Mine Islimye Taskin

Background/Objectives: All-trans retinoic acid (ATRA) and acetylsalicylic acid (ASA; aspirin) have been reported to influence cancer-associated signaling through distinct molecular mechanisms, but their combined effects on cervical cancer cells remain incompletely characterized. This study evaluated the individual and combined effects of ATRA and ASA on HeLa human cervical cancer cells and used computational analyses as supportive, hypothesis-generating mechanistic contextualization. Methods: Cell viability was assessed by MTT assay after treatment with increasing concentrations of ATRA and ASA for 24, 48, and 72 h. The abundance of total ERK1/2, phospho-AKT (Ser473), total p38 MAPK, and total JNK was assessed by Western blotting, while intracellular HIF-1α and VEGF concentrations were measured in cell lysates by ELISA. Computational analyses included cross-validated response modeling, bootstrap estimation of Bliss excess inhibition, STRING network topology and enrichment, SwissTargetPrediction/SEA consensus target prediction, TCGA-CESC survival analysis, and redocking-validated molecular docking. Results: ATRA and ASA reduced HeLa cell viability in a dose- and time-dependent manner. Treatment was associated with lower total ERK1/2 abundance and lower phospho-AKT (Ser473) abundance, whereas ASA-containing conditions were associated with higher stress-associated MAPK markers, particularly JNK. Intracellular VEGF concentrations were lower after ATRA, ASA, and combined treatment, while intracellular HIF-1α concentrations were not significantly altered under normoxic culture conditions. Computational response modeling showed high predictive accuracy for ATRA and ASA, while bootstrap Bliss analysis indicated dose-dependent interaction behavior rather than uniform synergy. STRING analysis supported pathway-level coherence among retinoid, COX/prostaglandin, MAPK/AKT, hypoxia, and angiogenesis-related modules. TCGA-CESC analyses associated VEGFA, HIF1A, and PTGS2 with adverse survival outcomes in adjusted models. Docking supported ATRA–RARG and salicylate–COX-2 pose plausibility but did not support direct VEGFR2 or AKT1 targeting by ASA or salicylate. Conclusions: These findings suggest that ATRA and ASA reduce HeLa cell viability and are associated with altered MAPK/AKT-related protein abundance and lower intracellular VEGF concentrations in HeLa cervical cancer cells. The computational results provide pathway-level support and target prioritization for future validation but should not be interpreted as proof of direct binding, causal pathway mediation, treatment efficacy, or clinical benefit.

Background/Objectives: Prognostic stratification of stage I endometrioid-type endometrial cancer remains imperfect when based on clinicopathological variables alone. This retrospective study evaluated immunohistochemical markers reflecting stress adaptation, inflammatory signaling, autophagy regulation, and apoptotic balance, and developed an exploratory Endometrioid Immunohistochemical Prognostic Score (EIPS) based on SIRT1, HMGB1, Bcl-2, and Caspase-3 expression. Methods: Using surgical specimens from 139 patients with stage I endometrioid-type endometrial cancer, EIPS was calculated by assigning one point for high SIRT1, high HMGB1, high Caspase-3, and low Bcl-2 expression. Associations with overall survival and model discrimination were evaluated using Kaplan–Meier analysis, Cox regression, ridge-penalized multivariable modeling, and ROC/AUC analysis. Results: During a median follow-up of 1577 days, 12 deaths occurred. High SIRT1, HMGB1, and Caspase-3 expression were associated with poorer overall survival, while low Bcl-2 was retained as a biologically plausible adverse component. EIPS stratified patients into ordered low-, intermediate-, and high-risk groups with increasing event rates and showed higher apparent mortality discrimination than the predefined LVSI/grade-based clinicopathologic grouping (AUC = 0.857 vs. 0.756). IE-EIPS provided a modest additional apparent improvement in discrimination (AUC = 0.876). Conclusions: EIPS may offer prognostic stratification in stage I endometrioid-type endometrial cancer by integrating biologically complementary immunohistochemical markers.

