What genetic change can lead to cancer via telomerase production?

The activation of telomerase plays a crucial role in the development of cancer by allowing cells to maintain their telomeres, which are the protective caps at the ends of chromosomes. Normally, telomeres shorten with each cell division, leading to eventual cellular senescence (the process by which cells stop dividing) or programmed cell death (apoptosis). This limitation acts as a barrier to unlimited cell proliferation.

In cancer cells, the reactivation or overexpression of telomerase enables them to maintain their telomeres, avoiding the senescence that typically accompanies extensive division. By preventing the natural shortening of telomeres, cancer cells can continue to divide indefinitely, contributing to tumor growth and the potential for metastasis. This transformation allows typically regulated cells to behave like stem cells, perpetuating the cell cycle without the normal controls that prevent excessive proliferation.

In contrast, the other genetic changes listed—such as inversions, duplications, or deletions—do not have a direct role in telomere maintenance. While these alterations can lead to various forms of genomic instability or dysregulation, they do not specifically enable the sustained cell division characteristic of cancer like the activation of telomerase does.