The paper:
C. Chen et al., "Molecular determinants of resistance to antiandrogen therapy," Nat Med, 10:33-9, 2004. (Cited in 176 papers)
The finding:
Using gene-expression profiling, Charles Sawyers then at the University of California, Los Angeles, and collaborators found consistently elevated levels of androgen receptor mRNA in hormone therapy-resistant prostate cancer xenografts.
The surprise:
In cells with elevated androgen receptor levels, they found that the anticancer drug flips from inhibiting cell growth to stimulating it. This could potentially explain a clinical observation that some prostate cancers grow when treated with anti-androgen therapy.
The follow-up:
Using cells that express high levels of androgen receptor, Sawyers' lab is hunting for compounds that function like the current anti-androgen drugs, without stimulating growth. One of these compounds has already been licensed by a small company for preliminary testing.
Sawyers' take:
"Our experiments led to this completely serendipitous and unexpected finding about the flip from ...
