Search Results (2,206)

Background/Objectives: This study evaluated the diagnostic accuracy of cervical cytology, CINtec^® (p16/Ki-67 dual staining), and PD-L1 immunohistochemistry, individually and in combination with high-risk HPV (HR-HPV) testing, for identifying histologically confirmed cervical lesions ranging from CIN1 to invasive carcinoma. Methods: We conducted a prospective cross-sectional study including 114 patients who underwent cervical cytology, CINtec^®, PD-L1 staining, HPV genotyping, and histopathologic confirmation at a tertiary clinical center between September 2024 and September 2025. Sensitivity, specificity, PPV, NPV, and ROC performance were calculated for each test across lesion categories. Multivariable logistic regression models incorporating HR-HPV status were used to assess added predictive value. Results: All tests showed poor performance for CIN1 (cytology AUC 0.488; CINtec^® 0.374; PD-L1 0.366). Diagnostic accuracy improved markedly with lesion severity. For CIN3, CINtec^® demonstrated the highest discriminative ability (AUC 0.826), with cytology and PD-L1 also performing well (AUC 0.820 and 0.753). Cytology achieved the strongest ROC performance for CIN2+ (AUC 0.937), CIN3+ (0.913), and invasive carcinoma (0.887). PD-L1 consistently showed lower accuracy across categories. Cytology + HR-HPV demonstrated the highest AUC across all lesion categories. Conclusions: Cytology and CINtec^® exhibited strong diagnostic accuracy for high-grade lesions, while PD-L1 showed limited utility as an independent screening marker. Combining cytology with HR-HPV testing enhanced predictive performance across all lesion categories. These findings support the continued use of cytology-based triage and highlight CINtec^® as a valuable adjunct for high-grade disease detection. Because this study used a high-prevalence referral cohort, specificity may be overestimated and not representative of population-based screening. Full article

Background: Experimental autoimmune thyroiditis is an important animal model for studying Hashimoto’s thyroiditis. Our aim was to develop the model using CBA/J-DR3 mice expressing human HLA-DR3, which is associated with autoimmune thyroiditis in humans, to better simulate human autoimmune thyroiditis. Such a humanized model can be used to test specific antigen therapies for autoimmune thyroiditis. Methods: CBA/J-DR3 mice were produced by back-crossing B6-DR3 mice to the CBA/J background. Female CBA/J-DR3 mice were immunized with human thyroglobulin (Tg) in complete Freund’s adjuvant on days 0 and 7. On day 21, mice were sacrificed, blood collected, spleen and thyroid harvested for analysis. Splenocytes were analyzed for T cell responses to Tg and its major T-cell epitope in human autoimmune thyroiditis, Tg.2098. Serum anti-thyroglobulin antibodies were measured by ELISA, and thyroid-stimulating hormone was measured using the Luminex assay. Thyroid histology and immunohistochemistry were examined. Results: Immunized CBA/J-DR3 mice showed significant T cell proliferation in response to Tg (stimulation index 3.4 ± 4.5) and Tg.2098 (1.5 ± 0.7). Anti-thyroglobulin antibody levels were elevated in immunized mice when compared to control mice (2.05 ± 0.75 vs. 0.15 ± 0.06, p < 0.0001). T cells demonstrated higher reactivity to thyroid antigens by enhanced production of pro-inflammatory cytokines. Thyroid immunohistochemistry revealed mild CD3-positive T-cell infiltration. Conclusions: This novel humanized CBA/J-DR3 mouse model of Hashimoto’s thyroiditis demonstrates key features of human autoimmune thyroiditis. The HLA-DR3 background and the immune response to Tg and Tg.2098 enhance translational relevance, making this a valuable model for studying thyroid disease pathogenesis and testing targeted immune-modifying therapies. Full article

