Date:2/16/2012

in a tumor-promoting way," Ford says. Patients whose tumors have high SIX1 or associated microRNAs are likely to benefit from "TGF-beta inhibitors" drugs that turn off the signal that are currently in clinical trials. Conversely, patients with low SIX1 are best left with TGF-beta signaling intact in this case, the signal is likely helping these breast cancer patients fight against their tumors.

In the future, Ford hopes to target SIX1 directly.

"Because we don't need it in most adult tissues, if we could target SIX1, we could probably inhibit the tumor on multiple fronts with few side effects," she says.

Stay tuned: now with the SIX1 target in sight, Ford and collaborators at the CU Cancer Center are developing novel drugs to stop this tumor-promoting factor.

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Contact: Garth Sundem garth.sundem@ucdenver.edu University of Colorado Denver Source:Eurekalert

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