Aims: This study aimed to evaluate preoperative HbA1c and serum 25-hydroxyvitamin D levels in patients with endometrial carcinoma and to investigate their associations with tumor grade and lymphovascular space invasion (LVSI).Methods: This retrospective study included 81 patients with histologically confirmed endometrial carcinoma and 30 control patients diagnosed with endometrial hyperplasia who underwent hysterectomy. Patients were categorized into four groups: grade 1-2 LVSI-negative, grade 1-2 LVSI-positive, grade 3 tumors, and controls. Preoperative glucose, HbA1c, and vitamin D levels were retrieved from medical records. Group comparisons were performed using Welch’s ANOVA with Games-Howell post hoc testing. Multivariate analysis of covariance (MANCOVA) was conducted adjusting for age and body-mass index.Results: Patients with endometrial carcinoma were significantly older and had higher BMI, glucose, and HbA1c levels, along with lower vitamin D concentrations compared with controls (all p

AimUterine septum is the most common Müllerian anomaly linked to primary infertility, preterm delivery, recurrent abortion, and fetal malpresentation. Hysteroscopic septum resection is a common treatment, but its impact on pregnancy outcomes remains debated. This study evaluates the effects of the procedure on pregnancy in women with poor obstetric history and primary infertility.Materials and MethodsPatients who underwent hysteroscopic septum resection in our clinic between 2015 and 2025 were retrospectively analyzed. Patients with incomplete follow-up or missing pregnancy outcome data were excluded from the study. A total of 107 patients were divided into two main groups: the group with a poor obstetric history and the primary infertility group. The effect of the surgery on pregnancy rates, term delivery rates, spontaneous abortion, and preterm birth rates in these groups was evaluated.Results In our study, a total of 107 patients were included, consisting of 62 primary infertile women (group 1) and 45 patients with a poor obstetric history (group 2). After hysteroscopic septum resection, 35 (56.5%) patients in group 1 and 27 (60.0%) patients in group 2 had a full-term delivery. The abortion rates were 6 (9.7%) and 3 (6.7%), respectively; the preterm birth rates were 3 (4.8%) and 3 (6.7%), respectively. As a complication, synechia was observed in only 3 patients.ConclusionOur study demonstrated hysteroscopic septum resection improved pregnancy outcomes in infertile women and patients with poor obstetric history, though no significant difference was found between the two groups.

This retrospective study compared the perioperative outcomes of vaginal natural orifice transluminal endoscopic surgery (V-NOTES) and total laparoscopic hysterectomy (TLH). This analysis included 62 patients: 32 underwent V-NOTES and 30 underwent TLH. Patients with a body mass index (BMI) >30, a history of endometriosis, multiple cesarean sections, or a uterine size >12 week were excluded. Perioperative data-including visual analog scale (VAS) scores, analgesia use, mobilization time, hospitalization duration, and hemoglobin deficit-were compared using independent sample t tests and Mann-Whitney U tests. There were no significant differences in BMI, number of pregnancies, or operative time (p > 0.05). VAS scores at 6 and 24 h were significantly lower in the V-NOTES group (p < 0.001). Patients in the V-NOTES group required less analgesia, had shorter mobilization and hospitalization periods, and returned to daily activities sooner (p < 0.001). However, the hemoglobin deficit was higher in the V-NOTES group (1.85 g/dl vs. 0.7 g/dl, p < 0.001). The neutrophil-to-lymphocyte ratio (NLR) was lower in the V-NOTES group (p = 0.013), whereas the platelet-to-lymphocyte ratio (PLR) and mean platelet volume (MPV) did not differ significantly between the two groups. V-NOTES offers advantages such as reduced postoperative pain and faster recovery compared to TLH. The higher hemoglobin deficit observed with V-NOTES may be related to the surgeon's experience. Further randomized studies are warranted to validate these findings and define appropriate patient selection criteria.

Aim: Peutz–Jeghers syndrome is a rare genetic disease with an increased risk of gastrointestinal and extragastrointestinal malignancies. Ovarian involvement of Sertoli–Leydig cell tumors is uncommon and even more rare in Peutz–Jeghers syndrome patients. This case report outlines the importance of primary ovarian Sertoli–Leydig cell tumor with bilateral adnexal involvement in a patient diagnosed with Peutz–Jeghers syndrome. Case: A 31‐year‐old female patient diagnosed with Peutz–Jeghers syndrome presented to our clinic with pelvic pain. Ultrasound examination revealed solid masses in both adnexa. Laparoscopic fertility‐preserving surgery was performed. Pathology confirmed the diagnosis of poorly differentiated solid ovarian Sertoli–Leydig cell tumor. Staging surgery was performed, and finally, the patient was referred to oncology for chemotherapy. Conclusion: This case report outlines the importance of Sertoli–Leydig cell tumors in the differential diagnosis of adnexal masses in patients with Peutz–Jeghers syndrome. Bilateral adnexal involvement is an unusual presentation of Sertoli–Leydig cell tumors. Despite unusual and different presentations, Sertoli–Leydig cell tumors should not be ignored or overlooked in patients with Peutz–Jeghers syndrome.

