the Value of Immunohistochemical Expression of Moesin in Endometrial Hyperplasia and Endometrial Carcinoma
Study Details
Study Description
Brief Summary
Endometrial carcinoma (EC) is the most prevalent invasive carcinoma of the female genital tract in developed countries, while it ranks as the second most frequently occurring neoplasm of women in developing countries, after carcinoma of the cervix uteri. The vast majority of ECs occur in perimenopausal and postmenopausal women .
ECs are classified into two distinct phenotypes; type I which represents more than 80% of all cases of ECs, it has a favorable prognosis. This type is linked to excess, unopposed hyper-estrogenic condition and it is almost always preceded by endometrial hyperplasia. On the contrary, type II endometrial carcinoma is less common than type I, representing less than 10% of all cases of ECs. Type II endometrial carcinomas are high grade, poorly differentiated and estrogen-independent tumors .
| Condition or Disease | Intervention/Treatment | Phase |
|---|---|---|
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Study Design
Arms and Interventions
| Arm | Intervention/Treatment |
|---|---|
| endometrial carcinoma smples
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Device: microscopic pathological evaluation
description of moesin expression between endometrial hyperplasia and endometrial carcinoma
|
| endometrial hyperplasia samples
|
Device: microscopic pathological evaluation
description of moesin expression between endometrial hyperplasia and endometrial carcinoma
|
Outcome Measures
Primary Outcome Measures
- The value of immunohistochemical expression of moesin in endometrial hyperplasia and endometrial carcinoma [1 year]
To evaluate immunohistochemical expression of moesin in normal, hyperplasic and neoplastic endometrial tissues , correlate this expression with different clinicopathologic parameters of endometrial carcinoma and to evaluate the role of moesin as prognostic marker in progression from preinvasive lesions of the endometrium to endometrial carcinoma.
Eligibility Criteria
Criteria
Inclusion Criteria:
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Hysterectomy specimens diagnosed as endometrial hyperplasia and endometrial adenocarcinoma.
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All cases of endometrial biopsies obtained by curettage (D&C) diagnosed as endometrial hyperplasia.
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Cases of cyclical endometrium obtained from endometrial curettage or hysterectomy specimens done for pathological conditions other than hyperplastic or neoplastic endometrial lesions.
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Complete clinical data.
Exclusion Criteria:
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Patients with a history of preoperative chemotherapy and /or radiotherapy.
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Biopsies with predominantly blood clots.
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Insufficient or tiny tissue biopsies.
Contacts and Locations
Locations
| Site | City | State | Country | Postal Code | |
|---|---|---|---|---|---|
| 1 | Sohag University Hospital | Sohag | Egypt |
Sponsors and Collaborators
- Sohag University
Investigators
None specified.Study Documents (Full-Text)
None provided.More Information
Publications
- Frose J, Chen MB, Hebron KE, Reinhardt F, Hajal C, Zijlstra A, Kamm RD, Weinberg RA. Epithelial-Mesenchymal Transition Induces Podocalyxin to Promote Extravasation via Ezrin Signaling. Cell Rep. 2018 Jul 24;24(4):962-972. doi: 10.1016/j.celrep.2018.06.092.
- Mandelbaum RS, Ciccone MA, Nusbaum DJ, Khoshchehreh M, Purswani H, Morocco EB, Smith MB, Matsuzaki S, Dancz CE, Ozel B, Roman LD, Paulson RJ, Matsuo K. Progestin therapy for obese women with complex atypical hyperplasia: levonorgestrel-releasing intrauterine device vs systemic therapy. Am J Obstet Gynecol. 2020 Jul;223(1):103.e1-103.e13. doi: 10.1016/j.ajog.2019.12.273. Epub 2020 Jan 21.
- Wang H, Xiao X, Li Z, Luo S, Hu L, Yi H, Xiang R, Zhu Y, Wang Y, Zhu L, Xiao L, Dai C, Aziz A, Yuan L, Cui Y, Li R, Gong F, Liu X, Liang L, Peng H, Zhou H, Liu J. Polyphyllin VII, a novel moesin inhibitor, suppresses cell growth and overcomes bortezomib resistance in multiple myeloma. Cancer Lett. 2022 Jul 1;537:215647. doi: 10.1016/j.canlet.2022.215647. Epub 2022 Mar 17.
- Yuan O, Ugale A, de Marchi T, Anthonydhason V, Konturek-Ciesla A, Wan H, Eldeeb M, Drabe C, Jassinskaja M, Hansson J, Hidalgo I, Velasco-Hernandez T, Cammenga J, Magee JA, Nimeus E, Bryder D. A somatic mutation in moesin drives progression into acute myeloid leukemia. Sci Adv. 2022 Apr 22;8(16):eabm9987. doi: 10.1126/sciadv.abm9987. Epub 2022 Apr 20.
- Soh-Med-22-10-04