Comparison of the expression of GATA-3 protein from the transcription factor family and pathological prognostic parameters in invasive ductal carcinomas of the breast

Author:

PARLAK Leymune1,KANDEMİR Olcay2

Affiliation:

1. Department of Pathology, University of Health Science Turkey, Mehmet Akif İnan Training and Research Hospital, Şanlıurfa, Turkey

2. Department of Pathology, University of Health Science Turkey ,Dr. Abdurrahman Yurtaslan Ankara Oncology Training and Research Hospital, Ankara, Turkey

Abstract

Background GATA binding protein 3 (GATA-3) is one of the six transcription factor family members and is important for glandular development in the breast. Its expression becomes important in breast cancer. We aimed to compare GATA-3 immunoreactivity and pathological prognostic factors in patients with invasive ductal carcinoma. Material and Methods Our study was conducted retrospectively with 300 breast invasive ductal carcinoma patients who were operated on in our hospital between May 2013 and June 2014. Patient reports, slides and blocks in the pathology archive were scanned. GATA-3 immunohistochemical (IHC) staining was evaluated according to the nuclear staining, intensity and percentage. The relationship between clinicopathological prognostic parameters and GATA-3 IHC staining results was investigated. Results A positive staining was observed in 286 (95.3%) cases. According to the GATA-3 staining intensity and percentage, 210 (70%) cases stained strongly and 246 (82%) stained +4, respectively. There was a significant relationship between GATA-3 immunoreactivity with ER, PR, Cerb-B2, Ki-67, mitotic degree, mitotic count and histological grade. Conclusions There was a correlation between the high expression of GATA-3 and good prognostic markers. Hormone receptors can be evaluated with Cerb-B2 and Ki-67 and used as prognosis determinants in breast cancers. They can be used to identify both primary and secondary breast tumors.

Publisher

Turkish Journal of Internal Medicine

Subject

General Medicine

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