Gene associated with breast cancer may play major role in prostate cancer ...( that the driving force for recurrence ...)

that the driving force for recurrence of prostate cancer is the reactivation of the androgen receptor, which normally requires the presence of androgen, and this reactivation of the androgen receptor underlies tumor progression of prostate cancer despite hormonal therapy. Exactly how this occurs, we're not sure, but our hypothesis is that activation of HER-2 tyrosine kinase leads to activation of the androgen receptor."

In testing their hypothesis, Whang and his co-authors inhibited HER-2 activity in two laboratory experiments involving human cancer cells. In the first, they used an artificial antibody to HER-2 delivered directly into the cells via a modified virus. In the second, they used an experimental drug that specifically inhibits HER-2 tyrosine kinase activity. The oral drug lapatinib (GlaxoSmithKline) is currently in an advanced clinical trial involving patients whose breast cancer is driven by HER-2.

In both experiments, tyrosine kinase activity and androgen receptor function were largely derailed.

"We discovered that inhibition of HER-2 strongly inhibits proliferation of prostate cancer cells and the function of androgen receptor," Whang said.

To properly carry out its function, the androgen receptor protein binds specifically to the regulatory DNA sequence of the genes regulated by androgens such as testosterone, he said. "And we have shown that inhibition of HER-2 impairs the androgen receptor function at this step of binding to the DNA sequence of critical genes such as prostate specific antigen."

The implication of this work, he added, is that HER-2 is important and necessary for prostate cancer viability and progression.

"This provides the rationale for initiating a clinical trial of this novel drug inhibiting HER-2, which is being planned for patients within several months," Whang said. "I envision this drug becoming one of several that could be used in combination with other specifically targeted drugs to prolong the
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Contact: L. H. Lang
llang@med.unc.edu
919-843-9687
University of North Carolina School of Medicine
20-Apr-2005

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