Background: GMK is a bioactive material newly identified from a water extract of mixed mushroom mycelia (Phellinus linteus, Inonotus obliquus, and Ganoderma lucidum). It has shown protective effects against glutamate-induced excitotoxicity and lipopolysaccharide-triggered neuroinflammation. However, whether GMK can ameliorate global cerebral ischemia–reperfusion injury (GCIRI) and its associated cognitive deficit remains to be elucidated. Methods: GCIRI was induced in male Sprague–Dawley rats by bilateral common carotid artery occlusion with hypovolemia (BCCAO/H). GMK (30 or 90 mg/kg, p.o.) was administered once daily for 14 days before surgery. Cognitive functions were evaluated using the Y-maze, Barnes maze, and passive avoidance tests. Hippocampal CA1 neuronal survival and glial activation were analyzed by cresyl violet staining and Iba1/GFAP immunohistochemistry. In parallel, PC12 cells were pretreated with GMK (100 or 200 μg/mL, 24 h) before oxygen–glucose deprivation and reoxygenation (OGD/R), and apoptosis (TUNEL, Bax/Bcl-2), oxidative stress markers (ROS, MDA, and NO), antioxidant enzymes including glutathione peroxidase (GPX) and catalase (CAT), and signaling proteins (p-ERK/ERK, iNOS) were examined. Results: GMK significantly ameliorated GCIRI-induced learning and memory impairments, protected CA1 pyramidal neurons, and reduced microglial and astrocytic activation. In OGD/R-challenged PC12 cells, GMK attenuated apoptosis, suppressed ROS, MDA, and NO production, normalized GPX and CAT activities, and favorably regulated p-ERK and iNOS pathways. Conclusions: These findings suggest that GMK confers dose-dependent behavioral and histopathological protection against GCIRI, potentially by modulating redox- and apoptosis-related signaling (Bax/Bcl-2, GPX/CAT, and ERK/iNOS pathways), with more consistent effects at a higher dose. Full article

Background: Atherosclerosis forms the background of several cardiovascular pathologies. LDL receptor knockout (LDLR-KO) mice kept on a high-fat diet (HFD) develop high cholesterol levels. Previously we found that vasodilation responses in HFD LDLR-KO mice were improved in the absence of type 1 cannabinoid receptors (CB₁Rs). We aimed to reveal the effects of HFD and CB₁Rs on vascular contractile and structural properties. Methods: Experiments were performed on LDLR-CB₁R double knockout and wild type (WT) mice, kept on an HFD or control diet (CD) for 5 months. Thoracic aortas were isolated for Oil Red plaque staining and abdominal aorta segments for myography to obtain phenylephrine (Phe)-induced (100 nM–10 µM) contractile responses. Aorta samples were subjected to histology stainings with hematoxylin–eosin and resorcin–fuchsin (elastin density) and for smooth muscle actin (SMA) immunohistochemistry. Results: Phe-induced contractions significantly increased in HFD groups (p < 0.05) similarly in all genotypes. However, contractions were stronger with CD in CB₁R-KO compared to WT. Plaque areas were increased in LDLR-KO mice compared to WT, significant in HFD groups (p < 0.05). SMA increased to HFD, while elastin density remained similar, with the highest value in double KO-HFD. Intima/media ratio significantly decreased in double KO-HFD vs. CD. Conclusions: Our results indicate that HFD-treated LDLR-KO mice develop atherosclerosis with functional contractile and structural alterations modulated by CB₁Rs: absence of CB₁Rs elicited higher contraction properties with some modification in vascular remodeling indicating contribution of the CB₁R to cellular signalization controlling wall thickness and elasticity in pathological conditions. Full article

Background: Autophagy, a self-destructive cellular mechanism with a paradoxical nature, plays a part in both tumor suppression and induction by providing cancer cells with metabolic substrates, resulting in cell proliferation and survival. In this study, we aim to investigate the clinical significance of four autophagy pathway components (BECLIN, p62/, LC3b, ATG3) in pathogenetic mechanisms of thymic epithelial tumors (TETs) with possible prognostic importance. Methods: Immunohistochemistry was used to evaluate the cytoplasmic expression of BECLIN, p62, LC3b, and ATG3 in tumor cells of 99 TETs, and possible correlations with clinicopathological parameters were examined. Results: Higher BECLIN and p62 expression was associated with male gender (p = 0.027 and p = 0.014, respectively). B3 thymomas and thymic carcinomas (TCs) displayed higher p62 expression (p = 0.019), while LC3b expression was marginally higher in non-B3/TC TETs (p = 0.098). A positive correlation between higher BECLIN expression and advanced Masaoka–Koga stage was also observed (p = 0.009). ATG3 was not associated with any of the investigated clinicopathological parameters (p > 0.05). There was also no significant correlation between any of the four examined molecules and overall survival or relapse. Conclusions: Our findings indicate autophagy activation in B3/TC and advanced Masaoka–Koga stage cases. Further studies are needed to explore the role of these autophagy related proteins as potential biomarkers and therapeutic targets in TETs. Full article

