Apoptosis, bcl-2 Expression, and Proliferation in Benign and Malignant Endometrial Epithelium: An Approach Using Multiparameter Flow Cytometry

Morsi, Hassan; Leers, Mathie P.G.; Radespiel‐Tröger, Martin; Björklund, Viveka; Kabarity, H. El; Nap, Marius; Jäger, Wolfram

doi:10.1006/gyno.2000.5744

Cited by 36 publications

(18 citation statements)

References 19 publications

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“…Since IGF-1 is an apoptosis blocker, the decreased expression of the corresponding gene is an indirect prerequisite for activation of apoptosis in hyperplastic endometrium. However, it is known that apoptosis in EHP increases just negligibly in comparison with the proliferation stage [8]. Its negative regulation in EHP can be seen from low activity of Ca 2+ /Mg 2+ -dependent endonucleases [2] participating in DNA degradation.…”

Section: Resultsmentioning

confidence: 99%

Disorders in Cytokine Gene Expression in Endometrial Hyperplasia and Effect of Hormone Therapy

et al. 2005

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We studied local expression of insulin-like growth factor 1, insulin-like growth factor receptor, epithelial growth factor, transforming growth factor beta2, PCNA, TNF-alpha, type I TNF receptor, Fas, FasL, IFN-gamma, IL-1beta, IL-4, IL-6, IL-8, IL-10, and IL-12 genes in intact and hyperplastic endometrium. Endometrial hyperplasia was associated with reduced production of TNF-alpha (p<0.05), PCNA (p<0.05), and epithelial growth factor mRNA and enhanced production of Fas mRNA (p<0.01). The expression of TNF-R1, IL-1beta, and IL-12 genes decreased only in glandular cystic hyperplasia (p<0.05 for all genes), expression of insulin-like growth factor 1 gene decreased only in adenomatous hyperplasia (p<0.05). Dufaston therapy of glandular cystic hyperplasia and zoladex therapy of adenomatous hyperplasia normalized expression of Fas receptor, PCNA, and insulin-like growth factor 1 genes, while the expression of IFN-gamma and IL-6 genes, which was normal in hyperplasia, decreased (p<0.05). Zoladex therapy decreased the production of transforming growth factor beta2 (p<0.05) and IL-1beta (p<0.01) mRNA, dufaston therapy decreased production of TNF-alpha (p<0.05) and IL-4 mRNA (p<0.05). Hence, both apoptosis and proliferative activity were suppressed in endometrial hyperplasia, and hormone therapy created prerequisites for transition of the endometrium into the normal proliferation stage.

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Section: Resultsmentioning

confidence: 99%

Disorders in Cytokine Gene Expression in Endometrial Hyperplasia and Effect of Hormone Therapy

et al. 2005

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“…However, the transition of the endometrial epithelium from hyperplasia to cancer may otherwise involve increased apoptosis. In a study evaluating apoptosis in malignant and benign endometrial samples quantitatively, the apoptotic activity increased significantly when normal and hyperplastic endometria were compared [17].…”

Section: Discussionmentioning

confidence: 99%

Apoptosis in the Endometrium of Postmenopausal Women Receiving Tibolone

Gökaslan

Öktem²,

Durmuşoğlu³

et al. 2003

Gynecol Obstet Invest

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Background/Aim: Tibolone, a synthetic derivative of the 19-nortestosterone family, induces atrophy of the endometrium, especially via its progestogenic Δ⁴ isomer. The aim of the study was to determine whether tibolone induces apoptosis in the endometrium of postmenopausal women. Methods: Twenty healthy postmenopausal women (mean age ± SD 52.4 ± 4.21 years) who had amenorrhea for at least 1 year and who had no history of any systemic illness and estrogen replacement therapy were enrolled in the study. All patients were offered office endometrial samplings, and then tibolone was prescribed (2.5 mg/day p.o., once daily) to all patients. Repeat endometrial samples were obtained after completion of the 6-month course of tibolone therapy. All samples were immunohistochemically analyzed for the presence of apoptotic cells. Results: There was no significant difference in the median proportion of apoptotic nuclei between the pre- and posttreatment samples (2 vs. 3%; p > 0.05). Conclusions: The results showed that tibolone did not affect the rate of apoptosis in the postmenopausal endometrium. Further studies are needed to clarify the role of apoptosis in overall effects of hormonal compounds on the postmenopausal endometrium.

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“…Flow cytometric evaluation of M30 and Bcl-2 expression levels, with SPF, in curettage specimens from post-menopausal patients complaining of bleeding provides a quantitative assessment of endometrial apoptosis, anti-apoptosis, and proliferation. Further studies are needed to determine the relationship among these three processes as indicators of the biological behavior of gynecological tumors [30]. …”

Section: Overviewmentioning

confidence: 99%

Predictive diagnosis of endometrial hyperplasia and personalized therapeutic strategy in women of fertile age

et al. 2013

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IntroductionEndometrial hyperplasia has a high risk for malignant transformation and relapses; existing mini-invasive treatments may lead to irrevocable endometrium destruction. The aims were to analyze receptor systems in endometrial hyperplasia, to evaluate the capabilities of ultrasonography, sonoelastography for diagnosis and treatment control, and to develop treatment algorithm.Materials and methodsWe included 313 women (20–45 years), assessed into the following: group 1 (n = 112) with glandular cystic hyperplasia, group 2 (n = 98) endometrial polyps, and group 3 (n = 103) atypical hyperplasia; and 82 controls who have undergone hysteroscopy before in vitro fertilization in tubal origin infertility were also included. Patients underwent clinical examination, transvaginal ultrasound, immunohistochemical study, and hormonal therapy/hysteroresectoscopy.ResultsIn patients with glandular hyperplasia, we registered increase of endometrium estrogen receptors (75.6% in the epithelium and 30.9% in the stroma; in controls, 43.3% and 29.6%, respectively); in polyps, there was a significant estrogen receptor increase in the stroma (48.2% vs 29.6% in controls), and in atypical hyperplasia, progesterone receptors significantly increased in the stroma. Ki-67 increased (40% to 50%) in the epithelium without changes in the stroma. Ultrasound has a sensitivity of 96% and a specificity of 85% for early detection of endometrial pathology and prediction outcome of intervention, and sonoelastography has a sensitivity of 91% and a specificity of 83% for polyp diagnosis. Personalized treatment was effective in 88.8%, relapse was diagnosed in 11.2% after 6 months, and conservative treatment of atypical hyperplasia was effective in 45%: in 25.8%, ablative hysteroresectoscopy was performed, while in 22.6% with comorbidities, hystero/oophorectomies were performed.ConclusionsThe evaluation of receptor status with ultrasound data in patients with endometrial hyperplasia allows for a clear definition of the treatment policy, avoidance of relapse, treatment optimization, and observation of such patients.

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Apoptosis, bcl-2 Expression, and Proliferation in Benign and Malignant Endometrial Epithelium: An Approach Using Multiparameter Flow Cytometry

Cited by 36 publications

References 19 publications

Disorders in Cytokine Gene Expression in Endometrial Hyperplasia and Effect of Hormone Therapy

Disorders in Cytokine Gene Expression in Endometrial Hyperplasia and Effect of Hormone Therapy

Apoptosis in the Endometrium of Postmenopausal Women Receiving Tibolone

Predictive diagnosis of endometrial hyperplasia and personalized therapeutic strategy in women of fertile age

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