the Value of Immunohistochemical Expression of Moesin in Endometrial Hyperplasia and Endometrial Carcinoma
NCT ID: NCT05619159
Last Updated: 2022-11-16
Study Results
The study team has not published outcome measurements, participant flow, or safety data for this trial yet. Check back later for updates.
Basic Information
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UNKNOWN
100 participants
OBSERVATIONAL
2022-11-30
2023-05-31
Brief Summary
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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 .
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Detailed Description
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Conditions
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Study Design
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CASE_ONLY
RETROSPECTIVE
Study Groups
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endometrial carcinoma smples
microscopic pathological evaluation
description of moesin expression between endometrial hyperplasia and endometrial carcinoma
endometrial hyperplasia samples
microscopic pathological evaluation
description of moesin expression between endometrial hyperplasia and endometrial carcinoma
Interventions
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microscopic pathological evaluation
description of moesin expression between endometrial hyperplasia and endometrial carcinoma
Eligibility Criteria
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Inclusion Criteria
* All cases of endometrial biopsies obtained by curettage (D\&C) diagnosed as endometrial hyperplasia.
* Cases of cyclical endometrium obtained from endometrial curettage or hysterectomy specimens done for pathological conditions other than hyperplastic or neoplastic endometrial lesions.
* Complete clinical data.
Exclusion Criteria
* Biopsies with predominantly blood clots.
* Insufficient or tiny tissue biopsies.
FEMALE
No
Sponsors
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Sohag University
OTHER
Responsible Party
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Nermin Abbas
resident doctor pathology in sohag oncology center
Locations
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Sohag University Hospital
Sohag, , Egypt
Countries
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Central Contacts
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afaf t el nashar, professor
Role: CONTACT
Facility Contacts
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Magdy M Amin, professor
Role: primary
References
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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.
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.
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.
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.
Other Identifiers
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Soh-Med-22-10-04
Identifier Type: -
Identifier Source: org_study_id
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