Objective: Chronic low-grade inflammation occurs in polycystic ovary syndrome (PCOS), and there are many contributing factors. In this study, we aimed to investigate Helicobacter pylori and Chlamydia trachomatis infections in patients with PCOS and to evaluate the association between these microorganisms and the inflammatory process in the etiology of the disease. Materials and Methods: This comparative cross-sectional clinical study was conducted at Balıkesir University Hospital and included 40 female patients diagnosed with PCOS in the gynecology outpatients clinic and 40 healthy female controls. Demographic data were recorded. Blood hormone profiles and biochemical parameters were analyzed. An enzyme-linked immunosorbent assay test kit was used to measure H. pylori IgG and C. trachomatis IgG. Results: According to the analysis of the study data, there was no significant association between the PCOS and non-PCOS groups with regard to the presence of Helicobacter pylori IgG (p = 0.1) and Chlamydia trachomatis IgG (p = 0.338). CRP levels were significantly higher in the PCOS group (p = 0.001). In the subgroup analyses, the CRP levels were not significantly different between the H. pylori and C. trachomatis antibody-positive and -negative groups. Diabetes mellitus was significantly associated with PCOS (p = 0.005). The smoking rate was significantly higher in the control group than in the PCOS group (p = 0.036). Compared to the control group, the BMI, LH, HOMA-IR, TSH, and TG levels were significantly higher in participants with PCOS (p = 0.000; p = 0.004; p = 0.001; p = 0.001; p = 0.043; p = 0.000). FSH was lower in PCOS patients compared to controls (p = 001). In the subgroup analyses, no significant differences were found between the H. pylori and C. trachomatis antibody-positive and -negative groups. Conclusions: PCOS is characterized by chronic nonspecific low-grade inflammation. The etiopathogenesis of PCOS involves comorbidities that cause a chronic inflammatory process. However, the possible infective causes still seem to be open to investigation. In particular, studies on microbiota and periodontal diseases in PCOS may provide important contributions.

Objective: Chronic systemic inflammation has been suggested to play a role in the development of polycystic ovary syndrome (PCOS). The aim of this study was to investigate the relationship between serum Chlamydia trachomatis and Helicobacter pylori infection and inflammatory processes in patients with PCOS and healthy controls and to analyse the factors associated with PCOS. Ma¬terials and Methods: This comparative cross-sectional clinical study was conducted at Balıkesir University Hospital and included 40 female patients diagnosed with PCOS in the gynaecology and obstetrics clinic and 40 healthy female controls. Demographic data were recorded. Blood hormone profiles and biochemical parameters were analyzed. A tube of blood was taken from the PCOS and control groups and analyzed in a biochemistry tube for H. pylori IgG and Clamidydia trachomatis IgG. Enzyme-linked immunosorbent test kit was used to measure H. pylori IgG and Clamidydia trachomatis IgG. Results: Diabetes mellitus and BMI were significantly associated with PCOS (p=0.005;p=0.000). Smoking rate was significantly higher in the control group than PCOS (p=0.036). Compared with the control group; BMI, LH, HOMA-IR, CRP, TSH, TG were significantly higher in subjects with PCOS (p=004;p=00;p=001;p=043;p=000), FSH in subjects with PCOS was lower than that in the controls (p=001). There was no significant association between the PCOS and non-PCOS groups with regard to the presence of Helicobacter pylori IgG (p=0.1) and Clamidydia trachomatis IgG (p=0.338). Conclusions: Abdominal obesity, oxidative stress endothelial dysfunction and gut microbiota have been shown to cause chronic low-grade inflammation, and chronic inflammation contributes to the processes leading to the metabolic and hormonal disorders of PCOS. Whether infections contribute to polycystic ovary syndrome has not yet been sufficiently clarified. However, regardless of infections, PCOS is characterized by chronic nonspecific low-grade inflammation.

