A potential downside of molecular therapies aiming to improve organ maintenance during ageing could be an increase in the cancer risk. It appears unavoidable that interventions that increase stem cell self-renewal and regeneration would also increase cancer risk if constantly applied. Transient interventions might be one option to avoid such side effects. A detailed understanding of the role of telomeres and telomerase in cancer initiation and progression is a prerequisite to begin to explore telomeres and telomerase as targets for regenerative medicine. Lenhard Rudolph summarizes data from mouse models and human data showing that telomere dysfunction has a dual role in carcinogenesis by increasing the rate of cancer initiation but suppressing cancer progression. The chapter summarizes molecular mechanisms that could explain an increased cancer risk in response to telomere dysfunction, including the induction of chromosomal instability and environmental alterations. In contrast, depending on the checkpoint response, telomere dysfunction may impair cancer progression. Maria Blasco extends the cancer section of the book by summarizing experimental evidence indicating that in addition to telomere length, telomere binding proteins can influence tissue deterioration during ageing and increase the cancer risk specifically in the context of short telomeres.

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