Laryngopharyngeal reflux disease (LPRD) results from the retrograde flow of gastric contents into the upper aerodigestive tract, causing epithelial injury. Progress in its management has been limited by the lack of objective biomarkers and reproducible in vivo models. This study aimed to establish a chronic, non-surgical mouse model of LPRD and to investigate the protective effect of N-acetylcysteine (NAC). Female C57BL/6 mice were randomly assigned to three groups: control (standard drinking water), study (acidified water, pH 3.0, for 12 weeks), and treatment (acidified water for 12 weeks plus NAC supplementation during the final 4 weeks). Body weight, food intake, and water consumption were monitored weekly. Pharyngeal tissues were analyzed by immunohistochemistry and Western blotting. Chronic acid exposure resulted in loss of membrane-localized E-cadherin, cytoplasmic redistribution, and upregulation of matrix metalloproteinase-7 (MMP-7). These molecular alterations were accompanied by enhanced phosphorylation of ERK and c-Jun, consistent with activation of the ROS–ERK–c-Jun signaling pathway. NAC supplementation was associated with partial restoration of E-cadherin, reduced MMP-7 expression, and attenuation of ERK/c-Jun phosphorylation. No systemic toxicity or weight loss was observed, indicating good tolerability of the model. This non-surgical ingestion-based model faithfully recapitulates key epithelial features of LPRD and provides a feasible platform for mechanistic investigation and exploratory therapeutic studies. NAC may exert protective effects against acid-induced epithelial injury in this model. Full article

Doxorubicin (DOX), a widely used chemotherapeutic, is constrained by its nephrotoxicity, characterized by endothelial injury, inflammation, and oxidative stress. Vascular endothelial growth factor (VEGF) signaling in the kidney serves a dual function. Under normal conditions, it supports the survival of glomerular endothelial cells and maintains vascular stability, but when excessively activated, it disrupts angiogenesis and contributes to kidney injury. In this context, we hypothesize that Nanocurcumin (CUR-NP), a nano-formulated curcumin derivative with enhanced bioavailability, can modulate the VEGF pathway and restore regular renal activity. Thus, this study aims to explore the potential protective effect of CUR-NP on DOX-induced renal injury in male rats. Thirty-two Wistar albino rats were used and distributed into four groups. CUR-NP (80 mg/kg dissolved in 1% CMC) was administered by oral gavage for two weeks. A single dose of DOX (15 mg/kg) (i.p.) was injected on day seven of the study. Results showed that DOX increased the circulating creatinine, urea, and urea-nitrogen levels, while pretreatment with CUR-NP markedly alleviated kidney function. In addition, CUR-NP treatment significantly normalized oxidative stress markers in renal tissues, such as NO, GSH, and SOD, and improved renal pro-inflammatory mediators, TNF-α, IL-6, and NF-κB-p65. DOX caused degeneration of glomeruli and tubules with degenerated epithelial lining and casts in their lumens. Conversely, CUR-NP maintained standard tubular and glomerular structure. Immunohistochemistry showed that DOX strongly upregulated VEGF and AhR, while CUR-NP markedly reduced their expression, countering VEGF/AhR pathway disruption and helping restore physiological signaling. Full article

Background: Vitamin D deficiency has been implicated in breast cancer pathogenesis and prognosis. However, the relationship between serum 25-hydroxyvitamin D [25(OH)D] levels and molecular breast cancer subtypes remains incompletely understood. Methods: This cross-sectional study included 168 women (89 breast cancer patients, 79 healthy controls) from Poland. Serum 25(OH)D was measured by electrochemiluminescence immunoassay. Blood samples were collected year-round, with 54% obtained during winter/spring months (October–March). Molecular subtypes (luminal A, luminal B, HER2-enriched, triple-negative) were classified by immunohistochemistry. Results: Mean 25(OH)D was 30 ± 13 ng/mL, with 55% showing insufficiency (<30 ng/mL). No significant differences were observed between patients and controls (p = 0.93). A borderline non-significant trend was observed across molecular subtypes (p = 0.055). HER2-enriched tumors showed descriptively higher concentrations (37.6 ng/mL, 95% CI: 29.5–45.8) compared to luminal A (31.0 ng/mL), luminal B (26.4 ng/mL), and triple-negative (25.9 ng/mL). A significant subtype × season interaction was detected (p = 0.015), though interpretation is limited by the absence of a main seasonal effect (p = 0.64). Age (OR = 1.06, p = 0.023) and BMI (OR = 1.06, p = 0.090) predicted vitamin D deficiency. Conclusions: Vitamin D insufficiency is prevalent in breast cancer patients and healthy women. In this exploratory analysis with limited statistical power, no definitive associations between 25(OH)D and molecular subtype were established. The descriptive trend suggesting higher vitamin D in HER2-enriched tumors requires validation. Limitations: Small sample sizes (n = 11–35 per subtype) and post-surgical blood collection limit interpretation; findings require validation in larger cohorts. Full article

