Background/Objectives: Endocrine-disrupting chemicals (EDCs) interfere with hormonal homeostasis and have been implicated in gynecological malignancy pathogenesis. This narrative review synthesizes current evidence regarding EDC exposure and breast, endometrial, ovarian, and cervical cancers, examining molecular mechanisms, epidemiology, and diagnostic and clinical implications. Methods: We conducted a literature review using PubMed/MEDLINE, Embase, Scopus, and Cochrane databases through April 2026, including systematic reviews, meta-analyses, prospective cohorts, case-control studies, and mechanistic investigations examining EDC-cancer associations. Methodological quality was appraised using the Newcastle-Ottawa Scale and AMSTAR-2, with overall certainty of evidence rated using the GRADE framework. Results: Major EDC classes—bisphenol compounds, phthalates, polychlorinated biphenyls, organochlorine pesticides, and per- and polyfluoroalkyl substances—demonstrate carcinogenic potential through estrogen receptor modulation, epigenetic alterations, oxidative stress, and oncogenic signaling disruption. Breast cancer shows the strongest evidence, with prenatal and early-life DDT/DDE exposure associated with up to a 3.7-fold increased risk. Endometrial cancer demonstrates associations with xenoestrogen mixtures exhibiting non-monotonic dose-responses, whereas ovarian and cervical cancers show emerging but limited associations. Common mechanisms include receptor crosstalk, epigenetic dysregulation with transgenerational effects, oxidative genomic instability, metabolic reprogramming, and cancer stem cell enrichment. Conclusions: Evidence supports EDC contributions to gynecological malignancy through convergent pathways, though causal inference remains constrained by observational epidemiology, long latency periods, and challenges in characterizing real-world mixture exposures. Diagnostic and prevention strategies should integrate EDC exposure into risk-prediction models, leverage multi-omics biomarkers for early detection, and emphasize exposure reduction during critical developmental windows alongside regulatory reform.

The Dietary Approaches to Stop Hypertension (DASH) diet, characterized by high consumption of fruits, vegetables, whole grains, low-fat dairy products, and limited intake of saturated fats, cholesterol, and refined sugars, has been suggested to reduce the risk of preeclampsia. This narrative review aimed to summarize and synthesize the evidence regarding the role of the DASH diet in preeclampsia prevention. PubMed/MEDLINE, Embase, Google Scholar, ScienceDirect, Scopus, and Web of Science databases were searched to identify relevant studies. Multiple observational and intervention studies examining DASH diet adherence and preeclampsia outcomes were included. Higher adherence to the DASH diet was associated with an approximately 35–45% reduced risk of preeclampsia in observational studies. Intervention trials in high-risk populations demonstrated improved blood pressure control and potential reductions in preeclampsia incidence. The DASH diet appears to exert protective effects through multiple mechanisms, including improved blood pressure regulation, enhanced antioxidant defense, reduced inflammation, and improved endothelial function. The heterogeneity in study designs, DASH diet assessment methods, and intervention protocols limited the strength of conclusions. Evidence for the effects of greater adherence to the DASH diet on preeclampsia prevention is promising but requires confirmation through larger randomized controlled trials. Future research should focus on standardized DASH diet assessment methods, optimal timing and duration of dietary intervention, and exploration of potential synergies with other preventive strategies.

