Growing evidence supports the antagonistic pleiotropy theory of mammalian aging. Accordingly, changes in gene expression following the pluripotency transition, and subsequent transitions such as the embryonic–fetal transition, while providing tumor suppressive and antiviral survival benefits also result in a loss of regenerative potential leading to age-related fibrosis and degenerative diseases. However, reprogramming somatic cells to pluripotency demonstrates the possibility of restoring telomerase and embryonic regeneration pathways and thus reversing the age-related decline in regenerative capacity. A unified model of aging and loss of regenerative potential is emerging that may ultimately be translated into new therapeutic approaches for establishing induced tissue regeneration and modulation of the embryo-onco phenotype of cancer.

The cost of monoclonal antibody therapies for cancer is soaring out of control. Healthcare payers and patients are increasingly struggling to meet the high costs, which can be up to US$100,000 a year. A number of methods have been proposed to control these costs-government price controls on cancer drugs, biosimilars and novel drug pricing strategies. This article discusses what the impact of these strategies would be in terms of their ability to reduce costs and their effect on innovative cancer drug discovery.

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