Fascia has traditionally been described as a passive connective tissue mainly composed of collagen types I and III. Recent research, however, has revealed its structural and functional complexity, suggesting the possible presence of additional collagen types. This study aimed to quantify the presence and distribution of collagen types I, III, VI, and XII in human superficial and deep fasciae to improve understanding of fascial extracellular matrix composition. Superficial and deep fascia samples were collected from 19 adult patients (ages 20–83 years; thigh and lumbar area). Histology, Azan Mallory staining, hydroxyproline quantification, Western blotting, and immunohistochemistry were performed. The results indicated that deep fascia contained significantly more total collagen than superficial fascia (0.55 ± 0.17 µg/mg vs. 0.36 ± 0.14 µg/mg, p < 0.01). Collagen type VI was the most abundant and widely distributed subtype in both superficial and deep fasciae (mean ratio equal to 0.24 ± 0.13 and 0.27 ± 0.10, respectively), nearly double that of collagen types I (0.12 ± 0.07 and 0.11 ± 0.08), III (0.13 ± 0.09 and 0.17 ± 0.11), and XII (0.13 ± 0.11 and 0.13 ± 0.04). Moreover, statistically significant anatomical differences were observed, despite considerable interindividual variability. Fasciae from the thigh showed higher levels of collagen types I and III (mean ratio of 0.17 and 0.27, respectively, in deep fascia; 0.14 for both types in superficial fascia), whereas fasciae of the lumbar region exhibited greater levels of collagen types VI and XII (ratio equal to 0.33 and 0.15, respectively, in deep fascia; 0.36 and 0.20 in superficial fascia). Overall, these findings highlighted the structural complexity and regional specialization of human fasciae, with potential functional implications for mechanotransduction and tissue adaptation. Full article

Background: Pulmonary fibrosis (PF) currently lacks effective therapeutic interventions. Roxadustat, an oral small-molecule inhibitor of hypoxia-inducible factor prolyl hydroxylase, has been shown in several studies to attenuate the progression of fibrotic diseases. However, its therapeutic efficacy in PF remains to be fully elucidated. The aim of this study was to evaluate roxadustat’s therapeutic benefits on PF as well as the underlying mechanisms of action. Methods: Bleomycin was administered intraperitoneally to establish a PF mouse model. H&E staining, Masson staining, and immunohistochemistry (IHC) were used to assess histopathological and fibrotic changes. Changes in the expression levels of inflammatory mediators, including IL-1β, TGF-β1, and TNF-α, were examined by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Network pharmacology combined with transcriptomic analysis was employed to identify potential target genes and associated signaling pathways. Subsequently, RT-qPCR and Western blot analyses were carried out to experimentally validate the predicted targets and pathways and to verify the protective effects of roxadustat in PF mice. Results: Roxadustat markedly ameliorated bleomycin-induced pulmonary fibrosis in mice. The therapeutic effect was evidenced by a reduction in alveolar damage, thinner alveolar septa, diminished infiltration of inflammatory cells, and decreased collagen deposition. Concomitantly, the expression levels of inflammatory mediators, including IL-1β, TGF-β1, and TNF-α, were significantly lowered. Integrated network pharmacology and transcriptomic analyses revealed the involvement of critical signaling pathways, specifically nuclear factor-kappa B (NF-κB) and peroxisome proliferator-activated receptor (PPAR). Experimental validation further demonstrated that roxadustat downregulated the expression of key genes (S100A8, S100A9, and Fos) in murine lung tissues. It also suppressed the protein ratios of phosphorylated p65 to total p65 and phosphorylated IκBα to total IκBα. Moreover, roxadustat treatment upregulated PPARγ protein expression. Conclusions: These data indicate that roxadustat ameliorates bleomycin-induced PF in mice, an effect associated with modulation of the NF-κB and PPAR signaling pathways. The findings provide a preclinical rationale for further investigation of roxadustat as a potential treatment for PF. Full article

