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Differential expression of STAT1 and IFN‐γ in primary and invasive or metastatic wilms tumors
Author(s) -
Liu Wei,
Zhang Lijuan,
Wu Rongde
Publication year - 2013
Publication title -
journal of surgical oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.201
H-Index - 111
eISSN - 1096-9098
pISSN - 0022-4790
DOI - 10.1002/jso.23364
Subject(s) - wilms' tumor , medicine , stat1 , immunohistochemistry , metastasis , concordance , cancer research , pathology , oncology , interferon , cancer , immunology
Background and Objectives IFN/STAT1 signaling has been found to be not only associated with an aggressive tumor phenotype but also activated and functional during metanephric development. This study was undertaken to evaluate STAT1 and IFN‐γ expression and its relation to histopathological features of primary and invasive/metastatic Wilms tumors. Methods Immunohistochemistry was used to determine the expression and cellular distribution of STAT1 and IFN‐γ in 18 pairs of primary and corresponding invasive/metastatic Wilms tumors and 40 primary tumors without invasion or metastasis. Results Positive rate of STAT1/IFN‐γ expression was 66.7%/61.1% and 72.2%/77.8% in 18 pairs of primary and associated invasive/metastatic Wilms tumor tissues, while 35.0%/27.5% in 40 primary tumors without invasion or metastasis. The expression of STAT1 and IFN‐γ was significantly associated with invasion/metastasis ( P = 0.025; P = 0.015). There was a positive correlation between STAT1 and IFN‐γ expression in all Wilms tumor tissues ( χ 2 = 23.408, P = 0.05, r = 0.555). The expression of STAT1 and IFN‐γ between primary and matched invasive/metastatic tissues was concordance, respectively ( P = 0.710 and P = 0.375). Conclusions These results suggest that IFN‐γ/STAT1 signaling might have clinical potential as a promising predictor to identify individuals with poor prognostic potential and as a possible novel target molecule of therapy for Wilms tumor. J. Surg. Oncol. 2013; 108:152–156 . © 2013 Wiley Periodicals, Inc.