Maintaining the ends of chromosomes, called telomeres, is a requisite feature of cells that are able to continuously divide and also a hallmark of human cancer. “Telomeres are much like the plastic cap on the ends of shoelaces -- they keep the ends of DNA from fraying,” says Roger Greenberg, MD, PhD, associate professor of Cancer Biology in the Perelman School of Medicine at the University ofPennsylvania. In a new study published this week in Cell, he and his colleagues describe a mechanism for how cancer cells take over one of the processes for telomere maintenance to gain an infinite lifespan.

Telomeres stay intact in most cancer cell types by means of a specialized enzyme called telomerase that adds the repetitive telomere DNA sequences to the ends of chromosomes. Cancer cells can also use a second method involving a DNA-repair-based mechanism, called alternative lengthening of telomeres, or ALT for short. In general, cancer cells take over either type of telomere maintenance machinery to become immortal. Overall, approximately fifteen percent of cancers use the ALT process for telomere lengthening, but some cancer types use ALT up to 40 to 50 percent of the time. 

Greenberg’s co-authors of the new findings are Nam Woo Cho and Robert L. Dilley, both MD/PhD students in his lab, and Michael A. Lampson, an associate professor of Biology at Penn. Greenberg is also an associate investigator at the Abramson Family Cancer Research Institute and director of Basic Science for the Basser Research Center for BRCA.

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