Endometriosis (EM) is a chronic inflammatory disease characterized by the growth of endometrial-like tissue outside the uterus, yet its molecular mechanisms remain poorly understood. This study investigated the expression of mucins (MUC1, MUC2, MUC5AC, MUC6, MUC16) and their O-glycans in endometriotic lesions, given their roles in epithelial protection, adhesion, and immune modulation. Using immunohistochemistry, Western blotting, lectin profiling, histochemical staining, and transcriptomic analysis, we compared mucin levels and glycosylation patterns in eutopic and ectopic tissues from women with and without endometriosis and measured mucin-derived tumor markers in serum (CA 125/MUC16 and CA 15-3/MUC1) and peritoneal fluid (CA 125/MUC16). The results showed significant upregulation of all mucins in EM biopsies, with increased MUC1 transcript levels, while MUC6 and MUC16 protein levels did not always align with transcripts. Yet, tumor markers CA 125 and CA 15-3 showed no significant differences between groups. Looking at mucin distribution in biopsies of peritoneal (pEM), deep infiltrating and ovarian EM, MUC1 was significantly overexpressed in lesions of all EM forms, while MUC5AC was significantly elevated in pEM. Lectin analysis revealed specific glycan changes, including elevated core-1 O-glycans and α(1-2)-linked fucosylation, while sialylation remained unchanged. These findings demonstrate consistent mucin dysregulation and glycan alterations, implicating their roles in epithelial adhesion, immune evasion, and lesion persistence. Mucin biology thus emerges as a promising target for diagnostic and therapeutic strategies in endometriosis. Full article

Background: The prognostic value of phosphatidylinositol-3-kinase p110α, a key catalytic subunit in the PI3K/AKT pathway, in breast cancer remains controversial. This study evaluated its prognostic significance in stage I–III invasive breast cancer. Methods: p110α protein expression was detected via immunohistochemistry (IHC) in 161 patient tissue samples. Its association with overall survival (OS) and relapse-free survival (RFS) was analyzed using Kaplan–Meier and Cox proportional hazards models. Results: p110α positivity was detected in 59.0% of specimens and showed significant correlation with histological grade (p = 0.034). Survival analysis revealed that p110α positivity was associated with worse OS (log-rank p = 0.008) and RFS (log-rank p = 0.018). In multivariate analysis, p110α expression was an independent predictor of poor prognosis for both OS (HR = 2.45, 95%CI: 1.25–4.78) and RFS (HR = 2.12, 95%CI: 1.14–3.94). This association with poor prognosis was particularly pronounced in stage I–II, hormone receptor (HR)-positive, and human epidermal growth factor receptor 2 (HER2)-negative subgroups. Supporting evidence from the PROGgeneV2 database showed that high PIK3CA mRNA levels predicted inferior survival in external cohorts. Conclusions: p110α protein expression is an independent biomarker for adverse outcomes in stage I–III invasive breast cancer. Its assessment could improve prognostic evaluation and guide personalized therapy. Full article

Melanocytic Tumors of Uncertain Malignant Potential (MELTUMPs) remain among the most challenging entities in dermatopathology due to overlapping morphologic features and marked inter-observer variability. This comprehensive review critically assesses the diagnostic and potential prognostic significance of combining p16 and methylthioadenosine phosphorylase (MTAP) immunohistochemistry (IHC) as a practical surrogate for genomic alterations involving the 9p21 (CDKN2A/MTAP) locus. We analyzed the molecular underpinnings of the CDKN2A/MTAP axis and systematically reviewed existing literature to define an integrated IHC strategy for ambiguous melanocytic lesions. The combined use of p16, a sensitive marker of CDKN2A inactivation, and MTAP, a highly specific marker for homozygous 9p21 deletion, was assessed for its diagnostic complementarity and potential clinical utility. p16 IHC demonstrates high sensitivity but limited specificity due to heterogeneous staining in borderline lesions. In contrast, MTAP loss exhibits near-absolute specificity for CDKN2A/MTAP co-deletion, albeit with lower sensitivity. Concordant loss of both markers strongly supports melanoma or high-risk melanocytoma, while MTAP retention may predict responsiveness to adjuvant interferon therapy. Combined p16/MTAP IHC provides a synergistic, biologically grounded approach that refines diagnostic accuracy in MELTUMPs. This dual-marker algorithm promotes a shift from purely morphology-based evaluation toward a reproducible, molecularly informed classification, improving both diagnostic confidence and patient management. Full article

