Please use this identifier to cite or link to this item: http://localhost:8080/xmlui/handle/123456789/7819
Title: Vitamin D receptor expression in hydatidiform mole and gestational trophoblastic neoplasia: A cross-sectional study
Authors: Sasotya, RM Sonny
Kustiandi, Arieff
Hidayat, Yudi Mulyana
Effendi, Jusuf Sulaeman
Permadi, Wiryawan
Harsono, Ali Budi
Mulyantari, Ayu Insafi
Hernowo, Bethy S.
Keywords: Gestational trophoblastic disease
Gestational trophoblastic neoplasia
Hydatidiform mole
Vitamin D
Vitamin D receptor
Issue Date: 2024
Publisher: Journal of Taibah University Medical Sciences
Series/Report no.: Original Article;184-189
Abstract: Objective: Vitamin D receptor (VDR) exerts anti-cancer properties in a variety of cancers. The purpose of this study was to investigate the expression of VDR in patients with hydatidiform mole (HM) and gestational trophoblastic neoplasia (GTN). Methods: This is a cross-sectional study involved 61 specimens of HM (n ¼ 37, 60.7%) and GTN (n ¼ 24, 39.3%) was collected from the biopsy. An immunohistochemistry was used to asses the VDR expression. Student’s t-test and ManneWhitney test were used to compare the expression of VDR, including VDR staining intensity, VDR distribution, and histoscore, between HM and GTN tissue specimens. Results: No significant differences in age and parity were noted between patients with HM or GTN (p > 0.05). The VDR staining intensity of GTN tissue specimens was significantly lower than that of HM tissue specimens (2.3 0.8 vs. 2.8 0.5, p ¼ 0.008). In addition, the histoscore for GTN tissues was significantly lower than that for HM tissues (7.3 3.2 vs. 9.4 28, p ¼ 0.016). However, no significant differences in VDR distribution between GTN and HM tissues were observed (3.3 0.8 vs. 3.3 1.0, p ¼ 0.525). Conclusion: Low VDR expression is associated with GTN, whereas high VDR expression is associated with HM, suggesting that the expression of VDR may regulate the severity of gestational trophoblastic disease.
URI: http://localhost:8080/xmlui/handle/123456789/7819
ISSN: 1658-3612
Appears in Collections:Vol 19 No 1 (2024)

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