A growing amount of experimental evidences has progressively shown that aging and carcinogenesis share many molecular pathways. During aging, the accumulation of genetic and epigenetic changes, the diminishing of telomere length, the progressive disruption of mechanisms for DNA damage repair, glucose metabolism regulation, cell cycle control, and stem cells self-renewal lead to induction of senescence or apoptosis and loss of replicative capacity. The same cellular dysfunctional mechanisms characterizing the aging process have been found to be involved, with different level of evidence, in cancerogenesis and are reviewed herein.