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Tissue repair is an extremely crucial part of clinical treatment. During the course of disease treatment, surgery, chemotherapy, and radiotherapy cause tissue damage. On the other hand, Normal tissue from accidental or therapeutic exposure to high-dose radiation can cause severe tissue damage. There is an urgent need for developing medical countermeasures against radiation injury for tissue repair. Tissue repair involves the regeneration, proliferation, differentiation, and migration of tissue cells; imbalance of local tissue homeostasis, progressive chronic inflammation; decreased cell activity and stem cell function; and wound healing. Although many clinical treatments are currently available for tissue repair, they are expensive. The long recovery time and some unavoidable complications such as cell damage and the inflammatory reaction caused by radiotherapy have led to unsatisfactory results. Extracellular vesicles (EVs) derived from mesenchymal stem cells (MSCs) have similar tissue repair functions as MSCs. In tissue damage, EVs can be used as an alternative to stem cell therapy, thereby avoiding related complications such as immunological rejection. EVs play a major role in regulating tissue damage, anti-inflammation, pro-proliferation, and immune response, thus providing a diversified and efficient solution for the repair of disease- and radiotherapy-induced tissue damage. This article reviews the research progress of mesenchymal stem cell-derived EVs in promoting the repair of tissue including heart, lung, liver, intestine, skin, blood system, central nervous system, and tissue damage caused by radiotherapy, thereby aiming to offer new directions and ideas for the radiotherapy and regenerative applications. [ABSTRACT FROM AUTHOR]

Immunotherapy has revolutionised the treatment landscape of non-small cell lung cancer (NSCLC), significantly improving survival outcomes and offering renewed hope to patients with advanced disease. However, the majority of patients experience limited long-term benefits from immune checkpoint inhibition (ICI) due to the development of primary or acquired immunotherapy resistance. Accurate predictive biomarkers for immunotherapy resistance are essential for individualising treatment strategies, improving survival outcomes, and minimising potential treatment-related harm. This review discusses the mechanisms underlying resistance to immunotherapy, addressing both cancer cell-intrinsic and cancer cell-extrinsic resistance processes. We summarise the current utility and limitations of two clinically established biomarkers: programmed death ligand 1 (PD-L1) expression and tumour mutational burden (TMB). Following this, we present a comprehensive review of emerging immunotherapy biomarkers in NSCLC, including tumour neoantigens, epigenetic signatures, markers of the tumour microenvironment (TME), genomic alterations, host–microbiome composition, and circulating biomarkers. The potential clinical applications of these biomarkers, along with novel approaches to their biomarker identification and targeting, are discussed. Additionally, we explore current strategies to overcome immunotherapy resistance and propose incorporating predictive biomarkers into an adaptive clinical trial design, where specific immune signatures guide subsequent treatment selection. [ABSTRACT FROM AUTHOR]

The genetic information that dictates the structure and function of all life forms is encoded in the DNA. In 1953, Watson and Crick first presented the double helical structure of a DNA molecule. Their findings unearthed the desire to elucidate the exact composition and sequence of DNA molecules. Discoveries and the subsequent development and optimization of techniques that allowed for deciphering the DNA sequence has opened new doors in research, biotech, and healthcare. The application of high-throughput sequencing technologies in these industries has positively impacted and will continue to contribute to the betterment of humanity and the global economy. Improvements, such as the use of radioactive molecules for DNA sequencing to the use of florescent dyes and the implementation of polymerase chain reaction (PCR) for amplification, led to sequencing a few hundred base pairs in days, to automation, where sequencing of thousands of base pairs in hours became possible. Significant advances have been made, but there is still room for improvement. Here, we look at the history and the technology of the currently available next-generation sequencing platforms and the possible applications of such technologies to biomedical research and beyond., (© 2025. The Author(s), under exclusive license to Springer Science+Business Media, LLC, part of Springer Nature.)

N1-methyladenosine (m1A), a methylation of RNA, is gaining attention for its role in diverse biological processes. However, the potential roles of m1A regulatory-mediated methylation modifications in multiple myeloma (MM) remain unclear. The mRNA expression of m1A regulators in normal plasma (NP; n=9) and MM (n=174) bone marrow plasma cells was investigated and the m1A modification patterns of 559 MM samples based on the expression of 10 m1A-related regulatory genes were comprehensively evaluated. Univariate Cox regression, Kaplan-Meier survival curve, unsupervised clustering and gene enrichment analyses were used to explore the associations between m1A-related regulatory genes and MM patient survival/prognosis. The m1A score model was subsequently constructed to quantify the m1A modification patterns of individual tumours, and its predictive performance was further assessed via receiver operating characteristic curves. Immunohistochemistry, Cell Counting Kit-8, flow cytometry and m1A dot blot assays were performed to investigate the potential role of YTH domain-containing family protein 2 (YTHDF2) in MM. Moreover, bioinformatics analysis was performed to predict the potential downstream regulatory mechanism of YTHDF2. In total, seven differentially expressed genes [tRNA methyltransferase 61A/B (TRMT61A/B), YTH N6-methyladenosine RNA binding protein (YTHD)F1/F2/F3/C1 and Alkb homolog 1, histone H2A dioxygenase (ALKBH1)] were identified in MM samples compared with those in NP samples. The forest map and Kaplan-Meier curve revealed that the expression of m1A-related regulatory genes could be favourable prognostic factors for patients with MM. A total of three distinct m1A modification patterns were determined, and Cluster B exhibited the worst outcome, which was accompanied by increased expression of YTHDF2, tRNA methyltransferase 6 non-catalytic subunit (TRMT6), tRNA methyltransferase 10 homolog C (TRMT10C) and TRMT61B. The m1Ascore model was subsequently constructed. A high m1A score was associated with clinical benefit and an improved treatment response. High expression of the reader protein YTHDF2 was associated with poor survival in patients with MM and was superior to other assessed proteins in terms of prognosis. Subsequent cell experiments demonstrated that YTHDF2 promoted the proliferation and inhibited the apoptosis of U266 cells. Notably, an evident increase in the m1A level was observed when YTHDF2 was overexpressed. A total of 150 genes related to YTHDF2 were identified, and these genes were enriched in the peroxisome proliferator-activated receptor signalling pathway, protein export, positive regulation of protein targeting to the membrane, and gamma-delta intraepithelial T-cell differentiation. Serine and arginine rich splicing factor 10 (SRSF10) was subsequently selected because SRSF10 expression was significantly positively correlated with YTHDF2 expression and was also associated with poor prognosis in patients with MM. The present study revealed the modification patterns and high prognostic value of m1A regulators and demonstrated that the reader protein YTHDF2 is a potentially crucial target for MM. [ABSTRACT FROM AUTHOR]