleason grade, the evaluation of IL-10 and IL-1Ra in PC may be significant in assessing for malignancy. (C) 2004 American Cancer Society.

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