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A question worth answering: why don’t cancer cells die?

Yale Medicine Magazine, 2003 - Winter


When cells become cancerous, they grow unrestrained and sometimes ignore signals that would normally induce them to die. “What are the genetic functions,” Nobel laureate Harold E. Varmus, M.D., asked in a November 1 campus talk, “responsible for sustaining the life of cancer cells?” Varmus, president and chief executive officer of Memorial Sloan-Kettering Cancer Center and the former director of the National Institutes of Health, gave the keynote address at the 2002 Graduate Student Research Symposium, an annual event that brings speakers to campus and provides graduate students a venue for presenting research in progress.

In his address Varmus described how his laboratory has used new ways to study those genetic functions in mouse models of lung and ovarian cancers. Varmus and colleagues controlled expression of a mutant gene by dosing mice with the antibiotic doxycycline: in this way they could induce lung cells to become cancerous. Halting the drug dosages abruptly reduced the expression of that gene, K-ras, and triggered the death of the tumor cells, causing the cancers to melt away.

His laboratory is attempting to understand how genes like K-ras “protect cells from cell death” and what happens when the cells lose K-ras function and die. From there, the goal will be to figure out “how to trigger a similar response in humans,” which, Varmus suggested, could prove key to developing new treatments for the deadly cancers.

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