Immunohistochemical expression of PTEN in normal, hyperplastic and malignant endometrium and its correlation with hormone receptors, bcl-2, bax, and apoptotic index


KAPUCUOĞLU N., Aktepe F., KAYA H., Bircan S. , Karahan N. , Ciris M.

PATHOLOGY RESEARCH AND PRACTICE, cilt.203, ss.153-162, 2007 (SCI İndekslerine Giren Dergi) identifier identifier identifier

  • Cilt numarası: 203 Konu: 3
  • Basım Tarihi: 2007
  • Doi Numarası: 10.1016/j.prp.2007.01.003
  • Dergi Adı: PATHOLOGY RESEARCH AND PRACTICE
  • Sayfa Sayıları: ss.153-162

Özet

PTEN is a tumor supressor gene that is frequently mutated in type I endometrioid endometrial carcinomas (EECs), and is involved in the control of cell proliferation, differentiation, and apoptosis. In this study, we aimed to assess the relationship between PTEN expression and estrogen, progesterone receptors (PRs), other apoptosis-related proteins, such as bcl-2 and bax, and apoptotic index (AI) in EEC, its precursor lesion hyperplasia, and cyclical endometrium. We also evaluated the relationship between PTEN expression and clinicopathologic parameters. PTEN, estrogen receptor (ER), PR,. and bcl-2 and bax expressions were evaluated immunohistochemically, and AI was evaluated in hematoxylin and eosin (HE)-stained slides in 23 cyclical and 37 hyperplastic endometria, and in 35 EECs. PTEN expression was higher in cyclical endometrium than in the carcinomas (p < 0.05). The PTEN expression level was significantly higher in non-atypical hyperplasias than in EEC, but there were no differences between atypical complex hyperplasia (ACH) and EEC and between hyperplasias. In the carcinomas, there was a negative correlation between grade and PTEN expression (r = -0.338, p = 0.047). In conclusion, we presume that PTEN is involved in the early phases of endometrial tumorigenesis, and it can be speculated that decreased PTEN expression with loss of differentiation in carcinoma can contribute to the emergence of tumors with a more aggressive phenotype. (c) 2007 Elsevier GmbH. All rights reserved.