One of the fundamental differences in the behavior of human normal versus tumor cells is that most normal cells divide for a limited number of times (Hayflick Limit) whereas tumor cells can proliferate indefinitely (one of the hallmarks of cancer). It is widely believed that the biological function of cellular aging (senescence) is to serve as a mechanism for restricting cancer progression. It is now established that almost all advanced cancers express telomerase, and this provides the molecular mechanism for the bypass of both telomere-associated senescence. The following topics/questions will be discussed in this lecture.

1. Evidence that the telomere-based mechanism of cellular aging in human cells has held the test of time

2. The role of telomerase in bypassing telomere-based replicative senescence proves that the growth arrest of human cells with critically short telomeres is a key molecular basis of human cell aging

3. Progress in using telomerase inhibitors in targeting cancer

4. Development of accurate methods to quantitatively measure the shortest telomeres

5. Methods for safely using telomerase or telomerase activators for identifying and treating telomere diseases associated with aging?

Goals and Objectives

1. To review the evidence that telomeres are a biomarker that is important in human aging and cancer.

2. To review the evidence that introduction of telomerase into normal cells does not lead to an increased risk of cancer and inhibition of telomerase can lead to cancer cell death

3. To review human diseases associated with telomere dysfunction and approaches to identifying and treating telomeropathies

Citation Format: Jerry W. Shay. The role of telomeres and telomerase in aging and cancer. [abstract]. In: Proceedings of the Eleventh Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2012 Oct 16-19; Anaheim, CA. Philadelphia (PA): AACR; Cancer Prev Res 2012;5(11 Suppl):Abstract nr PL01-01.

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