CSHL study shows that some malignant tumors can be shut down...(at shuts down the tumor. Using a ge...)

Using a genetic maneuver called chromosome engineering, the CSHL team has found that TAp63 staves off cancer via senescence. The maneuver enabled them to specifically wipe out the TAp63 proteins while leaving the other p63 proteins intact. When exposed to the cancer-causing protein Ras, normal cells underwent senescence and could not form tumors. But cells without TAp63 failed to undergo senescence and developed into massive tumors.

When p53 and TAp63 were both missing, Ras caused extremely rapid and aggressive tumors. This tumor growth was much more severe than in tumors lacking either TAp63 or p53, suggesting that the two related proteins, working together, pack a stronger anti-cancer punch than either one alone.

A future anti-cancer strategy?

The team found that TAp63 could also substitute for p53 in its ability to halt tumor growth. When TAp63 was turned on in Ras-producing cells that were missing p53, tumors never started. "This suggests that TAp63 overrides cancer-promoting signals and prevents cancer from even forming," explains Mills.

The team went a step further and showed that in addition to blocking the initiation of tumors, TAp63 could also shut down tumors that were already established. With help from Professor Scott Lowe, Ph.D., another researcher at CSHL, Mills' team genetically tricked tumors into producing TAp63 when they were exposed to a compound called doxycycline.

Now being able to turn on TAp63 at will, the team transplanted these cells (which lack p53 and overproduce Ras) into mice and monitored for tumors. Once the tumors formed, a "mouse clinic" was set up: half of the "patients" were treated with doxycycline to induce TAp63 production, whereas the other half received a placebo. Tumor growth continued in the placebo group, with the tumors becoming five times larger within a week. In contrast, the tumors in the mice exposed to doxycycline were abruptly s
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