supports the idea that if you have c-jun in a cancer cell, it could
be a drug target for those tumors that have it as a basis of the
mutation," Wisdom said.
comes to UC Davis from the Salk Institute for Biological Studies
in San Diego, where he was a postdoctoral researcher. Enthusiastic
about the clinical implications of his research, Chen is zeroing
in on how the hormone estrogen binds to receptors and how those
receptors turn on the engine of gene transcription. Estrogen fuels
breast cancer cell growth, as testosterone spurs prostate cancer.
Clinicians often treat these cancers with hormone therapy, drugs
that block estrogen or testosterone from binding to receptors, which
arrest cancer growth. But, at some point, this hormone blockade
therapy stops working and the cancer progresses.
are trying to understand exactly what happens when this occurs,"
said Chen, an assistant professor of biological chemistry. "This
is where the basic science kicks in."
the past 10 years, scien- tists had a cut-and-dried theory that
explained the biological basis for breast and prostate cancer: the
hormone receptor binds to the hormone and acts as the engine within
that cell to turn on genes that control cell growth.
now, a new theory has arisen.
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fellows in Cheněs lab collect cells grown on a plate for a functional
analysis of the genes.