4.2 Article

Inhibin/activin subunits beta-A (-beta A) and beta-B (-beta B) are differentially localised in normal, hyperplastic and malignant human endometrial tissue

Journal

ACTA HISTOCHEMICA
Volume 108, Issue 1, Pages 1-11

Publisher

ELSEVIER GMBH, URBAN & FISCHER VERLAG
DOI: 10.1016/j.acthis.2005.11.002

Keywords

endometrium; hyperplasia; malignant; immunohistochemistry; immunofluorescence; inhibin/activin beta subunits; immunoperoxidase

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Inhibins (INHs) are dimeric glycoproteins composed of an alpha (-alpha) subunit and one of two possible beta (beta-) subunits (beta A or beta B). The aims of this study were to determine the frequency and distribution of INH beta (beta A and beta B) subunits in normal, hyperptastic and malignant human endometrium. Endometrial tissue was obtained from normal, hyperptastic (simple, complex and atypical) and endometrioid adenocarcinoma (EC) and INH-alpha, -beta A and -beta B were labelled using immunohistochemistry and immunofluorescence. INH-beta A and -beta B tabetting was increased significantly between the proliferative and secretory phase (p<0.05). The lowest tabetting was demonstrated in EC, being significantly lower than in secretory phase (p<0.01) and in simple, complex and atypical hyperplastic tissue (p<0.05). For inhibin-beta B, the most intense tabetting was noted in atypical hyperplasia compared to EC (p<0.05). A strong colocalisation of inhibin-alpha and -beta A could be demonstrated in malignant endometrial tissue, suggesting the production of inhibin A within the tumour. Additionally, only limited colocalisation of inhibin-beta B with -alpha subunit could be observed, suggesting the synthesis of activin B rather than inhibin B in malignant endometrium. In conclusion, INH-beta A and -beta B were labelled in normal, hyperptastic and malignant endometrium. Hyperplastic tissue labelled more intensely than EC for the presence of INH-beta A and -beta B, suggesting a substantial function in endometrial pathogenesis and an important role in endometrial carcinogenesis. (C) 2005 Elsevier GmbH. All rights reserved.

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