Metformin, a widely prescribed treatment for type II diabetes, offers promising benefits beyond glycemic control, including improved lipid profiles and cardiovascular outcomes. It inhibits gluconeogenesis in the liver by activating AMPK, thereby reducing glucose production and enhancing glucose uptake in muscle. Recent studies highlight its potential anticancer effects, particularly through the suppression of the mTOR pathway via LKB1-dependent AMPK activation, which inhibits cell proliferation. This review explores metformin’s role as an adjunct therapy in pancreatic cancer, summarizing evidence on its molecular mechanisms and potential efficacy. The findings suggest metformin’s broader therapeutic applications, especially in oncology, warrant further investigation. The aim: The aim of this study is to analyze the role of metformin as an adjunct therapy in the treatment of pancreatic cancer, with particular focus on its molecular mechanisms, such as AMPK activation and mTOR pathway inhibition. The study aims to summarize the current scientific evidence regarding its potential effectiveness.

Purpose: Collet-Sicard syndrome (CSS) is a neurological condition secondary to various neoplastic and non-neoplastic lesions, manifesting as palsy of the lower cranial nerves. This article aims to disseminate knowledge and share insights into this disorder. Case description: A 58-year-old...

Introduction and purpose: Human skeleton-based sex estimation is a major topic of interest for forensic anthropologists. Various bones have been examined for sex heterogeneity. The most commonly used include skull and pelvis, however they may not always be used due to damage or fragmentation. The patella has been shown to be resistant to postmortem changes, which creates a potential use for determining the sex of unknown human remains. Materials and methods: The samples were gathered from patients examined by computed tomography angiography (CTA) of lower extremities in University Hospital No. 4 in Lublin. Exclusion criteria included patellar fractures, knee replacement and advanced osteoporosis. A total of 120 CTA examinations of 65 males and 55 females, were included in the analysis. Four measurements for every patella: craniocaudal patella dimension (CCP), transverse dimension (TP), anteroposterior dimension (APP) and patellar angle (PA), were obtained from CTA images. Results: The statistical analysis proved that sex differences of all variables, except for PA, were statistically significant (p < 0,001). Conclusions: Patellar measurements can be helpful in sex determination in the Polish population. CT is a useful tool for skeleton-based sex identification.

Background: The type of tumor is a huge determinant of survival and treatment outcomes, particularly with immunotherapy, which uses the immune system to target cancer cells. The response to immunotherapy varies depending on tumor types and is influenced by factors such as genetic mutations and the tumor microenvironment. Materials and methods: The present retrospective study analyzed records for 151 patients who underwent immunotherapy at a single center between 2019 and 2023. The cohort included adults diagnosed with solid tumors, primarily NSCLC (non-small cell lung cancer). Immunotherapy agents included pembrolizumab, nivolumab, and others. Data on age, cancer stage, treatment response, adverse events, overall survival (OS), and progression-free survival (PFS) were collected. Statistical analyses, including the Cox proportional hazards model, assessed the impact of tumor types and subtypes on survival outcomes. Results: The median age of the cohort was 69 (SD, 10.3) years, and the majority of the patients were men (64.9%). NSCLC was the predominant tumor type (78.1% of cases). In comparison to adenocarcinoma NSCLC, squamous NSCLC showed a significantly higher hazard ratio (HR) for OS (HR 1.49) and PFS (HR 1.47). Renal cell carcinoma and bladder cancer had lower HRs, suggesting a better prognosis. Conclusions: This study highlights how responses to immunotherapy can differ widely based on tumor type, emphasizing the importance of personalized therapy approaches. These insights underscore the need for further research to tailor immunotherapy more effectively to different cancer types.

Background: The dynamic advancement of pediatric hemato-oncology and intensified therapeutic protocols have significantly increased survival rates while simultaneously highlighting the challenge of long-term treatment complications. Within the cohort of adolescent and young adult (AYA) survivors, delayed neurocognitive deficits, often manifesting as the chemobrain phenotype, and psychosocial disorders constitute a particularly substantial burden. Contemporary neurogastroenterological evidence indicates a fundamental role of persistent dysbiosis and gut–brain axis dysfunction in the pathogenesis of these alterations. This review aims to critically synthesize translational evidence elucidating the impact of iatrogenic gut microbiota damage and modifiable dietary patterns on the development of long-term neurocognitive sequelae in survivors of early childhood cancer. Methods: A systematized narrative review was conducted in accordance with the SANRA guidelines by integrating data from in vivo models and observational studies. A comprehensive literature search across the PubMed, Embase, Cochrane Central, Scopus, and Web of Science databases up to June 2026 was performed utilizing the Population, Exposure, and Outcomes (PEO) framework. Results: Oncological therapies, including myeloablative conditioning and broad-spectrum antibiotic therapy, induce a microbial scar phenomenon characterized by the depletion of commensal Firmicutes in favor of resistant pathobionts. The subsequent decline in the synthesis of neuroprotective short-chain fatty acids (SCFAs) alongside the pathological activation of the kynurenine pathway disrupts central nervous system homeostasis. Translocation of lipopolysaccharides (LPSs) across the compromised intestinal barrier generates systemic inflammation recognized as inflammaging, which, in turn, stimulates neurotoxic microglial hyperreactivity. This pathophysiological cascade is accelerated by a pro-inflammatory Western diet, whereas anti-inflammatory interventions such as the MIND diet and postbiotics demonstrate measurable restorative potential. Conclusions: The pathophysiology of delayed neurotoxicity is largely a consequence of systemic neuroinflammation driven by intestinal dysbiosis. Implementing individualized dietary and microbiome-targeted strategies into survivorship care protocols constitutes a crucial direction for clinical prophylaxis. Validating their clinical efficacy in the AYA population necessitates prospective randomized controlled trials integrated with shotgun metagenomic sequencing.