<"It's not what a lot of people think," says Kantoff. "It's not a home run; this is not going to cure prostate cancer, it's not going to make tumors go away. But on the other hand, it improves survival.">
Dr. Kantoff likely said much more than that but that's the catchy part so it was quoted. The question that a critical reader should ask is why Provenge "improves survival" even though it did not "make tumors go away"?
The answer lies in how Provenge works. It trains the immune system to first hunt for stray tumor cells on a long term basis so that they cannot spread to other parts of the body and second to attack any existing tumors. The long-term hunt for stray tumor cells is what makes Provenge different from drugs such as Taxotere and Avastin that aim mostly at destroying established tumors on a short-term basis.
The key in the Provenge trials was that enrolled patients must be free of any sign of metastasis to vital organs. The long-term hunt for stray tumor cells prevented the disease from spreading to places that could kill. That's what improved the chance for survival of treated patients over placebo ones.
The same protective mechanism could make Provenge a potentially good treatment to use in the early phase of the disease before it gets out too far from the prostate. Circulating Tumor Cells counting (click here
) is gaining some acceptance as a predictor for survival and could be accepted as a surrogate endpoint for prostate cancer trials. IMO, it would be easy to test the effectiveness of Provenge in reducing CTCs.
As I posted earlier, perhaps a new trial of Provenge in the Androgen-Dependent PC stage could be started to test for CTCs. That could go fairly quickly and could even be timed to finish at the same time as the P-11 trial for its Time-To-Metastasis endpoint. Then, if P-11 succeeds, a label extension to ADPC can be attempted with the additional data in a few years - perhaps even 2012.