Lymphatic malformations (LMs) in children are characterized by a prolonged and fluctuating clinical course with a risk of continued growth or recurrent enlargement after treatment. Identification of independent predictors and development of a clinically applicable risk score may improve treatment planning and long-term follow-up strategies.

Purpose of the study. To identify independent clinical and anatomical predictors of continued growth or recurrent enlargement of lymphatic malformations in children after initiation of surgical treatment using multivariable analysis.

Patients and methods. A retrospective single-center cohort study was conducted between 2012 and 2022. A total of 115 patients aged 17 years or younger were included who underwent surgical treatment (including extensive resection procedures), sclerotherapy, or combined treatment. The primary endpoint was the first episode of continued growth or recurrent enlargement of LM, defined predominantly by contrast-enhanced magnetic resonance imaging findings. Receiver operating characteristic analysis was used to determine the optimal lesion volume threshold. Multivariable logistic regression with bootstrap validation and time-to-event analysis using Kaplan–Meier and Cox methods were performed.

Results. The median follow-up after the index intervention was 11.0 (3.2–27.0) months. The event occurred in 22 of 115 patients (19.1 %). At the last follow-up visit, a ≥50 % reduction in lesion volume or complete response was observed in 95 of 115 patients (82.6 %), a <50 % reduction in 15 of 115 patients (13.0 %), and ongoing growth in 5 of 115 patients (4.3 %). Independent risk factors included prenatal or neonatal onset (OR 4.08; 95 % CI 1.10–15.05; p = 0.035), preoperative lesion volume ≥ 90 cm³ (OR 4.06; 95 % CI 1.09–15.15; p = 0.037), and previous surgery outside a referral center (OR 5.93; 95 % CI 1.73–20.36; p = 0.005). Aggressive anatomical spread demonstrated a trend toward increased risk (OR 2.82; p = 0.092). Model discrimination was high (AUC 0.812; 95 % CI 0.708–0.916) and remained stable after internal validation (AUC_0.632+ = 0.812). The additive score stratified the risk of the event as 6.0 % (95 % CI 1.9–17.4) for patients with ≤1 point, 10.3 % (95 % CI 3.2–28.7) for those with 2 points, and 44.4 % (95 % CI 28.8–61.2) for those with ≥ 3 points. Median event-free survival was 65.2 months. No significant differences were observed between treatment approaches (log-rank p = 0.699).

Conclusion. In this cohort, the risk of continued growth in pediatric lymphatic malformations was primarily associated with early disease onset, baseline lesion volume, and previous surgery outside a referral center, whereas extensive anatomical involvement demonstrated a trend toward increased risk. The proposed risk stratification score may support individualized follow-up and treatment planning; however, external validation is required.

Purpose of the study. To assess the dynamics of the Peritoneal Adhesion Index (PAI) and the number of involved anatomical regions of the abdominal cavity in patients with ovarian cancer and peritoneal carcinomatosis during consecutive sessions of pressurized intraperitoneal aerosol chemotherapy (PIPAC).

Patients and methods. A single-center observational study with intraoperative assessment of adhesive status was performed in 87 patients. PAI and the number of involved abdominal regions were determined during three PIPAC sessions and at delayed diagnostic laparoscopy. Available completed paired observations were used for interval comparisons. The primary endpoint was the change in total PAI; secondary endpoints were changes in the number of involved regions and the overall direction of changes by the time of delayed laparoscopy. The statistical significance of paired changes was assessed using the sign test.

