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Telomeres are essential DNA–protein complexes at the ends of eukaryotic chromosomes, which keep the cell's genomic stability and integrity. Because conventional DNA polymerases cannot replicate the very ends of linearized DNA, telomeric sequence (TTAGGG repeat arrays) is gradually lost during cell division and aging. For example, normal peripheral blood mononuclear cells loose up to about 100-base pair telomeric sequence per year (Iwama et al., 1998). Deregulation of telomere length is associated with various diseases: accelerated telomere shortening exacerbates premature aging in the patients with Werner and Hutchinson–Gilford progeria syndromes, whereas inefficient telomere maintenance in the patients with dyskeratosis congenita causes bone marrow failure. Premalignant hyper-proliferative lesions give rise to shortened telomeres, which are eventually stabilized by telomerase-mediated telomere replenishment in cancer. Accordingly, telomere length is referred to not only as a “mitotic clock”, which counts the number of normal cell division, but also as a biological marker of aging. Recently, telomere length has also been established as a surrogate marker for disease and lifestyle: shortened leukocyte telomeres are associated with a wide range of threat to life, including cardiovascular disease and psychological stresses (Haycock et al., 2014, Lin et al., 2012).

Predicting Risk at the End of the End: Telomere G-tail as a Biomarker