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  1. Home
  2. Browse by Author

Browsing by Author "Kurtul O."

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    Hormone receptor expressions and proliferation markers in postmenopausal endometrial polyps
    (2006) Inceboz U.S.; Nese N.; Uyar Y.; Ozcakir H.T.; Kurtul O.; Baytur Y.B.; Kandiloglu A.R.; Caglar H.; Fraser I.S.
    Background/Aims: Endometrial polyps are quite common in the general population, they have a significant role in postmenopausal bleeding, and the pathogenesis is unclear. The aim of this study was to investigate proliferation markers and expression of estrogen and progesterone receptors in endometrial polyps in postmenopausal women. Methods: Endometrial polyps were removed by hysteroscopy from 36 women who presented with postmenopausal bleeding. None were using hormonal therapy. The control group consisted of 16 inactive-atrophic postmenopausal endometrial specimens removed at hysterectomy. Immunohistochemistry was used to demonstrate expression of estrogen and progesterone receptors and the cell growth and apoptosis markers, Ki67, bcl-2, c-erbB-2. Results: In both the glandular epithelium and stroma of endometrial polyps, estrogen and progesterone receptors, Ki67 and bcl-2 showed significantly more positive staining than the inactive endometrium from the control group. There was no difference in expression of c-erbB-2 between the two groups. Conclusions: Estrogen may have a role in the development of postmenopausal endometrial polyps, either by direct stimulation of localized proliferation or by stimulation of proliferation via other pathways, such as activation of Ki67 or through inhibition of apoptosis via bcl-2. c-erbB-2 is unlikely to play any role in development of these lesions. Copyright © 2006 S. Karger AG.
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    A comparative study of the effect of raloxifene and gosereline on uterine leiomyoma volume changes and estrogen receptor, progesterone receptor, bcl-2 and p53 expression immunohistochemically in premenopausal women
    (Elsevier Ireland Ltd, 2007) Baytur Y.B.; Ozbilgin K.; Cilaker S.; Lacin S.; Kurtul O.; Oruc S.; Koyuncu F.M.
    Objective: To compare the mechanism of action of raloxifene and gosereline induced shrinkage of leiomyomas via estrogen receptor, progesterone receptor, bcl-2 and p53 expression immunohistochemically. Study design: Thirty-two premenopausal women affected by uterine leiomyomas were randomized into two equal groups. Group A was treated with gosereline (3.6 mg subcutaneous injection monthly) and group B was treated with raloxifene (60 mg daily per os) for 3 months before undergoing surgery. At entry and at the end of the treatment the leiomyoma volume was measured ultrasonografically and the volume change was calculated. Immunohistochemical detection of estrogen receptor (ER), progesterone receptor (PR), bcl-2 and p53 were performed on leiomyoma tissue samples from group A, group B and the matched-control group. H-scores for ER, PR, bcl-2 and p53 were calculated. The mean volume changes of leiomyomas and immunohistochemical H-score differences of ER, PR, bcl-2 and p53 were compared between groups. Results: The leiomyoma volume decreased significantly after treatment in gosereline group from baseline of 65 cm 3 to 35 cm 3 , and in raloxifene group from 68 cm 3 to 50 cm 3 , p < 0.05. The difference between the before and after treatment leiomyoma volumes between the two treatments was not statistically significant. H-score of ER expression was significantly lower in gosereline group compared to control group (54.4 versus 113.2, p = 0.001), whereas H-score of PR expression was significantly lower with both gosereline and raloxifene groups compared to control group (64.8 for gosereline versus 94.6 for control, 73.6 for raloxifene versus 94.6 for control, p = 0.001). The bcl-2 expression was higher in both gosereline and raloxifene groups compared to control group (173.7 for gosereline versus 94.7 for control, 179.7 for raloxifene versus 94.7 for control, p = 0.001). The p53 expression was only lower with gosereline than the control group (169.4 versus 205.6, p = 0.001), whereas there was no significant change between the raloxifene group and the control group (201.9 versus 205.6) (p > 0.05). Conclusion: Raloxifene was as effective as gosereline in reducing leiomyoma volumes. Decreased PR expression may be a mechanism for tumor growth reduction in raloxifene treatment. In both treatment modalities, the mechanism of shrinkage of leiomyomas could not be increased apoptosis mediated by bcl-2 and p53 expression and should be investigated by further studies. © 2006 Elsevier Ireland Ltd. All rights reserved.

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