Every time a healthy cell divides, its telomeres become slightly shorter. Scientists often compare telomeres to the plastic tips on shoelaces because they help protect chromosomes from fraying or breaking apart.
Eventually, telomeres shrink to a critical length, triggering a process called replicative senescence. At that point, the cell can no longer divide. This natural limit acts as one of the body’s important defenses against cancer.
Tumors must bypass that barrier to survive.
Many cancers accomplish this by reactivating telomerase, an enzyme that rebuilds telomeres and extends a cell’s lifespan. In melanoma, mutations in the TERT gene, which produces telomerase, are especially common. About 75% of melanoma tumors carry these mutations.
But there was a puzzle researchers could not explain.
Eventually, telomeres shrink to a critical length, triggering a process called replicative senescence. At that point, the cell can no longer divide. This natural limit acts as one of the body’s important defenses against cancer.
Tumors must bypass that barrier to survive.
Many cancers accomplish this by reactivating telomerase, an enzyme that rebuilds telomeres and extends a cell’s lifespan. In melanoma, mutations in the TERT gene, which produces telomerase, are especially common. About 75% of melanoma tumors carry these mutations.
But there was a puzzle researchers could not explain.
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