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首页> 外文期刊>Human Reproduction >Effect of asoprisnil on uterine proliferation markers and endometrial expression of the tumour suppressor gene, PTEN.
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Effect of asoprisnil on uterine proliferation markers and endometrial expression of the tumour suppressor gene, PTEN.

机译：Asoprisnil对抑癌基因PTEN的子宫增生标志物和子宫内膜表达的影响。

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BACKGROUND: The selective progesterone receptor modulator asoprisnil suppresses uterine bleeding and decreases leiomyoma volume while maintaining follicular phase estrogen concentrations. For safety of potential clinical applications, any proliferative effect of asoprisnil on uterine tissues, particularly endometrium, needs to be established. METHODS: In a double-blind, randomized, placebo-controlled study (continuation of previously published trial No. NCT00150644 (Williams et al., 2007 and Wilkens et al., 2008)), 33 patients with symptomatic uterine leiomyomata received placebo, 10 or 25 mg asoprisnil daily for 12 weeks before hysterectomy. Proliferation markers Ki-67 and anti-phospho-histone H3 (PH3) were immunolocalized in endometrium, myometrium and leiomyoma tissue. Endometrial PTEN (phosphatase and tensin homologue, a tumour suppressor gene) expression was also assessed by immunohistochemistry. PH3-positive glandular and stromal cells were counted per measured endometrial area. Endometrial Ki-67 expression was assessed using stereological methods. Stained myometrial and leiomyoma cells were counted per 10 fields (x250). PTEN immunostaining was quantified using a histoscore. Each asoprisnil group was compared with placebo (secretory phase) with significance at 0.05 level. RESULTS: Endometrial epithelial proliferation and PTEN expression were not significantly different between placebo and asoprisnil groups. Decreased stromal Ki-67 expression (P < 0.05) suggested any effect of asoprisnil on endometrial proliferation to be inhibitory. Immunolocalization of PTEN expression was not different between treatment groups in any tissue compartments. Myometrial Ki-67 expression decreased following asoprisnil 25 mg (P < 0.05). CONCLUSIONS: Asoprisnil does not induce proliferation of uterine tissues and does not suppress endometrial PTEN expression.
机译：背景：选择性孕激素受体调节剂阿普瑞尼可抑制子宫出血并减少平滑肌瘤体积，同时保持卵泡期雌激素浓度。为了确保潜在临床应用的安全性，需要确定Asoprisnil对子宫组织（尤其是子宫内膜）的任何增殖作用。方法：在一项双盲，随机，安慰剂对照研究中（继续先前发表的试验号NCT00150644（Williams等，2007和Wilkens等，2008）），有33例有症状子宫平滑肌瘤患者接受了安慰剂，10或在子宫切除术前12周每天服用25 mg阿索非尼。增殖标记Ki-67和抗磷酸组蛋白H3（PH3）免疫定位在子宫内膜，子宫肌层和平滑肌瘤组织中。子宫内膜PTEN（磷酸酶和张力蛋白同源物，一种抑癌基因）的表达也通过免疫组织化学评估。每个测量的子宫内膜面积对PH3阳性的腺体和基质细胞计数。使用立体学方法评估子宫内膜Ki-67表达。每10个视野（x250）计数染色的子宫肌层和平滑肌瘤细胞。使用组织评分对PTEN免疫染色进行定量。将每个asoprisnil组与安慰剂（分泌期）进行比较，其显着性水平为0.05。结果：安慰剂组和Asoprisnil组之间的子宫内膜上皮增殖和PTEN表达没有显着差异。基质Ki-67表达的降低（P <0.05）表明，阿泊瑞尼对子宫内膜增生的任何抑制作用都是抑制性的。在任何组织隔室中的治疗组之间，PTEN表达的免疫定位没有差异。 25 mg阿索普利尼后肌层Ki-67表达下降（P <0.05）。结论：Asoprisnil不会诱导子宫组织增殖，也不会抑制子宫内膜PTEN的表达。

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