Re: Role of Telomeres and Telomerase in Cancer

The most important difference between cancer and normall cells is the ability to continuous proliferation. This activation works due to telomeres and telomerase enzyme. Fifty years ago, Leonard Hayflick discovered that cultured normal humans cells have a limited capacity to divide. Today, this withdrawal from the cell cycle after a certain number of cellular divisions (replicative senescence(definition)) is known to be triggered as a result of shortened telomeres. Studies on telomeres and telomerase have begun to provide additional information about aging and cancer development and have created new opportunities in the field of regenerative medicine for telomeropathies. Progressive telomere(definition) shortening from cell division (replicative aging) provides a barrier for tumor progression. Continuous cell growth in malignancy correlates with the reactivation of telomerase. Telomerase is a cellular reverse transcriptase that adds new deoxyribonucleic acid (DNA) onto the telomeres that are located at the ends of chromosomes. Telomeres consist of many kilobases of TTAGGG nucleotide repeats. The telomeric nucleotide repeats shorten with each cell division due to replication problems (DNA repair) and oxidative damage. Quiescent/senescent state of the cell bypass can be accomplished by abrogating cell cycle checkpoint genes (such as TP53, p16INK4a, pRb). Telomerase is detected in approximately 90% of all malignant tumors. This telomerase activation has emerged as a target for cancer treatment. Telomerase therapeutics are classified as gene therapy (hTERT-telomerase catalytic protein component, hTR-telomerase functional), immunotherapy (Imetalstat-telomerase template antagonist), and small molecule inhibitors. In the near future, more specific researches on telomers and telomerase will contribute to aging/immortality studies (as stem cells) and to discover new biomarkers for malignant tissue or anticancer therapeutics.