MicroRNAs (miRNAs) are small RNA molecules that do not have coding functions but play essential roles in various biological processes. In lung cancer, miRNAs affect the processes of tumor initiation, progression, metastasis, and resistance to treatment by regulating gene expression. Tumor-suppressive miRNAs inhibit oncogenic pathways, while oncogenic miRNAs, known as oncomiRs, promote malignant transformation and tumor growth. These dual roles position miRNAs as critical players in lung cancer biology. Studies in recent years have shown the significant potential of miRNAs as both prognostic and diagnostic biomarkers. Circulating miRNAs in plasma or sputum demonstrate specificity and sensitivity in detecting early-stage lung cancer. Liquid biopsy-based miRNA panels distinguish malignant from benign lesions, and specific miRNA expression patterns correlate with disease progression, response to treatment, and overall survival. Therapeutically, miRNAs hold promise for targeted interventions. Strategies such as miRNA replacement therapy using mimics for tumor-suppressive miRNAs and inhibition of oncomiRs with antagomiRs or miRNA sponges have shown preclinical success. Key miRNAs, including the let-7 family, miR-34a, and miR-21, are under investigation for their therapeutic potential. It should be emphasized that delivery difficulties, side effects, and limited stability of therapeutic miRNA molecules remain obstacles to their clinical use. This article examines the roles of miRNAs in lung cancer by indicating their mechanisms of action, diagnostic significance, and therapeutic potential. By addressing current limitations, miRNA-based approaches could revolutionize lung cancer management, offering precise, personalized, and minimally invasive solutions for diagnosis and treatment.

Background. Unmanipulated haploidentical stem cell transplantation (haploSCT) with post-transplant cyclophosphamide is an option for patients with advanced hematologic malignancies. It offers a platform both for non-major histocompatibility complex-restricted alloimmunity due to killer-like immunoglobulin receptor (KIR)-mediated mechanisms of natural killer lymphocyte regulation and for classical T-cell mediated antileukemic effects. Objectives. The devastating long-term sequelae after total body irradiation (TBI) in children are encouraging omission of irradiation techniques in pediatric stem cell transplantations (SCT). Material and methods. Five children, 4 with acute leukemia and 1 with hemophagocytic lymphohistiocytosis, aged from 1 to 10 years, underwent haploSCT with post-transplantation cyclophosphamide. In all children, the conditioning regimen consisted of chemotherapy without TBI. The graft material was bone marrow (BM) in 4 cases and peripheral blood stem cells in 1 case. Three out of 5 leukemic patients showed better KIR haplotype associated with augmented alloreactivity. Results. Engraftment with complete donor chimerism was achieved in 4 patients, and 1 recipient died before leukocyte recovery. Three patients developed skin acute graft-versus-host-disease (aGvHD), 1 gut aGvHD and 1 liver aGvHD. In 2 recipients, chronic graft-versus-host-disease (cGvHD) was observed (1 limited and 1 extensive). The 4 engrafted patients were alive and in complete remission 3, 9, 32, and 36 months after transplantation. A T-cell count of 200 cells/uL was reached 90 days after haploSCT in all patients. Conclusions. HaploSCT with TBI-free protocols can be a viable option for heavily pretreated patients with advanced malignancies.

Hospital environments host diverse microbial communities that may contribute to nosocomial infections. Moisture-retaining surfaces such as cleaning sponges and faucet edges represent high-contact, under-investigated hygiene hotspots, particularly in wards caring for immunocompromised patients. Environmental samples were collected from cleaning sponges (n = 14) and faucet edges (n = 4) across multiple hospital rooms of a paediatric haematology–oncology unit, with domestic physician sponges as controls (n = 3). DNA was extracted and sequenced targeting the V3–V4 and V7–V9 hypervariable regions of the 16S rRNA gene on the Illumina MiSeq platform. Taxonomic composition and alpha/beta diversity were assessed using QIIME 2 and R. Sponge samples were dominated by Moraxellaceae, particularly Acinetobacter and Enhydrobacter, and showed significantly lower alpha diversity than faucet samples (Shannon index: Kruskal–Wallis H = 8.4, p = 0.01; Faith’s phylogenetic diversity: H = 9.17, p = 0.01). Faucet samples were enriched in human-associated genera including Staphylococcus, Streptococcus, and Chryseobacterium. Statistically significant beta-diversity differences were detected between sponge and faucet communities by PERMANOVA based on Bray–Curtis dissimilarity (p = 0.01), whereas no significant clustering by room or floor location was observed (p = 0.29). Potentially pathogenic taxa including Aeromonas, Pseudomonas, and Enterobacteriaceae were identified across both surface types. Domestic control sponges showed distinct microbiome profiles from hospital samples. Microbial communities differ significantly between hospital sponges and faucets, with surface type rather than location as the primary determinant of community structure. The presence of opportunistic pathogens on both surface types highlights the importance of enhanced hygiene protocols, inclusion of faucet edges and sink drains in routine decontamination schedules, and regular microbiological surveillance in clinical settings caring for immunocompromised patients.