Professor Elizabeth Blackburn

 

Telomeres are important because they are critical to how cells stop multiplying. Telomeres generally shorten as cells divide, or undergo DNA replication stress, and/or chemical damage including as oxidative damage. Telomerase, a specialized ribonucleoprotein reverse transcriptase, replenishes the DNA at telomeres and is important for long-term eukaryotic cell proliferation and genomic stability. Humans' relatively long lifespan is a key factor in how telomere maintenance, in complex intelplay with genetic and non-genetic factors, determines human healthspan and disease.

Accumulated data indicate that loss of telomere protection (measured as shortening of telomeres) is both linked to and, in some cases, causally contributes to, human aging and aging-related diseases. These include cardiovascular disease, stroke, osteoporosis, inflammatoly diseases, dementia, diabetes and certain cancers.

While new cancer treatments are imperative, telomere biology is highly relevant to the emerging Importance of cancer prevention and interception. However, it is too simplistic and even dangerous to suggest that extending telomere length will invariably extend healthspan. Disease mechanisms are interconnected and manipulating one mechanism has the potential to positively or negatively impact other mechanisms. Telomerase is highly active m many human malignancies, and a potential target for anti-cancer stratagems. But conversely, genetic deficiency of telomerase causes certain hemopoietic, skin and gastrointestinal cancers. Hence human telomerase activity and telomere maintenance present delicate balancing acts throughout human life. Further understanding about their control via molecular and environmental switches is anticipated to lead to applications in disease treatment and interception.