Introduction: Cancer of the uterine cervix (CUC) is still one of the most frequent oncological diagnoses in women. The specific interactions between the tumor cells of CUC and the cells and tissues in the tumor microenvironment can affect cancer cells’ invasive and metastatic potential and can modulate tumor’s progression and death. CD47 is a trans-membranous immunoglobulin, expressed in many cells. It protects the cells from being destroyed by the circulating macrophages. Aim: We aimed to evaluate the prognostic role of CD47 expressed in the tumor tissues of patients with CUC for tumor progression and to find the most sensitive immunohistochemical score for defining the cut-off significantly associated with tumor biology and progression. Materials and methods: Paraffin-embedded tumor tissues from 86 patients with CUC were included in the study. Clinico-morphological data for patients, such as age and stage at diagnosis according to FIGO and TNM classification, were obtained from the hospital electronic medical records. Immunohistochemical staining was performed with rabbit recombinant monoclonal CD47 antibody (Clone SP279). The final result was interpreted based on three reporting models in immunohistochemistry: H-score, Allred score and combined score. Results: The expression of CD47 was higher in tumors limited in the cervix compared with those invading other structures, and it did not depend on the nodal status. The results of immunohistochemical staining were similar regardless of which immunohistochemical method was used. The most significant correlation with TNM stage was observed with the H-score (p = 0.00018). The association with the Allred and combined score was less significant, with p values of 0.0013 and 0.0002, respectively. Conclusion: The expression of CD47 in the cancer cells is prognostic for tumor invasion in the surrounding structures, independent of lymph node engagement. The H-score is the most sensitive immunohistochemical score to describe tumor stage. To the best of our knowledge, this is the first study evaluating the significance of CD47 expression in CUC.

High-risk human papillomaviruses (HPVs), particularly types 16 and 18, drive carcinogenesis by rewiring host metabolism and mitochondrial function. The oncoproteins E5, E6, and E7 collectively induce mitochondrial fragmentation, increase reactive oxygen species (ROS), and promote a metabolic shift from oxidative phosphorylation (OXPHOS) to glycolysis (the Warburg effect). A redox-sensitive mitochondrial protein, Reactive Oxygen Species Modulator 1 (ROMO1), has emerged as a key mediator of these processes. ROMO1 contributes to mitochondrial morphology, regulates ROS homeostasis, and interacts with key stress-response pathways. While ROMO1 is overexpressed in many cancers and correlates with poor prognosis, recent data suggest that HPV-associated cervical lesions exhibit a unique biphasic expression pattern, with high ROMO1 levels in early stages and reduced expression in advanced tumors. The underlying molecular mechanisms remain unclear, but may involve HPV genome integration, NF-κB suppression, or epigenetic silencing. Key mechanisms such as how HPV modulates ROMO1 expression and how this contributes to stage-dependent metabolic vulnerability remain incompletely understood. This review highlights the current understanding of how HPV oncoproteins impact mitochondrial structure and function, emphasizes the role of ROMO1 in this context, and compares findings with other cancer types. Although no ROMO1-targeted therapies currently exist, the protein may serve as a redox-sensitive biomarker and potential vulnerability in HPV-driven tumors. We propose that targeting mitochondrial fragmentation, ROS signaling, or metabolic reprogramming may offer new avenues for therapeutic intervention. Further research is needed to clarify ROMO1’s dual role in early vs. late-stage disease and to validate its relevance as a clinical target. Our review fills a gap in the current literature by being the first to systematically explore ROMO1’s contribution to HPV-induced mitochondrial dysfunction and metabolic rewiring, and we outline research priorities for future studies.

More than 95% of the cases of Cervical cancer (CC) are now linked to infection with Human papilloma virus (HPV) but the infection alone is not sufficient for starting the oncogenesis. Reactive Oxygen Species (ROS) can promote CC cancerogenesis. ROMO1 is a protein that regulates the production of intracellular ROS and influences cancer cell invasion and proliferation. We aimed to investigate the impact of ROS in CC progression, measured by the expression of ROMO1. This is a retrospective study of 75 patients treated at the Department of Oncogynecology, Medical University of Pleven, Bulgaria. Paraffin embedded tumor tissues were immunohistochemically tested for the levels of expression of ROMO1. The results for both Allred score and H-score were investigated for association with tumor size, lymph node status and FIGO stage. Levels of ROMO1 were significantly higher in FIGO1 stage compared to FIGO2 and FIGO3 according to both scores (for H-score FIGO1 vs FIGO2 p = 0.00012; FIGO 1 vs FIGO3 p = 0.0008; for Allred score FIGO1 vs FIGO2, p = 0.0029; FIGO1 vs FIGO3 (p = 0.012). Statistically significant difference was found according to the H-score between patients with and without metastatic lymph nodes (p = 0.033). To the best of our knowledge this is the first study testing immunohistochemically the expression of ROMO1 for CC progression. The levels of ROMO1 were significantly higher in early stage tumors compared to advanced. Bearing in mind that only 75 patients were tested, further studies are required to evaluate the value of ROS in CC.

