UCSF scientists halt tumor growth by manipulating telomerase enzyme

differently than cells extracted directly from patients.)

If the strategy proves viable, one possible therapeutic approach, says Blackburn, would be conducting gene "anti-therapy," as was done in the current study. Another would be using an as yet-to-be-identified "small molecule" drug that could warp telomerase and mimic the mutation in the same portion of the telomerase enzyme as the mutated gene.

In either case, the goal would be to target therapy directly and exclusively at the cancer cells, rather than systemically, thereby avoiding the drawback of many current cancer drugs, which often damage normal tissues.

The fact that telomerase is not activated in the healthy cells of many tissues could help this effort. For instance, in its earliest stages, breast cancer has not spread to the cells of the breast epithelium or the surrounding stroma. These healthy cells do not express telomerase, and therefore would not be vulnerable to a mutated gene or drug that targeted the enzyme in the breast.

In prostate cancer, targeted telomerase therapy also might be possible. Prostate cells have certain activated genes that are inactive in all other cells types. Given this, the mutated telomerase gene theoretically could be placed under the "promoter" region of a prostate-specific gene, which would make its expression only take place in prostate cells. As the first step in prostate cancer treatment is to remove the prostate, any prostate cells remaining in the body could be presumed to be cancerous.

While it's too early to know whether the approach identified by Blackburn's team will bear out, the revelation that human cancer cells are acutely sensitive to mutations in the telomerase enzyme is worth exploring further, she says. "Success will depend on the details and identifying a method of delivery, but it is one of many reasonable targets out there."


Contact: Jennifer O'Brien
University of California - San Francisco

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