The expansion of genome-wide studies has identified widespread transcription that may result in previously unstudied transcripts, such as divergent long non-coding RNAs.

As depicted in the graphics, the classical NHEJ pathway can either take place in cells with DSBs or normal lymphocytes, reinforcing the stability of genome, and simultaneously maintaining the function of the immune system. While complete deletion causes immunodeficiency and tumourigenesis, some inhibitions could promote cancer therapies.

Annexin A (AnxA) family members, including AnxA1, AnxA2, AnxA5, AnxA6, AnxA7 and AnxA8, play diverse roles in the development and progression of atherosclerosis and present promising therapeutic targets for its treatment.

This review elucidates distinct (hepatitis B virus [HBV] DNA integration, oncoproteins; hepatitis C virus [HCV] metabolic dysregulation, fibrosis) and shared (chronic inflammation, epigenetic alterations, genomic instability) molecular mechanisms driving viral hepatitis (HBV/HCV)-induced hepatocellular carcinoma. It highlights how viral infection remodels the tumour microenvironment and discusses emerging diagnostic, preventive and therapeutic strategies targeting these pathways.

Molecular ageing mechanisms including genomic instability, cellular senescence, and epigenetic alterations drive cancer development while affecting therapeutic response. Artificial intelligence-powered biomarkers and ageing clocks enable precision oncology approaches that optimize treatment selection based on biological rather than chronological age, improving outcomes for older cancer patients.