University of Central Florida (UCF) BSC2010C Biology I Practice Exam 3

Cancer cells have a unique ability to maintain or even lengthen their telomeres, which allows them to divide indefinitely and evade normal cellular aging processes. Normally, as cells divide, telomeres—protective caps at the ends of chromosomes—shorten, leading eventually to cellular senescence or apoptosis (programmed cell death). However, cancer cells often express the enzyme telomerase, which can extend telomeres by adding repetitive nucleotide sequences back to the ends of the chromosomes. This action effectively stabilizes the telomeres and provides the cancer cells with a survival advantage, contributing to their uncontrolled proliferation.

Understanding this mechanism is crucial in cancer biology, as it highlights a potential target for therapeutic interventions aimed at inhibiting telomerase activity, thereby inducing senescence in cancerous cells. This contrasts with normal somatic cells, where telomerase is typically inactive, and telomere shortening serves as a cellular clock that limits the number of divisions a cell can undergo.