The article reviews the emerging connections between cancer and aging, tracing the origins of this interdisciplinary research to a series of unethical events involving Henrietta Lacks' biopsy sample in 1951. The review highlights five key areas where cancer biology and aging share common mechanisms: cellular senescence, genomic instability, telomere biology, autophagy, and mitochondrial metabolism. Cellular senescence, a stress-induced barrier to tumor formation, is linked to both cancer and aging through the activation of tumor suppressor pathways and the DNA damage response. Genomic instability, a hallmark of both cancer and aging, is influenced by factors such as p53, ATM, and BRCA1. Telomere shortening, crucial for chromosomal stability, is a common feature of both processes and can lead to cellular senescence and aging. Autophagy, the process of cellular waste management, plays a role in both cancer and aging by regulating the degradation of damaged proteins and organelles. Mitochondrial metabolism, which is critical for energy production, is also linked to both cancer and aging through pathways involving p53, mTOR, and forkhead transcription factors. The article concludes by emphasizing the complex and interconnected nature of these processes, suggesting that strategies to prevent cancer may also influence aging, and vice versa.The article reviews the emerging connections between cancer and aging, tracing the origins of this interdisciplinary research to a series of unethical events involving Henrietta Lacks' biopsy sample in 1951. The review highlights five key areas where cancer biology and aging share common mechanisms: cellular senescence, genomic instability, telomere biology, autophagy, and mitochondrial metabolism. Cellular senescence, a stress-induced barrier to tumor formation, is linked to both cancer and aging through the activation of tumor suppressor pathways and the DNA damage response. Genomic instability, a hallmark of both cancer and aging, is influenced by factors such as p53, ATM, and BRCA1. Telomere shortening, crucial for chromosomal stability, is a common feature of both processes and can lead to cellular senescence and aging. Autophagy, the process of cellular waste management, plays a role in both cancer and aging by regulating the degradation of damaged proteins and organelles. Mitochondrial metabolism, which is critical for energy production, is also linked to both cancer and aging through pathways involving p53, mTOR, and forkhead transcription factors. The article concludes by emphasizing the complex and interconnected nature of these processes, suggesting that strategies to prevent cancer may also influence aging, and vice versa.