People have always sought eternal life and everlasting youth. Recent technological breakthroughs and our growing understanding of aging have given strength to the idea that a cure for human aging can eventually be developed. As such, it is crucial to debate the long-term goals and potential impact of the field. Here, I discuss the scientific prospect of eradicating human aging. I argue that curing aging is scientifically possible and not even the most challenging enterprise in the biosciences. Developing the means to abolish aging is also an ethical endeavor because the goal of biomedical research is to allow people to be as healthy as possible for as long as possible. There is no evidence, however, that we are near to developing the technologies permitting radical life extension. One major difficulty in aging research is the time and costs it takes to do experiments and test interventions. I argue that unraveling the functioning of the genome and developing predictive computer models of human biology and disease are essential to increase the accuracy of medical interventions, including in the context of life extension, and exponential growth in informatics and genomics capacity might lead to rapid progress. Nonetheless, developing the tools for significantly modifying human biology is crucial to intervening in a complex process like aging. Yet in spite of advances in areas like regenerative medicine and gene therapy, the development of clinical applications has been slow and this remains a key hurdle for achieving radical life extension in the foreseeable future.

No abstract

Ageing is the biggest risk factor for cancer, but the mechanisms linking these two processes remain unclear. We compared genes differentially expressed with age and genes differentially expressed in cancer among nine human tissues. In most tissues, ageing and cancer gene expression surprisingly changed in the opposite direction. These overlapping gene sets were related to several processes, mainly cell cycle and the immune system.Moreover, cellular senescence signatures derived from a meta-analysis changed in the same direction as ageing and in the opposite direction of cancer signatures. Therefore, transcriptomic changes in ageing and cellular senescence might relate to a decrease in cell proliferation, while cancer transcriptomic changes shift towards an increase in cell division.Our results highlight the complex relationship between ageing, cancer and cellular senescence and suggest that in most human tissues ageing processes and senescence act in tandem while being detrimental to cancer. Our work challenges the traditional view concerning the relationship between cancer and ageing and suggests that ageing processes may hinder cancer development.

A major task for genetics is searching for genetic variants associated with disease. But we may well be missing a large number of “unknown unknown” alleles in the “fog of genetics”.