Results. Between the 1st and 2nd PIPAC sessions, a decrease in PAI was recorded in 57 patients (65.5 %), no change in 24 (27.6 %), and an increase in 6 (6.9 %); the mean change was – 2.7 points (p < 0.0001). Between the 2nd and 3rd PIPAC sessions, a decrease in PAI was observed in 35 patients (38.9 %), no change in 53 (58.9 %), and an increase in 2 (2.2 %); the mean change was 0.89 points (p < 0.0001). Between the 3rd PIPAC session and delayed laparoscopy, a decrease in PAI was observed in 14 patients (16.1 %), no change in 70 (80.5 %), and an increase in 3 (3.4 %); the mean change was 0.10 points (p = 0.006). Overall, a decrease in PAI from baseline to delayed laparoscopy was recorded in 56 patients (64.4 %), no change in 22 (25.3 %), and an increase in 9 (10.3 %); the mean cumulative change was 3.7 points (p < 0.0001). A similar pattern was observed for the number of involved regions: an overall decrease was recorded in 54 patients (62.1 %), no change in 24 (27.6 %), and an increase in 9 (10.3 %); the mean cumulative change was 1.32 points (p < 0.0001).

Conclusion. The sequential use of PIPAC was associated with a reduction in the severity and extent of abdominal adhesions, indicating a favorable safety profile of PIPAC and the technical feasibility of repeated laparoscopic procedures.

Mitochondria play a key role in cellular metabolism, steroid hormone synthesis, and the regulation of redox homeostasis. However, the role of mitochondrial steroidogenesis in the progression of endometrial adenocarcinoma (EA), particularly in the presence of type 2 diabetes mellitus (T2DM), remains poorly understood.

Purpose of the study. To determine the concentrations of steroid hormones and their receptors in the mitochondrial fraction of G1–G3 endometrial adenocarcinoma tissue compared with intact endometrium and to evaluate the modifying effect of type 2 diabetes mellitus on these parameters.

Patients and methods. Mitochondria were isolated by differential centrifugation from tumor tissue obtained from 92 patients with endometrial adenocarcinoma (G1–G3) and from morphologically normal endometrium (control group). Standard enzyme-linked immunosorbent assay (ELISA) kits were used to determine the concentrations of estradiol (E2), estriol (E3), estrone (E1) and their receptors (ERα, ERβ), testosterone (T) and the androgen receptor (AR), progesterone (P4) and the progesterone receptor (PR), as well as cortisol and cholesterol. Statistical analysis was performed using Statistica 10 software.

Results. In the mitochondria of G1–G2 endometrial adenocarcinomas, the estradiol level was approximately twofold higher than in the control group, whereas G3 tumors demonstrated an approximately twofold increase in estriol concentration. Testosterone and cortisol levels were elevated in the mitochondria of all tumors by 1.6-fold and more than twofold, respectively. Progesterone content was increased by 2.3–3.8-fold in the mitochondria of G1–G2 tumors but decreased by 4.3–5.9-fold in comparison with the control mitochondria. The levels of androgen and estrogen receptors were elevated in the mitochondria of all tumors, whereas the ERα/ERβ ratio decreased by 1.7–3.6-fold. Progesterone receptor levels were increased in G1–G2 mitochondria only in patients with T2DM, whereas in G3 tumors they were elevated regardless of T2DM status. Type 2 diabetes mellitus was associated with cholesterol accumulation in the mitochondria of all tumors.

Conclusion. Regardless of tumor differentiation grade and the presence of type 2 diabetes mellitus, endometrial adenocarcinoma mitochondria are characterized by increased levels of testosterone, cortisol, and sex hormone receptors, reflecting profound metabolic reprogramming of these organelles. Estradiol predominates in G1–G2 tumors, whereas estriol is the dominant estrogen in G3 tumors, which may contribute to increased tumor aggressiveness. Type 2 diabetes mellitus is associated with mitochondrial cholesterol accumulation, which may partly explain the more severe clinical course of endometrial adenocarcinoma in these patients.

Purpose of the study. Evaluation of the therapy optimization for patients with solid tumors using comprehensive genomic profiling (CGP).

Patients and methods. The article presents the results of a study involving patients from the Yamalo-Nenets Autonomous Okrug with malignant neoplasms of various localizations: breast cancer (n = 4), colorectal cancer (n = 3), gastric cancer (n = 1), cervical cancer (n = 1), ovarian cancer (n = 1), and prostate cancer (n = 1). Molecular genetic testing was performed using the Sentis™ Cancer+Discovery Panel (BGI). Biological material included FFPE tumor tissue sections containing >20 % tumor cells. Next-generation sequencing (NGS) parameters were as follows: sequencing depth > 900× for tumor samples and >300× for matched control samples (venous blood); insertion size ~140–210 bp; Q30 > 80 %; target coverage > 90 %. The analysis included 689 genes, microsatellite instability (MSI), tumor mutational burden (TMB), and germline pathogenic variants.