Pre-eclampsia, a major obstetric syndrome with an estimated global incidence of 2–8% of all pregnancies, ranks among the foremost causes of adverse maternal and perinatal outcomes worldwide. The Systemic Immune-Inflammation Index (SII)—derived as the product of platelet and neutrophil counts divided by the lymphocyte count—is a composite hematological parameter first established in oncological research that simultaneously captures neutrophil activation, lymphocyte dysfunction, and platelet alterations—three immunohematological disturbances implicated in pre-eclampsia pathophysiology. This narrative review synthesizes the current evidence regarding SII in pre-eclampsia, examining the biological rationale, clinical study findings, comparative performance against established inflammatory biomarkers, practical advantages, and limitations. A comprehensive literature search encompassing PubMed/MEDLINE, Scopus, Web of Science, and Google Scholar was conducted, covering all available records up to January 2026. The available data reveal substantial heterogeneity in both the direction of association (elevated versus paradoxically decreased SII in pre-eclampsia) and diagnostic performance across populations. While some studies report significantly elevated first-trimester SII values in women who subsequently develop pre-eclampsia, others demonstrate lower values or no significant predictive capacity. The only available meta-analysis reported non-significant pooled results for the pre-eclampsia-specific subgroup. Although SII’s derivation from routine complete blood count testing presents the advantages of cost-effectiveness and universal accessibility, methodological limitations—including retrospective study designs, the absence of standardized thresholds, the inconsistent discriminatory performance, and the conflicting directionality of association—preclude clinical implementation at present. Integration within multiparametric prediction models may optimize SII’s clinical utility. Future research should prioritize prospective validation studies across diverse populations, mechanistic investigations, and randomized controlled trials to establish evidence-based clinical translation.

Background/Objectives: Cervical insufficiency affects 1–2% of pregnancies and represents a significant cause of second-trimester loss and spontaneous preterm birth. This review synthesizes current evidence across the clinical spectrum of cervical insufficiency, providing evidence-based management guidance and identifying areas requiring further investigation. Methods: We conducted a comprehensive review of the current literature, evidence-based clinical guidelines, and landmark randomized controlled trials examining diagnostic frameworks, therapeutic interventions, and clinical outcomes across different presentations of cervical insufficiency. Our analysis incorporated data from major obstetric databases, professional society recommendations, and recent comparative effectiveness research. Results: Cervical insufficiency diagnosis encompasses three primary categories: history-based, ultrasound-based, and physical examination-based. Vaginal progesterone achieves a 31% reduction in preterm birth before 33 weeks (RR 0.69, 95% CI 0.55–0.88; NNT= 14). Ultrasound-indicated cerclage achieves a 30% relative risk reduction for delivery <35 weeks. The landmark SuPPoRT trial (n = 386) demonstrated no statistically significant differences among cerclage, pessary, and progesterone (p = 0.4), though formal equivalence trials have not been conducted. Multiple gestations show no benefit from singleton-derived interventions (RR 0.99–1.04). Conclusions: Optimal cervical insufficiency management emphasizes individualized approaches based on comprehensive risk stratification and objective cervical assessment, with vaginal progesterone and cervical cerclage serving as cornerstone therapies supported by robust clinical evidence.

Background: Low-dose aspirin started before 16 weeks' gestation is the only prophylaxis of established benefit for pre-eclampsia, yet one in twelve screen-positive women still develops the disorder. Low-molecular-weight heparin (LMWH) has anti-inflammatory, endothelial-protective and pro-angiogenic actions distinct from those of aspirin, but trials of combined therapy have used heterogeneous populations and fixed doses, and their results conflict.Objectives: To assess whether adding weight-adjusted tinzaparin to aspirin reduces pre-eclampsia and improves the angiogenic and inflammatory biomarker profile in women identified as high risk by first-trimester screening.Methods: preGO is a single-centre, open-label, parallel-group randomised controlled trial at a university hospital in Greece. One hundred women with a Fetal Medicine Foundation first-trimester risk above 1:150 for preterm pre-eclampsia are randomly allocated 1:1 to aspirin 160 mg daily alone or with weight-adjusted tinzaparin 4500–8000 anti-Xa IU once daily (≈75 anti-Xa IU/kg), from before 16 until 36 weeks' gestation. The primary outcome is pre-eclampsia by the 2021 ISSHP criteria. Secondary outcomes include early-onset and preterm pre-eclampsia, gestational hypertension, small-for-gestational-age birth, placental histopathology, and placental growth factor, soluble fms-like tyrosine kinase-1, their ratio, interleukin-6 and the systemic immune-inflammation index at 20–24, 32–34 and 36 weeks. The trial is powered for the biomarker outcomes; the clinical outcome is exploratory. Analysis is by intention to treat.Ethics and Dissemination: The trial was approved by the institutional ethics committee (approval 11/29-11-2022). Results will be published irrespective of direction and posted to the trial registry.Registration: ClinicalTrials.gov NCT07361679 (registered 21 December 2025; registered retrospectively).