Many cancers have shortened telomeres, including pancreatic, bone, prostate, bladder, lung, kidney, and head and neck. Measuring telomerase may be a way to detect other types of cancer as well. And if scientists can learn how to stop telomerase, they might be able to fight cancer by making cancer cells age and die. In one experiment, researchers blocked telomerase activity in human breast and prostate cancer cells growing in the laboratory, prompting the tumor cells to die. But there are risks. Blocking telomerase.

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​Progressive telomere shortening occurs with each cell division up to a point termed “replicative senescence” in most mature human  cells72. Basic biology studies have established that telomere shortening is a fundamental feature of dividing cells and directly related to the age of the cell lineage, and that telomere crisis in the present of defective cell-cycle control can lead to chromosomal instability and a malignant phenotype73. The dysfunctional telomeres will result in chromosomal fusions, continuous “breakage-fusion-bridge” cycles, derived chromosome imbalances, gene amplifications, and ultimately the generation of complex non-reciprocal translocations, a hallmark feature of adult solid tumors and genomic instability in general74. At the population level, the high incidence of cancer has prompted that shortening of telomeres promotes tumor development and several studies have found that patients with shorter telomeres in peripheral blood cells have a higher risk of developing carcinomas75.