Background: High grade serous ovarian carcinoma (HGSOC) is the most lethal type of epithelial ovarian cancer, with a prevalence of germline BRCA1/2 mutations as high as 20%. Our objective is to determine whether the location of mutations in the different domains of the BRCA1/2 genes affects the clinical outcome of HGSOC patients. Methods: A total of 51 women with BRCA1 or BRCA2 mutated ovarian cancer were identified. Progression-free survival (PFS) and overall survival (OS) were analyzed. Results: In our study cohort, 35 patients were carriers of germline mutations in BRCA1 and 16 in BRCA2. The median PFS time following completion of the primary therapy was 23.8 months (95% CI 20.1–27.5) and the median OS was 92.9 months (95% CI 69.8–116.1) in all BRCA carriers. After multivariate analysis, no significant association among the location or type of BRCA1/2 mutation with PFS or OS was identified. Notably, significant differences in PFS between carriers of identical mutations in the same BRCA gene were detected. Conclusions: Among HGSOC patients, BRCA1/2 carriers with mutations in different locations of the genes show no significant difference in survival outcomes, in terms of PFS and OS, suggesting the potential effect of other genetic abnormalities and co-contributing risk factors.

Neurological paraneoplastic syndromes are a rare subgroup of diseases commonly related to neuroendocrine tumors. However, they have been associated with uterine malignancies (sarcomas, endometrial carcinomas, and neuroendocrine cancers). Their presentation often correlates with a cancer diagnosis or cancer recurrence underlining their clinical significance. The most common neurological paraneoplastic syndrome in uterine cancer is cerebral degeneration with a comprehensive clinical presentation of pancerebral dysfunction. However, other neurological syndromes present with various symptoms leading to delayed diagnosis. Less common paraneoplastic neurological syndromes associated with uterine cancer are encephalitis, encephalomyelitis, subacute sensory neuropathy, sensory-motor neuropathy, dermatomyositis, cancer-associated retinopathy, opsoclonus, Guillain-Barre syndrome, necrotizing myopathy, and stiff-person syndrome. Herein, we reviewed published cases of neurological paraneoplastic syndromes in uterine cancer in order to raise awareness of these rare syndromes. We recorded patients' clinical presentation, antibodies detected, treatment, and clinical outcomes.

Ovarian cancer is the gynecologic malignancy that bears the highest mortality rate in the Western world. This is attributed to late diagnosis and limited therapeutic progress. Recent advances in molecular oncology have highlighted the pivotal role of epigenetic modifications—including DNA methylation, histone modifications, non-coding RNAs, chromatin remodeling, and RNA methylation—in ovarian cancer development, progression, and treatment resistance. DNA methylation patterns affect key tumor suppressors and oncogenes, while histone modifications alter chromatin accessibility, influencing gene expression. Chromatin remodeling complexes, particularly the SWI/SNF complex, are frequently mutated in specific ovarian cancer subtypes, which is central in shaping their biological behavior. Non-coding RNAs, including microRNAs and long non-coding RNAs, further regulate tumor cell behavior and the immunosuppressive tumor microenvironment. Epigenetic profiles vary among histological subtypes and hold promise for biomarker development, early detection, prognosis, and therapeutic monitoring. Liquid biopsy approaches leveraging circulating tumor DNA methylation show diagnostic potential superior to conventional markers. Moreover, targeting epigenetic regulators—such as DNMT and HDAC inhibitors, EZH2 antagonists, and RNA-modifying enzymes—offers novel avenues for treatment, particularly in reversing chemoresistance and sensitizing tumors to immunotherapy. While promising, these strategies require further validation through clinical research to translate into effective clinical interventions. This review aims to summarize the current literature and highlights potential applications of epigenetic manipulation in day-to-day practice.