Results. Clinically significant somatic biomarkers were identified in 8 of 11 cases (72.7 %), enabling optimization of treatment strategies toward the most effective therapeutic approaches. In 5 of these 8 cases (62.5 %), treatment plan modification included the potential use of off-label therapy following approval by a multidisciplinary tumor board. Germline (inherited) variants were detected in 4 of 11 cases (36.4 %), indicating the need for genetic counseling and evaluation of relatives.

Conclusion. The implementation of CGP in clinical practice expands the possibilities for a personalized approach to the treatment of patients with metastatic and progressive malignant neoplasms through the identification of additional potential biomarkers of sensitivity or resistance to targeted anticancer agents and immunotherapy. Further evaluation of CGP effectiveness in a larger patient cohort appears warranted.

Purpose of the study. To study changes in the copy number of genes whose products are involved in maintaining the structure and function of mitochondria in tissues of benign neoplasms and endometrioid adenocarcinoma (EA) of the uterine body of varying degrees of differentiation.

Materials and methods. The study utilized tumor tissue and normal uterine tissue from 42 patients with endometrioid adenocarcinoma (EA) and 15 patients with uterine fibroids. The tumor burden in the EA patients was between stages Ia and Ib, and neoadjuvant treatment was not administered. DNA was isolated from tumor and normal uterine tissue fragments using phenol-chloroform extraction, and relative gene copy numbers were determined using real-time PCR (real-time qPCR). Statistical analysis was performed using the Mann-Whitney U-test with a Bonferroni correction.

Results. In patients with EA G1, a decrease in the copy number of nuclear and mitochondrial genes was observed (MT-CO1 = 0.5, mtTFB = 0.4, mtSSB = 0.6, MT-RNR2 = 0.3, NRF1 = 0.4) (p < 0.005) and an increase in the copy number of MGME1 (2.4) (p < 0.005). In patients with EA G2, a picture similar to G1 is observed: a decrease in the copy number of the genes MT-CO1; mtTFB, MT-RNR2 and NRF1 (p < 0.005), except for mtSSB. An increase in the copy number of MGME1 (3.1) and POLRMT (1.8) (p < 0.005) was also recorded. In patients with EA G3, the most pronounced decrease in the copy number of mtSSB and MT-RNR2 by 5.0 times relative to normal tissue was found, as well as a decrease in the copy number of MGME1 by 3.3 times, which is the opposite of the results in G1/G2.

Conclusion. Significant differences in the copy number of genes involved in mitochondrial function were identified between benign uterine tissues and endometrioid adenocarcinoma. The most prominent alterations included reduced copy numbers of key mitochondrial genes (MT-CO1 and MT-RNR2), the nuclear gene mtSSB, and aberrant MGME1 copy number changes in tumor tissues. These findings provide new insights into the molecular mechanisms underlying endometrioid adenocarcinoma development and may contribute to the identification of potential diagnostic and prognostic biomarkers.

In clinical practice, one of the key methods for monitoring the effectiveness of soft tissue wound treatment is the assessment of wound surface area. Neural network technologies represent a promising approach for calculating wound surface area, identifying signs of wound healing progression, and planning personalized treatment according to clinical dynamics.

Purpose of the study. To analyze the results of wound surface area measurements obtained using the WoundVision software.

Materials and methods. The study was conducted in three stages: bench testing using schematic wounds and wound models, experimental testing in laboratory animals, and clinical evaluation in patients with trophic ulcers. The accuracy of wound surface area assessment was compared using the L. N. Popova method, ImageJ, UniversalDesktopRuler, and WoundVision computer software, as well as the ImitoWound mobile application.

