Telomere integrity and length and cancer risk

Telomeres consist of tandem arrays of short repetitive, non-coding sequences (TTAGGG in humans) and associated proteins at the ends of each chromosome (Blackburn 2005, Blackburn et al. 2006). Telomeres form a loop structure that caps the chromosomes and prevent chromosomes from erosion, end-to-end fusion, irregular recombination, and other damaging chromosomal events (Blackburn 2005, Blackburn et al. 2006). In somatic cells under normal physiological conditions, telomeres are progressively shortened during each mitotic cell division due to the “end replication problem”, resulting in progressive shortening of the chromosomes after each cell division. Because telomeres consist of repetitive, non-coding sequences and sit at both ends of each chromosome, the cells can afford to lose a few hundred base pairs of telomeres without losing genetic information. However, when telomeres become too short, the loop structures and associated proteins are disrupted and the protective function of telomere is lost. Critically short telomeres can have dire consequences, causing apoptosis and replicative senescence, and have been linked to the development of many chronic diseases.