Uterine serous carcinomas are an aggressive minority of endometrial cancers. They are characterized by mutations in TP53 and extensive copy number alterations and are primarily classified in the copy number-high/p53abn molecular prognostic group, highlighting a unique molecular profile that is crucial for understanding their behavior and treatment responses. Clinical studies have shown that molecular categorization via biomarkers can facilitate proper treatment selection, and this is now widely used. In this context, the scope of this systematic review is to identify molecular characteristics with prognostic significance for these neoplasms to further inform on their treatment needs. We performed a comprehensive literature search of all articles written in English using the PubMed/Medline and Cochrane databases through February 2025. Our review led to the inclusion of 95 studies, from which we identified a total of 66 distinct molecular characteristics along with new cancer signatures that may impact prognosis. These findings have the potential to inform clinical practice by aiding in the development of tailored treatment strategies for patients with uterine serous carcinoma, ultimately improving outcomes in this challenging malignancy.

Background/Objectives: Survival rates for ovarian cancer remain distressingly low. Despite established prognostic factors, the need to identify modifiable parameters to influence survival outcomes is imperative. Overweight and obesity, both prevalent conditions, have been implicated in cancer development and potentially poor survival. However, conflicting data on the associations of body mass index (BMI) with progression-free survival (PFS) and overall survival (OS) in ovarian cancer patients necessitate further exploration. This study aims to investigate the prognostic role of BMI before chemotherapy in women with ovarian cancer, specifically focusing on PFS and OS. Methods: A retrospective analysis encompassed 1,136 patients diagnosed with ovarian carcinomas between 1995 and 2018. Patients were categorized based on BMI at presentation, and a comprehensive examination of clinicopathological, treatment, and survival data was conducted. Results: In the patient population, normal weight patients (BMI < 25 kg/m²) demonstrated a median PFS of 12.8 months (95% CI 11.7–13.9 months), while overweight/obese patients (BMI ≥ 25 kg/m²) exhibited a significantly longer median PFS of 14.9 months (95% CI 13.6–16.4 months, P = 0.006). No statistically significant difference was noted in median OS between the two BMI groups. Subgroup analysis for different histological subtypes revealed a statistically significant benefit for overweight and obese patients with serous and endometrioid histology (mPFS 12.9 months, 95% CI 11.7–14.0 vs. 15.6 months, 95% CI 13.9–17.3, P = 0.012 and 14.6 months 95% CI 13.7–15.5 vs. 25.6 months, 95% CI 9.5–41.7, P = 0.031, respectively). Additionally, BMI ≥ 25 kg/m² demonstrated a significant advantage in advanced-stage disease. Conclusions: The study underscores the intricate association between BMI and ovarian cancer prognosis. While a statistically significant difference in progression-free survival was noted between normal weight and overweight/obese patients, with the latter group experiencing a survival benefit, no such difference was observed in overall survival.

Background: Uterine serous carcinoma (USC) represents a rare but aggressive subtype of endometrial cancer, accounting for a disproportionate number of disease-related deaths. Although molecular classification has improved risk stratification, prognostic heterogeneity highlights the need for new prognostic markers. Methods: We retrospectively analyzed 83 patients with USC treated at our institution between 1 January 2015 and 31 December 2023. Clinicopathological characteristics, treatment strategies, molecular biomarkers accessed by immunohistology (TP53, ER, PR, HER2, and MMR status), and survival outcomes were collected. Patients were first staged by FIGO 2009 and retrospectively reclassified by FIGO 2023. Disease-free survival (DFS), progression-free survival (PFS), and overall survival (OS) were assessed using Kaplan–Meier and Cox regression analyses. Results: The majority of patients were presented with advanced disease (FIGO stage IIIC-IV). TP53 mutations were found in 88% of cases, HER2 amplification in 18%, and ER expression in 57.8%. ER-positive patients showed significantly improved DFS in the adjuvant setting compared with ER-negative patients, whereas no significant associations were observed for first-line PFS or OS in multivariable analyses. HER2 amplification was not associated with inferior survival in our cohort. The advanced stage remained an independent predictor of worse OS. Conclusions: USC is a biologically heterogeneous disease, and its treatment should be guided by its molecular profile. ER expression identifies a subset of patients with improved DFS, suggesting potential prognostic relevance in this high-risk histology.