Results. The accuracy of wound area calculation was found to depend on contour shape and surface curvature. ImageJ and UniversalDesktopRuler systematically underestimated measurements, with an average accuracy of 80–88 %. The ImitoWound application demonstrated stable results with an average accuracy of 92 %, although its performance decreased on curved surfaces. Due to the implementation of neural network technologies and 3D scanning, the WoundVision software demonstrated the best results across all study groups. When using WoundVision, the mean accuracy of wound area measurements was 98.27 ± 0.65 % for schematic wounds, 99.19 ± 0.49 % for wound models, 98.52 ± 4.17 % for wounds in laboratory animals, and 98.52 ± 4.17 % for trophic ulcers in patients.

Conclusion. The developed WoundVision software demonstrated the highest accuracy among the evaluated methods. However, several limitations remain, including the need for a specialized camera. Nevertheless, the L. N. Popova method remains the most accurate currently available technique, although it is labor-intensive because of the time required for its implementation and its practical limitations.

The spectrum of bioactive metabolites identified in the fruits of Empetrum nigrum L. collected in the Kamchatka Territory is of particular interest for the prevention and correction of disorders associated with age-related diseases.

Purpose of the study. To investigate the effects of a liquid extract of black crowberry (Empetrum nigrum) fruits on metabolic and oxidative disturbances in rats with alloxan-induced diabetes.

Materials and methods. Following the identification of phenolic compounds and saponins in Empetrum nigrum fruits, the biological activities of these compounds were screened using the online Prediction of Activity Spectra for Substances (PASS) software. Experimental studies were conducted to evaluate the hypoglycemic, hepatoprotective, and antioxidant effects of the liquid extract of black crowberry fruits in rats with alloxan-induced diabetes. Assessments were performed using standard biochemical assays and conventional analytical methods on a Mindray BC-480 analyzer. The effects of the Empetrum nigrum liquid extract on antioxidant defense parameters following alloxan administration were evaluated spectrophotometrically by measuring malondialdehyde (MDA) levels and the total antiradical activity index. The comet assay was used to assess the genotoxic effects of alloxan and of the investigated extract.

Results. In the rat model of diabetes mellitus, administration of the liquid extract of Empetrum nigrum fruits resulted in a 23.9 % reduction in hyperglycemia (blood glucose level), a 38.7 % decrease in malondialdehyde concentration, and a 38.3 % increase in total antiradical activity compared with the control group (p < 0.05). The comet assay demonstrated the damaging effect of alloxan on liver cells: the number of necrotic and apoptotic cells in the control group was 1.6-fold higher than in the group receiving the black crowberry fruit extract (p < 0.05). Changes in absolute and relative liver weight, as well as biochemical parameters, further confirmed the beneficial effects of Empetrum nigrum L. fruit extract administration. The observed effects were compared with those of the reference compound rutin (a quercetin diglycoside).

Conclusion. The present study expands current knowledge regarding the hypoglycemic, hepatoprotective, and antioxidant properties of Empetrum nigrum, highlighting its potential relevance for pharmaceutical development and clinical applications.

Purpose of the study. Based on a synthesis of systematic review data using standard meta-analysis methodology, to evaluate the current state of radiomics model development, analyze sources of methodological heterogeneity, and present a standardized evidence-based algorithm to improve the quality and reproducibility of future studies.

Materials and methods. A systematic search was conducted in the PubMed/MEDLINE, Embase, Scopus, Web of Science, and Cochrane Library databases for studies published between January 2020 and December 2025. Keywords related to radiomics, magnetic resonance imaging (MRI), and prostate cancer (PCa) were used. According to the PICOS criteria, 27 studies involving 5,945 patients were included. Diagnostic performance was assessed using a random-effects meta-analysis, while methodological quality was evaluated independently by two reviewers using the Radiomics Quality Score (RQS) and METRICS instruments.

