Alireza Maghsoudi
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Alireza Maghsoudi has a total of 10 co-authors. Here are the top co-authors by number of shared publications:
- Berivan Guzelbag
Department of Obstetrics and Gynecology, Haseki Training and Research Hospital, University of Health Sciences Türkiye, 34265 Istanbul, Türkiye
2 shared publications - Ali Cetin
Department of Obstetrics and Gynecology, Haseki Training and Research Hospital, University of Health Sciences, 34265 Istanbul, Türkiye
1 shared publication - Cagseli Goksu Ozgun Selcuk
Division of Perinatology, Department of Obstetrics and Gynecology Haseki Training and Research Hospital Affiliated with Health Sciences University Istanbul Turkey
1 shared publication - Emine Yılmaz Güler
Department of Anesthesiology and Reanimation, Haseki Training and Research Hospital University of Health Sciences İstanbul Turkey
1 shared publication - Engin Oral
Department of Obstetrics and Gynecology, Norrland University Hospital, Umeå University, 90187 Umea, Sweden
1 shared publication - Hadice Karahan
Molecular Biology and Genetics Department, Faculty of Natural Sciences and Engineering, Biruni University, 34020 Istanbul, Türkiye
1 shared publication
Latest Publications
- Open Access
- 26 March 2026
- Published by MDPI AG in International Journal of Molecular Sciences
- Vol. 27 (7) , 3034
Reduced GEN1 Expression Is Associated with Elevated DNA Damage and Impaired Proliferation in Endometriosis-Derived Endometrial Organoids
Endometriosis affects approximately 10% of reproductive-age women and is associated with genomic instability; however, the contribution of specific DNA repair deficiencies remains poorly understood. This study investigated the expression and function of GEN1, a Holliday junction resolvase critical for homologous recombination, in patient-derived endometrial epithelial organoids (EEOs). Endometrial tissue was obtained by pipelle biopsy from women with laparoscopically confirmed endometriosis (n = 3, stage III–IV) and controls without endometriosis (n = 3). GEN1 mRNA and protein expression were reduced in primary endometrial cells from endometriosis patients compared with controls (mRNA: 0.52 ± 0.14 vs. 1.00 ± 0.19, p = 0.05; immunofluorescence intensity: 0.54 ± 0.18 vs. 1.00 ± 0.22, p = 0.05). Patient-derived EEOs from the endometriosis group showed trends toward lower formation efficiency (18.4 ± 5.6% vs. 25.2 ± 6.8%, p = 0.10) and reduced mean diameter (124.6 ± 34.2 vs. 155.8 ± 32.6 µm, p = 0.10). RNA interference (RNAi)-mediated GEN1 knockdown reduced proliferation in both groups, with a more pronounced effect in endometriosis-derived EEOs (49.7% vs. 39.5% reduction, p = 0.05). Endometriosis-derived EEOs exhibited elevated baseline γH2AX (phosphorylated histone H2AX) immunofluorescence compared with controls (2.32 ± 0.44 vs. 1.00 ± 0.28, p = 0.05), indicating increased DNA double-strand break accumulation. Furthermore, GEN1 knockdown directly increased γH2AX intensity in both groups, with endometriosis-derived EEOs showing a greater absolute increase (Δ1.26 vs. Δ0.72). To our knowledge, this study provides the first organoid-based evidence that GEN1 is downregulated in endometriosis and functionally linked to impaired proliferation and elevated DNA damage, suggesting a potential contribution of homologous recombination dysregulation to endometriosis pathogenesis.
- 26 March 2026
- Published by MDPI AG in International Journal of Molecular Sciences
- Vol. 27 (7) , 3034
Open AccessReduced GEN1 Expression Is Associated with Elevated DNA Damage and Impaired Proliferation in Endometriosis-Derived Endometrial Organoids
Endometriosis affects approximately 10% of reproductive-age women and is associated with genomic instability; however, the contribution of specific DNA repair deficiencies remains poorly understood. This study investigated the expression and function of GEN1, a Holliday junction resolvase critical for homologous recombination, in patient-derived endometrial epithelial organoids (EEOs). Endometrial tissue was obtained by pipelle biopsy from women with laparoscopically confirmed endometriosis (n = 3, stage III–IV) and controls without endometriosis (n = 3). GEN1 mRNA and protein expression were reduced in primary endometrial cells from endometriosis patients compared with controls (mRNA: 0.52 ± 0.14 vs. 1.00 ± 0.19, p = 0.05; immunofluorescence intensity: 0.54 ± 0.18 vs. 1.00 ± 0.22, p = 0.05). Patient-derived EEOs from the endometriosis group showed trends toward lower formation efficiency (18.4 ± 5.6% vs. 25.2 ± 6.8%, p = 0.10) and reduced mean diameter (124.6 ± 34.2 vs. 155.8 ± 32.6 µm, p = 0.10). RNA interference (RNAi)-mediated GEN1 knockdown reduced proliferation in both groups, with a more pronounced effect in endometriosis-derived EEOs (49.7% vs. 39.5% reduction, p = 0.05). Endometriosis-derived EEOs exhibited elevated baseline γH2AX (phosphorylated histone H2AX) immunofluorescence compared with controls (2.32 ± 0.44 vs. 1.00 ± 0.28, p = 0.05), indicating increased DNA double-strand break accumulation. Furthermore, GEN1 knockdown directly increased γH2AX intensity in both groups, with endometriosis-derived EEOs showing a greater absolute increase (Δ1.26 vs. Δ0.72). To our knowledge, this study provides the first organoid-based evidence that GEN1 is downregulated in endometriosis and functionally linked to impaired proliferation and elevated DNA damage, suggesting a potential contribution of homologous recombination dysregulation to endometriosis pathogenesis.