Osteoporosis, the most common bone disorder, profoundly impacts women’s health, especially during postmenopausal phases. Characterised by diminished bone mineral density (BMD), it increases the risk of fractures, affecting mobility, quality of life, and potentially mortality. The present review analyses the intricate interactions among physiological alterations, diseases, and medications that lead to bone mineral density reduction in women. It underscores the importance of gynaecologists in the prevention, diagnosis, and management of osteoporosis via early risk assessment, suitable hormone treatment, and lifestyle modifications. Essential considerations encompass the categorisation of osteoporosis into primary (age-related) and secondary (attributable to diseases or pharmacological treatments) types, with particular emphasis on predisposing conditions such as premature menopause, hormone deficits, and cancer therapies. The significance of diagnostic instruments such as DXA and novel methodologies like trabecular bone score and quantitative ultrasonography is emphasised for precise evaluation and surveillance. The review also addresses nutritional methods, physical exercise, and pharmaceutical interventions, including hormone replacement therapy (HRT), selective oestrogen receptor modulators (SERMs), and other anti-resorptive drugs, to preserve bone health. This review highlights the important role of gynaecologists in maintaining women’s bone health, promoting a proactive strategy to avert osteoporosis-related complications and enhance long-term results.

Reactive oxygen species modulator 1 (ROMO1) is a nuclear-encoded inner mitochondrial protein known for its dual role as a modulator of reactive oxygen species (ROS) and a non-selective ion channel. Initially identified for its role in ROS production, ROMO1 has garnered attention for its functional properties as a non-selective ion channel that regulates ion homeostasis in mitochondria. This article examines ROMO1 from both perspectives, emphasizing its structural and functional characteristics, physiological roles, and implications in health and disease. Understanding ROMO1’s dual functionality provides insight into its potential as a therapeutic target for oxidative stress-related disorders, especially cancer progression.

Background: The individual and social burden of endometriosis is high, and the diagnosis is usually delayed by 7–10 years. Menstrual effluent (ME) represents an accessible and uniquely informative biofluid. This systematic review evaluated the pathophysiological relevance and diagnostic potential of ME in endometriosis. Methods: Following PRISMA 2020 guidelines, we systematically searched PubMed/MEDLINE, EBSCOhost (Academic Search Premier, APA PsycArticles, APA PsycInfo, CINAHL, and MEDLINE), Semantic Scholar, and Google Scholar from inception to 30 November 2025. Original studies analyzing human ME or ME-derived cells in women with endometriosis versus controls were eligible. We extracted study design, analytic methods, diagnostic accuracy metrics (AUC, sensitivity, and specificity), mechanistic pathways, and risk of bias (QUADAS-2 for diagnostic, and NIH tools for mechanistic studies). Results: Thirty-five studies were included. ME consistently captured key pathophysiological mechanisms of endometriosis, including impaired decidualization and progesterone resistance, immune dysregulation with diminished cytotoxic clearance, pro-angiogenic and invasive phenotypes, heightened stem/progenitor cell survival, cellular senescence and DNA damage, and altered extracellular-vesicle signaling. Diagnostic accuracy was reported in nine studies. Aromatase mRNA showed the highest performance (AUC 0.977), followed by TGF-β1 (AUC 0.973) and IGFBP1 (AUC 0.92). A lipidomic two-marker model achieved an AUC of 0.87. All diagnostic assessments were based on case–control studies; none conducted prospective validation. Conclusions: ME is a biologically relevant, non-invasive, and patient-acceptable biospecimen reflecting core endometriosis mechanisms and yielding promising diagnostic accuracy. The highest diagnostic performance was achieved for assays reflecting steroidogenic and growth-factor pathways (e.g., aromatase and TGF-β1). Standardization and prospective validation are needed before clinical adoption.