Ageing and cancer are the edges within the same spectrum of molecular biologic processes. Ageing is the process of gradual accumulation of senescence cells with concomitant deterioration of different organ functions. The ineffective clearance of these cells leads to a proinflammatory phenotype with genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, deregulated nutrient-sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion and altered intercellular communication. On the contrary, cancer is a continuous and uncontrolled regeneration of a transformed cell. The proposed models for the development of cancer are the clonal genetic model (a mutation in a single gene accompanied by a series of mutations that offer genomic instability and plasticity),the epigenetic dysregulation model (global hypomethylation and specific gene hypermethylation or hypomethylation that activates oncogenes and inhibits tumor suppressor genes), the reprogramming model (alteration in genes responsible for transition states) and the non-resolved inflammation model (cancer is related to chronic inflammation and the secretion of IL-6, IL-8 and TNF-a cytokines from the tumor cell or the microenvironment).