Osteosarcoma (OS) is the most common primary malignant bone tumor, predominantly affecting children, adolescents, and young adults. Epithelial–mesenchymal transition (EMT), a process in which epithelial cells lose their cell–cell adhesion and gain migratory and invasive properties, has been extensively studied in various carcinomas. However, its role in mesenchymal tumors like osteosarcoma remains less explored. EMT is increasingly recognized as a key factor in the progression of osteosarcoma, contributing to tumor invasion, metastasis, and resistance to chemotherapy. This narrative review aims to provide a comprehensive overview of the molecular mechanisms driving EMT in osteosarcoma, highlighting the involvement of signaling pathways such as TGF-β, transcription factors like Snail, Twist, and Zeb, and the role of microRNAs in modulating EMT. Furthermore, we discuss how EMT correlates with poor prognosis and therapy resistance in osteosarcoma patients, emphasizing the potential of targeting EMT for therapeutic intervention. Recent advancements in understanding EMT in osteosarcoma have opened new avenues for treatment, including EMT inhibitors and combination therapies aimed at overcoming drug resistance. By integrating biological insights with clinical implications, this review underscores the importance of EMT as a critical process in osteosarcoma progression and its potential as a therapeutic target.

Silicone implants are frequently used for breast augmentation and reconstruction. However, late complication, such as capsular contracture, remain the most important side effect. In this study we compare different methods for reducing the inflammatory reaction around the silicone implant by introducing one microtextured breast implant in wistar rats. The rats were dividing in 4 groups: the first one was the control group that received untreated implant; in the second we used silicone implants impregnated with rifampin solution, the third one had implant combined with intramuscular dexamethasone injection and the last one had silicone implant associated with autologous centrifuged fat introduced in the implant pocket. The implants and the capsular tissue surrounding were removed after eight weeks. Capsule samples were submitted to histological evaluations. The present study demonstrated that fat grafting may have a role in reducing and preventing capsular contractures after breast augmentation with silicone implants by decreasing the inflammatory process.

Metabolically-dysfunction-associated steatotic liver disease (MASLD) represents the most common chronic liver disease in the pediatric population, and its prevalence has doubled over the past decade. The etiology is multifactorial, including genomic risk factors, perinatal and developmental or behavioral factors. Still, many cases of MASLD are associated with being overweight and obesity, particularly in children who have poor dietary habits and sedentary lifestyles that contribute to excessive weight gain. Given the progressive and heterogeneous nature of MASLD, early identification of high-risk patients before the development of severe liver disease is a major clinical priority. Recent studies indicate that disorders of amino acid metabolism are closely linked to both obesity and MASLD, reflecting profound alterations in systemic metabolic homeostasis. The reported data sustain significant changes in circulating amino acid profiles, particularly elevated levels of branched-chain amino acids (BCAAs) and aromatic amino acids. These alterations are thought to reflect fundamental metabolic disturbances, including insulin resistance, compromised mitochondrial activity, and altered hepatic lipid metabolism. Consequently, alterations in amino acid metabolism have been proposed as potential biomarkers for disease progression and metabolic dysfunction in MASLD. This review aims to evaluate the correlation between the amino acid profile and histological changes in pediatric MASLD, including steatosis, steatohepatitis, and fibrosis.

Background/Objectives: Gonadal germ cell tumors (GCTs) arise in the testis and ovary from primordial germ cells. Despite shared origins, they display distinct molecular and genetic features. Understanding these differences is essential for clarifying tumor pathogenesis and improving diagnostic and therapeutic strategies. This review aims to compare these features and to better define the biological differences between testicular and ovarian GCTs. Methods: We reviewed cytogenetic alterations, epigenetic modifications, and somatic mutations reported in testicular and ovarian GCTs. Comparative analysis was performed to identify common and site-specific mechanisms. Results: Isochromosome 12p is a hallmark of testicular GCTs, while ovarian GCTs show diverse chromosomal changes. DNA methylation and other epigenetic marks differ by tumor subtype and gonadal origin. Somatic mutations affect pathways regulating cell cycle, pluripotency, and differentiation, with overlapping and unique patterns between testicular and ovarian tumors. Collectively, these findings define a molecular framework that explains both shared biology and gonadal-specific divergence in GCTs. Conclusions: Understanding molecular similarities and differences across gonadal GCTs can refine classification, guide biomarker discovery, and inform translational research. This comparative perspective highlights core pathogenetic mechanisms and gonadal-specific features relevant to clinical and experimental oncology.