Background. Endometrial cancer (EC) is one of the most common gynecologic malignancy, mostly in postmenopausal women. The gold standard treatment for EC is surgery, but in the early stages, it is possible to opt for conservative treatment. In the last decade, different clinical and pathological markers have been studied to identify women who respond to conservative treatment. A lot of immunohistochemical markers have been evaluated to predict response to progestin treatment, even if their usefulness is still unclear; the prognosis of this neoplasm depends on tumor stage, and a specific therapeutic protocol is set according to the stage of the disease. Objective. (1) To provide an overview of the conservative management of Stage 1A Grade (G) 2 endometrioid EC (FIGO) and the oncological and reproductive outcomes related; (2) to describe the molecular alterations before and after progestin therapy in patients undergoing conservative treatment. Materials and Methods. A systematic computerized search of the literature was performed in the main electronic databases (MEDLINE, Embase, Web of Science, PubMed, and Cochrane Library), from 2010 to September 2021, in order to evaluate the oncological and reproductive outcomes in patients with G2 stage IA EC who ask for fertility‐sparing treatment. The expression of several immunohistochemical markers was evaluated in pretreatment phase and during the follow‐up in relation to response to hormonal therapy. Only scientific publications in English were included. The risk of bias assessment was performed. Review authors’ judgments were categorized as “low risk,” “high risk,” or “unclear risk” of bias. Results. Twelve articles were included in the study: 7 observational studies and 5 case series/reports. Eighty‐four patients who took progestins (megestrol acetate, medroxyprogesterone acetate, and/or levonorgestrel‐releasing intrauterine devices) were analyzed. The publication bias analysis turned out to be “low.” 54/84 patients had a complete response, 23/84 patients underwent radical surgery, and 20/84 had a relapse after conservative treatment. Twenty‐two patients had a pregnancy. The length of follow‐up was variable, from 6 to 142 months according to the different studies analyzed. Several clinical and pathological markers have been studied to identify women who do not respond to conservative treatment: PR and ER were the most studied predictive markers, in particular PR appeared as the most promising; MMR, SPAG9, Ki67, and Nrf2‐survivin pathway provided good results with a significant association with a good response to progestin therapy. However, no reliable predictive markers are currently available to be used in clinical practice. Conclusions. The conservative treatment may be an option for patients with stage IA G2 EEC who desire to preserve their fertility. The immunohistochemical markers evaluation looks promising in predicting response to conservative treatment. Further large series and randomized clinical trials are needed to confirm these results.

Background: Polycystic ovary syndrome (PCOS) is a complex and multifactorial disorder affecting reproductive, endocrine, and metabolic functions in women of reproductive age. While environmental and lifestyle factors play a role, increasing evidence highlights the contribution of genetic and epigenetic mechanisms to its pathogenesis. Objective: This narrative review aims to provide an updated overview of the current evidence regarding the role of genetic variants, gene expression patterns, and epigenetic modifications in the etiopathogenesis of PCOS, with a focus on their impact on ovarian function, fertility, and systemic alterations. Methods: A comprehensive search was conducted across MEDLINE, EMBASE, PubMed, Web of Science, and the Cochrane Library using MeSH terms including “PCOS”, “Genes involved in PCOS”, and “Etiopathogenesis of PCOS” from January 2015 to June 2025. The selection process followed the SANRA quality criteria for narrative reviews. Seventeen studies published in English were included, focusing on original data regarding gene expression, polymorphisms, and epigenetic changes associated with PCOS. Results: The studies analyzed revealed a wide array of molecular alterations in PCOS, including the dysregulation of SIRT and estrogen receptor genes, altered transcriptome profiles in cumulus cells, and the involvement of long non-coding RNAs and circular RNAs in granulosa cell function and endometrial receptivity. Epigenetic mechanisms such as the DNA methylation of TGF-β1 and inflammation-related signaling pathways (e.g., TLR4/NF-κB/NLRP3) were also implicated. Some genetic variants—particularly in DENND1A, THADA, and MTNR1B—exhibit signs of positive evolutionary selection, suggesting possible ancestral adaptive roles. Conclusions: PCOS is increasingly recognized as a syndrome with a strong genetic and epigenetic background. The identification of specific molecular signatures holds promise for the development of personalized diagnostic markers and therapeutic targets. Future research should focus on large-scale genomic studies and functional validation to better understand gene–environment interactions and their influence on phenotypic variability in PCOS.

We have developed a biopsy technique aimed at preoperative evaluating the extent of Paget’s vulvar disease in order to plan subsequent radical vulvar surgery. The aim is to find all possible lesion sites that are not visible macroscopically, to obtain a clear evaluation of the disease spread and to tailor the radical surgical procedure to remove even microscopic lesions, avoiding recurrences and excessively destructive surgery, adopting as conservative an approach as possible. We used this procedure for the first time to establish the radicality of the surgical intervention in a 68-year-old patient initially suffering from a single invasive vulvar Paget’s lesion.

