IMR Press / EJGO / Volume 19 / Issue 5 / pii/1998198

European Journal of Gynaecological Oncology (EJGO) is published by IMR Press from Volume 40 Issue 1 (2019). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with S.O.G.

Open Access Original Research

Correlation between immunoreactivity for transglutaminase K and for markers of proliferation and differentiation in normal breast tissue and breast carcinomas

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1 Department of Gynecology, University of the Saarland, Hamburg, Germany
2 Department of Dermatology, University of the Saarland, Hamburg, Germany
3 Department of Pathology, University of the Saarland, Hamburg, Germany
Eur. J. Gynaecol. Oncol. 1998, 19(5), 444–448;
Published: 10 October 1998
Abstract

We investigated immunohistochemically localization and expression of transglutaminase K (TGK) in normal breast tissue (n = 10) and in breast carcinomas (n = 30). Transglutaminase K was compared with the staining patterns of cytokeratin 10, Ki-67, p53, estrogen and progesterone receptors in these tumors. Weak to strong membrane bound immunoreactivity to TGK was detected in 17 out of 30 breast carcinomas analyzed. TGK staining was heterogeneous with visual differences between individual tumour cells. Ninety percent of normal breast tissues revealed no immunoreactivity to TGK. Both intensity of TGK immunostaining and number of TGK­positive cells were upregulated in breast carcinomas as compared to normal breast tissue. Analyzing coexpression of TGK with cytokeratin 10, Ki-67, p53, ER and PR, no statistically significant correlation was found. Our findings indicate that: (I) TGK is upre­gulated in breast carcinomas as compared to normal breast tissue. (II) Upregulation of TGK in breast carcinoma is not exclusively induced by alterations of epithelial differentiation or proliferation, but by different, unknown mechanisms. (III) Upregulation of TGK in breast carcinomas may play an important role in the regulation of tumour cell invasive properties by modulating cell-matrix interactions or by facilitating the assembly of matrix and tissue remodeling.

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