Colon cancer remains a significant global health challenge, with inflammatory pathways such as TNF-α playing a central role in its progression. TNF-α, a key proinflammatory cytokine, is implicated in various stages of colon cancer development, including inflammation, tumor growth, and metastasis. This review provides a comprehensive overview of the molecular mechanisms through which TNF-α contributes to colon cancer progression, with a focus on its interaction with signaling pathways like NF-κB and the Wnt/β-catenin in humans. TNF-α’s involvement in promoting tumorigenesis and its complex role in the tumor microenvironment highlight its potential as both a therapeutic target and a challenge for effective treatment. This review explores the potential of anti-TNF-α therapies and the emerging role of combination strategies with immune checkpoint inhibitors. Despite promising preclinical findings, clinical application faces challenges due to the dual role of TNF-α in both promoting and inhibiting tumor progression. Future research should aim to overcome resistance mechanisms, develop personalized therapeutic strategies, and balance the effects of TNF-α in cancer therapy.

Background/Objectives: Colon cancer remains a significant health challenge world-wide, with inflammatory pathways such as tumor necrosis factor-alpha (TNF-α) playing a central role in its progression. TNF-α, a key proinflammatory cytokine, is implicated in various stages of colon cancer development, including inflammation, tumor growth, and metastasis. This review provides a comprehensive overview of the molecular mechanisms through which TNF-α contributes to colon cancer progression, with a focus on its interaction with signaling pathways like NF-κB, oxidative stress, and Wnt/β-catenin. Methods: A comprehensive review of the literature was conducted to elucidate the role of tumor necrosis factor-alpha in the pathogenesis of colon cancer. Peer-reviewed clin-ical and preclinical studies involving human subjects were identified through electronic databases, including PubMed, Scopus, and Web of Science. Selection criteria focused on studies examining the molecular mechanisms of TNF-α signaling, its interaction with key oncogenic pathways and therapeutic interventions targeting TNF-α. Data were synthesized to highlight both mechanistic insights and therapeutic applications. Results: TNF-α’s involvement in promoting tumorigenesis and its complex role in the tumor microenvironment highlight its potential as both a therapeutic target and a challenge for effective treatment. The review also delves into the potential of an-ti-TNF-α therapies and the emerging role of combination strategies with immune checkpoint inhibitors. Despite promising preclinical findings, clinical application faces challenges due to the dual role of TNF-α in both promoting and inhibiting tumor pro-gression. Conclusion: Future research should focus on overcoming resistance mechanisms, de-veloping personalized therapeutic strategies, and balancing the effects of TNF-α in cancer therapy.

Introduction: Chronic kidney disease (CKD) is a progressive illness with high morbidity and mortality that warrants early and accurate risk stratification for optimal management. The traditional biomarkers, serum creatinine and estimated glomerular filtration rate (eGFR), are insufficient for detecting early CKD and long-term prognosis. Novel biomarkers have emerged as effective tools to complement CKD diagnosis, prognosis, and therapeutic monitoring. Aim: The aim of this research was to determine the potential of novel biomarkers in CKD risk stratification and their clinical significance for improving early detection, monitoring disease progression, and developing individualized treatment strategies. Methods: A literature review was conducted by searching the PubMed, Scopus, and Embase databases to identify studies on novel CKD biomarkers, including cystatin C, neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), and specific microRNAs. Results: Emerging evidence suggests that novel biomarkers provide superior predictive abilities compared to traditional markers. Cystatin C is more accurate in kidney function estimation, whereas NGAL and KIM-1 are markers of early kidney injury. MicroRNAs show potential in distinguishing between CKD subtypes and predicting disease progression. Clinical application of these biomarkers may enhance CKD risk stratification, allowing more targeted intervention strategies. Conclusion: New biomarkers in CKD risk stratification represent a watershed moment in nephrology, offering improved early detection and prognostic accuracy. While promising, additional large-scale research and clinical validation are required before they can be used routinely.