Results. Twenty-seven studies were included. The pooled diagnostic performance of radiomics models was high (AUC = 0.847); however, substantial heterogeneity was observed (I² = 70.32 %). The mean RQS score was 15.2 ± 3.4 (42.3 % of the maximum possible score), while the mean METRICS score was 67.5 ± 9.0 %. Systematic methodological weaknesses were identified, including retrospective study design (96.3 %), lack of external validation (77.8 %), absence of clinical utility assessment (70 %), and failure to report missing-data handling procedures (100 %). Meta-regression demonstrated that a high risk of bias was associated with inflated AUC estimates (p = 0.009).

Conclusion. The currently reported high performance of PCa radiomics models should be interpreted with caution because of methodological limitations. The proposed standardized algorithm, incorporating recommendations on prospective study design, validation, data processing, and model development, provides a practical methodological guidance for future research. Its implementation may be key to improving methodological rigor, reproducibility, and the clinical translational value of future studies in this field.

The diagnosis of adrenocortical tumors has undergone substantial changes in recent years owing to the introduction of reproducible morphological scoring systems combined with validated immunohistochemical and molecular markers. Updates to the WHO Classification of Endocrine and Neuroendocrine Tumours (2025), ICCR datasets, and contemporary clinical guidelines have strengthened requirements for morphological diagnostic standards, immunohistochemical profiling, and interpretation of pathological findings.

Purpose of the study. To systematize contemporary morphological, immunohistochemical, and molecular criteria for adrenocortical tumors and to provide a practical algorithm for their stepwise application in pathological diagnosis.

Materials and methods. An analytical review of publications from 2021 to 2025 on the pathology and molecular oncoendocrinology of adrenocortical tumors was performed, including the WHO-2025 classification, ICCR datasets, updates to European clinical guidelines, and multicenter studies.

Results. Classical morphological criteria, including assessment of mitotic activity, capsular and vascular invasion, and cytological atypia, remain fundamental for the diagnosis of adrenocortical tumors. The review systematizes the principal morphological tools, including the Weiss criteria and their modifications, the Helsinki score, and the reticulin algorithm. Diagnostic features of oncocytic (Lin–Weiss–Bisceglia), myxoid, and pediatric variants of adrenocortical tumors are discussed. Current evidence regarding the role of SF-1 as a highly specific marker of adrenocortical origin is summarized, together with the significance of a high Ki-67 index as one of the most important diagnostic and prognostic indicators of malignancy, taking into account established threshold values and strict counting methodology. Increased IGF2 expression is also highlighted as an additional marker of malignancy. Furthermore, the review provides a comprehensive overview of major molecular drivers, including TP53, CTNNB1/β-catenin, ZNRF3, and TERT-promoter alterations, as well as DNA methylation signatures and microRNA profiles (miR-483). The contribution of single-cell and spatial transcriptomics and emerging noninvasive biomarkers, including steroid metabolomics and liquid biopsy, is also discussed.

Conclusion. The transition toward integrated morphomolecular stratification improves diagnostic and prognostic accuracy in adrenocortical tumors, enhances the comparability of pathology reports, and facilitates patient selection for surveillance and treatment.

Breast cancer (BC) remains one of the most common oncological diseases among women worldwide, ranking among the leading causes of both cancer incidence and mortality. The main cause of unfavorable outcomes in BC is distant metastasis. The brain is one of the most frequent sites of distant metastatic spread, which significantly complicates treatment and worsens prognosis. This is the blood–brain barrier, which limits the penetration of many chemotherapeutic agents, as well as the aggressive biology of the tumor.
This article presents a clinical case of effective use of modern targeted agents in a patient with diagnosed breast cancer who initially had an unfavorable prognosis and disease progression after previous therapy. Particular attention is paid to treatment strategy selection and the use of contemporary targeted therapies that demonstrated clinical efficacy.
The described case illustrates the potential of a personalized approach in the treatment of this category of patients, including the possibility of disease control and improvement of clinical outcomes. The analysis of the presented clinical case indicates the need for further development of systemic maintenance therapy, as well as broader implementation of targeted and combined treatment approaches. Individualization of therapeutic strategies taking into account tumor biological characteristics and prior treatment history may contribute to improved treatment efficacy and quality of life.