The biology of cancer and ageing shares common mechanisms, as highlighted in this review. The discovery of HeLa cells in 1951 marked a pivotal moment in cancer research, leading to a deeper understanding of cellular senescence and its role in both cancer and ageing. Cellular senescence, a process where cells stop dividing, is linked to tumour formation and is triggered by various stresses, including telomere shortening and DNA damage. The CDKN2a locus, which includes p16INK4a and p19ARF, plays a key role in this process, and its dysregulation is associated with both cancer and ageing. Genomic instability, another common feature of both cancer and ageing, is influenced by factors such as DNA repair defects and mutations in genes like P53 and BRCA1. Telomeres, the protective caps at the ends of chromosomes, shorten with age and are maintained by telomerase. Defects in telomere maintenance are linked to premature ageing syndromes and cancer. Autophagy, a cellular process that removes damaged components, is also involved in both cancer and ageing, with impaired autophagy contributing to tumour development and accelerated ageing. Metabolic pathways, including those regulated by mTOR and p53, are crucial for both processes, as they influence cell growth, survival, and energy homeostasis. The review emphasizes the complex interplay between these mechanisms and suggests that understanding them could lead to new strategies for cancer prevention and ageing research. The story of Henrietta Lacks highlights the importance of her cells in advancing our understanding of cancer and ageing.The biology of cancer and ageing shares common mechanisms, as highlighted in this review. The discovery of HeLa cells in 1951 marked a pivotal moment in cancer research, leading to a deeper understanding of cellular senescence and its role in both cancer and ageing. Cellular senescence, a process where cells stop dividing, is linked to tumour formation and is triggered by various stresses, including telomere shortening and DNA damage. The CDKN2a locus, which includes p16INK4a and p19ARF, plays a key role in this process, and its dysregulation is associated with both cancer and ageing. Genomic instability, another common feature of both cancer and ageing, is influenced by factors such as DNA repair defects and mutations in genes like P53 and BRCA1. Telomeres, the protective caps at the ends of chromosomes, shorten with age and are maintained by telomerase. Defects in telomere maintenance are linked to premature ageing syndromes and cancer. Autophagy, a cellular process that removes damaged components, is also involved in both cancer and ageing, with impaired autophagy contributing to tumour development and accelerated ageing. Metabolic pathways, including those regulated by mTOR and p53, are crucial for both processes, as they influence cell growth, survival, and energy homeostasis. The review emphasizes the complex interplay between these mechanisms and suggests that understanding them could lead to new strategies for cancer prevention and ageing research. The story of Henrietta Lacks highlights the importance of her cells in advancing our understanding of cancer and ageing.