Serum lactate dehydrogenase (LDH) is a recognized prognostic biomarker in human lymphomas, yet its clinical significance in canine lymphoma remains insufficiently characterized. This study aimed to quantify serum LDH levels in healthy dogs and dogs with high-grade multicentric lymphoma (ML) (predominantly B-cell) and to investigate correlations between LDH levels and established clinical and laboratory prognostic indicators. Twenty-seven dogs were prospectively enrolled: healthy controls (G1, n = 7) and dogs with high-grade ML (G2, n = 20). Immunophenotyping was performed by immunohistochemistry (CD3/CD79a). LDH concentrations were measured at diagnosis (T0) and after six weeks of CHOP-based induction chemotherapy (T1). Statistical analyses included Kruskal–Wallis, Wilcoxon signed-rank, Pearson’s correlation, and mixed-effects models. Dogs with high-grade ML exhibited significantly elevated LDH levels compared to controls (median 545.5 U/L, range: 288.2–2816 U/L vs. 143 U/L, range: 66–272; p < 0.001). Dogs with thrombocytopenia had higher baseline LDH (median 746 U/L, range: 612–921; p = 0.006) and greater reductions following chemotherapy (median −1011.7 U/L, range: −159 to −2064; p = 0.004). LDH levels declined significantly after treatment (overall median reduction 50.7%; post-chemotherapy range: 60.4–752 U/L; n = 15; p = 0.013), with normalization achieved in 77.8% of dogs with complete response versus 16.7% with partial or progressive disease (p = 0.02). We confirmed that serum LDH is significantly elevated in dogs with high-grade ML and declines following effective chemotherapy, supporting its utility as a dynamic biomarker of tumor burden and treatment response. Thrombocytopenic dogs may represent a biologically distinct subset warranting further investigation. Full article

Background/Objectives: Early and accurate characterization of endometrial cancer (EC) is crucial for patient management, but current imaging modalities lack in diagnostic accuracy and ability to assess molecular profiles. The aim of this study is to evaluate hybrid [¹⁸F]FDG PET/MRI’s diagnostic accuracy in EC staging and role in predicting tumor aggressiveness, molecular characterization, and recurrence. Methods: A prospective study (ClinicalTrials.gov, ID:NCT04212910) evaluating EC patients undergoing [¹⁸F]FDG PET/MRI before surgery (2018–2024). Histology, immunohistochemistry, and patients’ follow-up (mean FU time: 3.13y) were used as the reference standard. [¹⁸F]FDG PET/MRI, PET only, and MRI only were independently reviewed to assess the diagnostic accuracy (ACC), sensitivity (SN), specificity (SP), and positive/negative predictive value (PPV, NPV). Imaging parameters were extracted from [¹⁸F]FDG PET and pcT1w, T2w, DWI, and DCE MRI. Spearman’s correlations, Fisher’s exact test, ROC-AUC analysis, Kaplan–Meier survival curves, log-rank tests and Cox proportional hazards models were applied. Results: Eighty participants with primary EC (median age 63 ± 12 years) were enrolled, with 17% showing LN involvement. [¹⁸F]FDG PET/MRI provided ACC = 98.75%, SN = 98.75%, and PPV = 100% for primary tumor detection, and ACC = 92.41%, SN = 84.62%, SP = 93.94%, PPV = 73.33%, and NPV = 96.88% for LN detection. PET/MRI parameters predicted LN involvement (AUC = 79.49%), deep myometrial invasion (79.78%), lymphovascular space invasion (82.00%), p53abn (71.47%), MMRd (74.51%), relapse (82.00%), and postoperative administration of adjuvant therapy (79.64%). Patients with a tumor cranio-caudal diameter ≥ 43 mm and MTV ≥ 13.5 cm³ showed increased probabilities of recurrence (p < 0.001). Conclusions: [¹⁸F]FDG PET/MR showed exceptional accuracy in EC primary tumor and LN detection. Derived parameters demonstrated potential ability in defining features of aggressiveness, molecular alterations, and tumor recurrence. Full article