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Telomeres and telomerase have a dual role in cancer initiation and progression. Telomere shortening can induce chromosomal instability, environmental alterations, and cancer initiation. In contrast, telomere shortening induces checkpoints that limit tumor progression, and the stabilization of telomeres represents an essential step during tumorigenesis. The disclosure of molecular mechanisms downstream of telomere dysfunction, as well as of mechanisms that can stabilize telomere function, will likely be of clinical value to improve cancer treatment, prevention, and screening.

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