Background: Adenomyosis and endometriosis are complex, estrogen-dependent gynecological conditions increasingly diagnosed in adolescents. While traditionally considered diseases of reproductive-age women, emerging evidence suggests a possible developmental origin in some cases, with genetic and epigenetic susceptibility playing a central role. Understanding the contribution of hereditary and molecular factors in adolescent-onset forms may offer insights into early pathogenesis, personalized risk stratification and tailored prevention strategies. Objectives: The objectives of this study were to explore the current evidence supporting a genetic contribution to the development of adenomyosis and endometriosis in adolescents and to identify specific genetic variants, molecular pathways and epigenetic mechanisms potentially involved in early-onset disease. Methods: A narrative literature review was conducted using PubMed and Scopus databases up to September 2025. Studies investigating the genetic basis of adenomyosis and endometriosis in adolescents, including familial aggregation, twin studies, GWAS and candidate gene analyses, were included. Results: Evidence from familial clustering and twin studies suggests a significant heritable component in both conditions. Genome-wide association studies have identified susceptibility loci, particularly involving WNT4, VEZT and ESR1, that may be relevant to adolescent-onset disease. Candidate gene studies further highlight the roles of estrogen signalling, inflammatory pathways, extracellular matrix remodelling and emerging epigenetic alterations, including aberrant DNA methylation and chromatin remodelling, which may influence early lesion development. However, most data are derived from adult cohorts, with limited adolescent-specific analyses. Conclusions: Genetic and epigenetic predispositions appear to contribute significantly to the pathogenesis of endometriosis and possibly adenomyosis in adolescents. Further studies targeting early-onset disease are needed to unravel developmental mechanisms and gene–environment interactions unique to this population.

Uterine myomas are the most common gynecological disease in reproductive-aged women, present several symptoms, and require effective medical and/or surgical strategies. This study aimed to compare robotic-assisted laparoscopic myomectomy (RALM) with laparoscopic myomectomy (LM) in terms of operative times, intraoperative estimated blood loss, pre- and post-hemoglobin levels drop, and length of hospital stay. Data from 50 clinical records (25 RALM in Group A and 25 LM in Group B) of patients with uterine fibroids were collected from December 2022 to December 2023 at Gynecological Unit of DAI Materno-Infantile Federico II in Naples, Italy. Patients aged 30–49 years with symptomatic fibroids were included. Data on peri-operative outcomes, including operative time for myomectomy (OTM), overall operative time (OOT), intraoperative estimated blood loss (EBL), pre- and post-operative hemoglobin levels, and length of hospital stay were analyzed. The OTM in the presence of > 5 myomas was 59 [52–65] vs 69 min [61–96] (p < 0.001) for RALM and LM groups, respectively. Moreover, also in presence of ≤ 5 myomas, a difference was observed in the RALM group 48[43–55] compared to the LM group 53[50–61] min (p = 0.07). The OOT was also statistically significant for Group A compared to Group B (83[65–93] vs 72[56–110] min, p < 0.001). There were no significant differences between the two groups in terms of pre- and post-operative hemoglobin levels and EBL (p = 0.178). Group A demonstrated a notably shorter hospital stay 1.2 [1–2] days compared to Group B 2.9[3–3.75] days (p = 0.007). Our study suggests potential advantages of RALM over LM in terms of reduced operative times and shorter hospital stays. The standardized approach and extensive surgical experience likely contributed to the favorable outcomes of RALM.

Background: Robotic-assisted surgery (RAS) has progressively expanded in gynecologic practice. Although its technical advantages are recognized, its economic sustainability and equitable accessibility remain debated. Methods: This clinical update provides a critical narrative review of current evidence on RAS in gynecology, integrating data on clinical outcomes, cost-effectiveness, diffusion patterns, and health equity across different healthcare settings. Results: In both benign and oncologic indications, RAS demonstrates consistent perioperative advantages over open surgery, including reduced blood loss, shorter hospital stay, and lower conversion rates. In routine cases, outcomes are largely comparable to conventional laparoscopy. However, robotic approaches appear particularly beneficial in complex scenarios, such as obesity, advanced malignancy, and technically demanding procedures. Economic evidence is heterogeneous. Short-term hospital-based studies report higher direct costs for RAS, especially in benign surgery. Conversely, cost–utility models in oncologic settings suggest that RAS may achieve acceptable cost-effectiveness when long-term outcomes, quality-adjusted life years, and institutional volume are considered. Accessibility remains strongly influenced by reimbursement policies, procedural volume, infrastructure, and workforce training. In the absence of structured reimbursement frameworks, robotic surgery may contribute to socioeconomic and geographic disparities. Conclusions: RAS represents an important component of modern gynecologic surgery, particularly in high-complexity and high-risk cases in which its technical advantages may translate into meaningful perioperative benefit. Its long-term sustainability depends on appropriate patient selection, institutional volume, reimbursement models, and health system organization. Future research incorporating long-term and societal economic perspectives is required to support balanced and equitable implementation.