Telomere length maintenance mechanisms in cancer

chromosomes and are composed of TTAGGG hexanucleotide repeats. In somatic cells, telomeres shorten upon each cell division ultimately resulting in activation of DNA damage response followed by senescence or cell death. However, cancer cells activate telomere length maintenance mechanisms (TMM) to overcome telomere attrition and attain replicative immortality which therefore represents one of the principle hallmarks of cancer. Two major pathways are employed by cancer cells to maintain telomeres. First is activation of telomere elongating enzyme called telomerase and second is alternative lengthening of telomeres (ALT). In addition, telomeres are bound by an end protection complex called as shelterin which has an essential role in regulating telomere length maintenance. Thus, TMM and telomere structure and function regulatory pathways represent an attractive target for development of anticancer therapeutics.