Background: Oncostatin M, a novel adipokine, plays a role in oogenesis, lipogenesis, and inflammation and may contribute to polycystic ovary syndrome pathogenesis and related metabolic problems. Adipokines are believed to contribute to developing polycystic ovary syndrome and its accompanying metabolic parameters, such as dyslipidemia, insulin resistance, and cardiovascular diseases. Methods: In this case–control study, the patients were grouped in a 1:1 ratio into either the polycystic ovary syndrome (n = 32) or the control group (n = 32). Serum levels of fasting glucose, insulin, C-reactive protein, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, triglyceride, white blood cell count, thyroid-stimulating hormone, luteinizing hormone, follicle-stimulating hormone, total testosterone, prolactin, estradiol, homeostasis model assessment of insulin resistance, and oncostatin M were analyzed. Results: Oncostatin M levels were significantly lower, but C-reactive protein levels were substantially higher in the polycystic ovary syndrome group than in the control group (p = 0.002, p = 0.001, respectively). Oncostatin M was inversely correlated with total cholesterol, non-high-density lipoprotein cholesterol, fasting glucose, and the luteinizing hormone/follicle-stimulating hormone ratio (ρ = −0.329, p =0.017; ρ = −0.386, p = 0.005; ρ = −0.440, p = 0.001; ρ = −0.316, p = 0.023, respectively). Conversely, there was no correlation between oncostatin M and total testosterone level (ρ = 0.220; p = 0.118). In the context of inflammation and metabolic parameters, oncostatin M was inversely correlated with C-reactive protein, homeostatic model assessment for insulin resistance score, and low-density lipoprotein cholesterol (ρ = −0.353, p = 0.019; ρ = −0.275, p = 0.048; ρ = −0.470, p < 0.001, respectively). Conclusions: Plasma oncostatin M levels were considerably lower in patients with polycystic ovary syndrome than in the control group, and this was inversely correlated with the hormonal and metabolic parameters of polycystic ovary syndrome. Thus, oncostatin M may be a novel therapeutic target for polycystic ovary syndrome and its metabolic parameters.

Background: Polycystic ovary syndrome is a common reproductive and endocrinological disease characterized by ovulatory dysfunction, polycystic ovaries, and hyperandrogenism. Adipokines are believed to contribute to developing polycystic ovary syndrome and its accompanying metabolic complications such as dyslipidemia, insulin resistance, and cardiovascular diseases. Oncostatin M, a novel adipokine, plays a role in oogenesis, lipogenesis, and inflammation and may contribute to polycystic ovary syndrome pathogenesis and its related metabolic problems. Methods: In this case-control study, the patients were grouped in a 1:1 ratio into either the polycystic ovary syndrome (n = 32) or the control group (n = 32). Blood samples were obtained between the third and fifth days of the menstrual cycle. Serum levels of fasting glucose, insulin, C-reactive protein, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, triglyceride, white blood cell count, thyroid-stimulating hormone, luteinizing hormone, follicle-stimulating hormone, total testosterone, prolactin, estradiol, homeostasis model assessment of insulin resistance and oncostatin M were analyzed. Results: Oncostatin M levels were significantly lower, but C-reactive protein levels were substantially higher in the polycystic ovary syndrome group than in the control group (p = 0.002, p = 0.001, respectively). Oncostatin M was inversely correlated with total cholesterol, non-high-density lipoprotein cholesterol, fasting glucose, and the luteinizing hormone/follicle-stimulating hormone ratio (ρ = -0.329, p =0 .017; ρ = -0.386, p = 0.005; ρ = -0.440, p = 0.001; ρ = -0.316, p = 0.023, respectively). Conversely, there was no correlation between oncostatin M and total testosterone level (ρ = 0.220; p = 0.118). In the context of inflammation and metabolic parameters, oncostatin M was inversely correlated with C-reactive protein, homeostatic model assessment for insulin resistance score, and low-density lipoprotein cholesterol (ρ = -0.353, p = 0.019; ρ = -0.275, p = 0.048; ρ = -0.470, p < 0.001, respectively). The diagnostic performance of oncostatin M, C-reactive protein, homeostasis model assessment of insulin resistance, and non-high-density lipoprotein cholesterol for polycystic ovary syndrome is as follows: Oncostatin M, sensitivity: 50%, specificity: 75%, Accuracy: 63%, p = 0.009; C-reactive protein, sensitivity: 84%, specificity: 61%, Accuracy: 74%, p = 0.004; homeostasis model assessment of insulin resistance, sensitivity: 72%, specificity: 81%, Accuracy: 77%, p < 0.001; and non-high-density lipoprotein cholesterol; sensitivity: 72%, specificity: 75%, accuracy: 73%, p < 0.001. Conclusions: Plasma oncostatin M levels were considerably lower in patients with polycystic ovary syndrome than in the control group, and this was inversely correlated with the hormonal and metabolic parameters of polycystic ovary syndrome. Thus, oncostatin M may be a novel therapeutic target for polycystic ovary syndrome and its metabolic complications.