How can telomeres and telomerase contribute to cancer development?

Telomeres are repetitive nucleotide sequences at the ends of chromosomes that protect them from deterioration or fusion with neighboring chromosomes. Each time a cell divides, its telomeres shorten, which eventually leads to cellular senescence or programmed cell death (apoptosis). Telomerase is an enzyme that adds nucleotide sequences to the ends of telomeres, effectively extending their length and allowing for continued cell division.

In the context of cancer development, the activation of telomerase is significant because many cancer cells reactivate this enzyme, which helps maintain their telomere length despite repeated divisions. By preventing telomere shortening, cancer cells can bypass the normal limits on cell division, which contributes to their uncontrolled growth and proliferation. This ability to sustain telomere length allows cancer cells to evade the typical aging process that other somatic cells undergo, thus facilitating tumor progression and development.

The other options highlight processes that do not align with the behavior of telomeres and telomerase in cancer cells. It is important to understand the role of telomerase in maintaining telomere length to grasp how it impacts cancer biology and the potential avenues for targeting cancer therapies that involve telomere regulation.