Maintaining a balanced skin microbiota is essential for skin health, whereas disruptions in skin microbiota composition, known as dysbiosis, can contribute to the onset and progression of various skin disorders. Microbiota dysbiosis has been associated with several inflammatory skin conditions, including atopic dermatitis, seborrheic dermatitis, acne, psoriasis, and rosacea. Recent advances in high-throughput sequencing and metagenomic analyses have provided a deeper understanding of the skin microbial communities in both health and disease. These discoveries are now being translated into novel therapeutic approaches aimed at restoring microbial balance and promoting skin health through microbiome-based interventions. Unlike conventional therapies that often disrupt the microbiota and lead to side effects or resistance, microbiome-based products offer a more targeted strategy for preventing and managing inflammatory skin diseases. These products, which include probiotics, prebiotics, postbiotics, and live biotherapeutic agents, are designed to modulate the skin ecosystem by enhancing beneficial microbial populations, suppressing pathogenic strains, and enhancing immune tolerance. As a result, they represent a promising class of products with the potential to prevent, manage, and even reverse inflammatory skin conditions. However, realizing the full therapeutic potential of microbiome-based strategies in dermatology will require continued research, robust clinical validation, and clear regulatory frameworks.

The resilience of sarcomas, tumors characterized by resistance to therapy and high metastatic potential, is largely driven by the unique characteristics of a small population known as cancer stem cells (CSC). Although ascorbic acid (AA) and its oxidized form, dehydroascorbic acid (DHA), have shown potential for selectively targeting cancer cells, their effects on sarcoma CSCs remain insufficiently explored. Still, recent research indicates that AA can affect the specific characteristics of CSC and lead to their cytotoxicity. To investigate the sensitivity of sarcoma CSCs to ascorbate, CSCs were isolated from six sarcoma patient-derived samples using a sphere assay, and their stem identity was evaluated through gene expression profiling and dye-efflux assays. Cytotoxicity testing of AA and DHA showed that DHA has a selective cytotoxic effect on cancer stem cells. The presence of basic fibroblast growth factor (bFGF), which is commonly used to support the self-renewal of CSCs, had an influence on the cytotoxic effect of DHA. To evaluate the difference in the effect of AA and DHA, a seven-day treatment of CSCs with these forms of ascorbate was performed. The gene expression analysis revealed that DHA in the presence of bFGF had a stronger impact on response to oxidative stress and cellular metabolism. Also, investigation of somatic mutations of oncogenes and tumor suppressors revealed that in liposarcoma and rhabdomyosarcoma, there are mutations that induce proliferative signals. These proliferative signals, joined with bFGF in the presence of DHA, do not lead to proliferation but instead cause cell death.