Resumo Introdução: Doença renal crônica (DRC) é uma doença progressiva, com elevada morbimortalidade, demandando estratificação precoce e precisa do risco para um manejo ideal. Biomarcadores tradicionais - creatinina sérica, taxa de filtração glomerular estimada (TFGe) - são insuficientes para detecção precoce da DRC e do prognóstico em longo prazo. Novos biomarcadores surgiram como ferramentas eficazes para complementar o diagnóstico, prognóstico e monitoramento terapêutico da DRC. Objetivo: Determinar o potencial de novos biomarcadores na estratificação do risco de DRC e sua significância clínica para aprimorar a detecção precoce, monitorar a progressão da doença e desenvolver estratégias terapêutica individualizadas. Métodos: Realizou-se revisão da literatura por meio de buscas nas bases de dados PubMed, Scopus e Embase para identificar estudos sobre novos biomarcadores da DRC, incluindo cistatina C, lipocalina associada à gelatinase neutrofílica (NGAL), molécula de lesão renal 1 (KIM-1) e microRNAs específicos. Resultados: Evidências emergentes sugerem que novos biomarcadores oferecem capacidades preditivas superiores comparados aos biomarcadores tradicionais. A cistatina C demonstra maior precisão na estimativa da função renal, enquanto NGAL e KIM-1 são biomarcadores de lesão renal precoce. MicroRNAs apresentam potencial para distinguir entre subtipos de DRC e predizer progressão da doença. A aplicação clínica desses biomarcadores pode aprimorar a estratificação do risco de DRC, permitindo estratégias de intervenção mais direcionadas. Conclusão: Novos biomarcadores na estratificação do risco de DRC representam um marco na nefrologia, oferecendo detecção precoce aprimorada e maior precisão no prognóstico. Embora promissores, são necessários estudos adicionais em larga escala e validação clínica antes que possam ser utilizados rotineiramente.

Background: Breast reconstruction is essential for restoring physical and psychological well-being in mastectomy patients. With possible benefits including decreased immunogenicity and fewer complications, dermal autografts (DAs) have become a more affordable option to acellular dermal matrices (ADMs). This systematic review evaluates the long term clinical outcomes and cost effectiveness of DA, compared to ADM in implant based breast reconstruction. Methods: A PRISMA-based systematic review was conducted using PubMed, Scopus, Google Scholar and EMBASE databases, up until February 2025. Included studies reported on DA outcomes (complications, reoperations, costs) in English. Eligible designs included randomized controlled trials (RCTs), cohort studies, and case series reporting complications, costs, graft survival, or patient satisfaction. Two reviewers independently assessed risk of bias using the Newcastle-Ottawa Scale (NOS) and National Institutes of Health (NIH) tools. Results: Five studies (175 patients) met the inclusion criteria. DA demonstrated comparable complication rates (e.g., infection, reoperation) to ADM but with significantly lower costs (DA: $3,924–$12,685 vs. ADM: $9,088–$66,832). Quality appraisal revealed considerable heterogeneity in study designs and outcome reporting, with one study assessed as being of ‘good’ quality. Conclusions: DA is a safe, cost-saving alternative to ADM in breast reconstruction, with comparable complication rates and superior economic value. Larger prospective trials are needed to validate long-term outcomes and standardize techniques.

The human gut microbiome makes up a highly diverse microbial ecosystem that is crucial for host metabolism, immunological modulation, and intestinal barrier integrity. The bacteria phyla Firmicutes, Bacteroidetes, Proteobacteria, and Actinobacteria dominate the intestinal microbiota, contributing to metabolic processes such as dietary polysaccharide fermentation and the synthesis of bioactive microbial metabolites. Dysbiosis, or disruptions in microbial composition and function, has been linked to the development of autoimmune disorders. Microbial mechanisms that relate dysbiosis to disease include the growth of pro-inflammatory microbial taxa, decreased synthesis of short-chain fatty acids (SCFAs), altered microbial metabolic pathways, and loss of epithelial barrier integrity. Among autoimmune disorders, inflammatory bowel disease (IBD), which encompasses Crohn’s disease and ulcerative colitis, is one of the best-studied cases of microbiome-associated pathology. In this review, we focus on the role of gut microbiome alterations in the pathogenesis of IBD, highlighting microbial dysbiosis, changes in microbial metabolites, and host–microbiome interactions that contribute to intestinal inflammation. This review also examines microbiome-targeted therapeutic strategies, including probiotics, prebiotics, fecal microbiota transplantation, and postbiotics, alongside emerging artificial intelligence–based approaches to personalized treatment, and consider how comorbid systemic conditions may shape microbial homeostasis in IBD patients. Understanding these microbial pathways may open new possibilities for microbiome-based diagnostics and therapeutic approaches in IBD.