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FHIT expression in neoplastic, hyperplastic, and normal endometrium
  1. S. K. ÖZKARA* and
  1. *Department of Pathology, Faculty of Medicine, Kocaeli University, Kocaeli, Turkey
  2. Department of Obstetrics and Gynecology, Faculty of Medicine, Kocaeli University, Kocaeli, Turkey
  1. Address correspondence and reprint requests to: Dr Sevgiye Kaçar Özkara, Associate Professor of Pathology, Mustafa Paşa Mah., Bağdat Cad. 0712, Sok. No. 19/6, 41400-Gebze, Kocaeli, Turkey. Email: emrecan1999{at}


Fragile histidine triad (FHIT), a candidate of tumor suppressor protein, expression was examined on paraffin-embedded specimens in proliferative, secretory, hyperplastic, and neoplastic human endometrium by immunohistochemistry. The results of FHIT immunoreactivity in endometrial carcinomas were compared with prognostic indicators as well as with p53 overexpression. Forty-four cases of endometrial carcinoma, 30 normal functional (15 proliferative, 15 secretory), and 24 hyperplastic endometrium (12 without atypia, 12 with atypia) specimens were studied using polyclonal FHIT antibody. The streptavidin–biotin–peroxidase detection system was used, and the intensity and the distribution of immunoreactivity were evaluated semiquantitatively. There were no significant differences in FHIT expression in the proliferative, secretory, hyperplastic, either with or without atypia, or carcinomatous endometria. No significant difference in FHIT expression of endometrial carcinomas was detected when prognostic parameters or p53 overexpression were considered. Loss or reduced FHIT expression was not found to predict disease-free or cumulative survivals. This study showed that loss or reduction in FHIT protein expression is present in normal functional and hyperplastic endometria as well as in neoplastic endometrium. FHIT protein seems not to be involved directly in endometrial carcinogenesis, but rather, it regulates cell proliferation both in physiologic and in pathologic conditions of endometrium.

  • carcinoma
  • endometrium
  • FHIT
  • fragile histidine triad
  • hyperplasia
  • p53

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