GATA3 immunohistochemical expression in invasive urothelial carcinoma

被引:22
作者
Mohammed, Kareem Hosny [1 ]
Siddiqui, Momin T. [1 ]
Cohen, Cynthia [1 ]
机构
[1] Emory Univ, Sch Med, Dept Pathol & Lab Med, Atlanta, GA 30322 USA
关键词
GATA3; expression; Genitourinary tumors; IHC; GENE-EXPRESSION; BREAST; DIFFERENTIATION; PROSTATE; MARKERS;
D O I
10.1016/j.urolonc.2016.04.016
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Introduction: GATA binding protein 3 (GATA3) is a transcription factor, which belongs to a distinct family of tumor suppressor genes. It is involved in human cancer cell growth and differentiation, and plays an important role in cell proliferation and apoptosis. Although, its expression has been reported in various cancers, there are limited data in genitourinary malignancies. Recent studies found GATA3 to be a sensitive marker for urothelial carcinoma (UC) and associated with prognostic pathologic features. Its level of expression was found to be an independent factor predicting cancer recurrence. Methods and materials: In this article, immunohistochemical evaluation of GATA3 expression in genitourinary malignancies (invasive UC, renal cell carcinoma, and prostatic adenocarcinomas) was performed. Results: GATA3 was positive in 56/79 (70.8%) of invasive UC, and was negative in all renal cell carcinoma and prostatic adenocarcinomas. The pattern of GATA3 staining, when positive, was intensely nuclear within the clusters of malignant cells. No cytoplasmic staining was noted. Negative controls were all negative. High GATA3 expression was associated with larger tumor size in invasive UC (3.19cm vs. 1.65cm, P = 0.01). GATA3 expression did not correlate with other clinicopathologic parameters in UC. Conclusions: This data suggest that GATA3 is a sensitive marker in confirming invasive UC, and may be helpful in differentiating it from metastatic tumors of renal and prostatic origin. Furthermore, strong GATA3 expression was noted to have an effect on tumor size in patients with UC. (C) 2016 Elsevier Inc. All rights reserved
引用
收藏
页码:432.e9 / 432.e13
页数:5
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