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By February 2008, Foley's PSA had risen drastically—hitting 22—and his cancer spread to half a dozen lymph nodes. He had just returned from a conference in California, where more than 700 prostate cancer patients met to share stories, learn about how to live with their disease, and hear about new treatment options. “It was so encouraging to hear that the fact that I had slipped into advanced prostate cancer wasn't a death sentence,” says Foley. “There were still treatments that would allow me to keep going.”
When Foley returned to New York, Morris presented him with an alternative to chemotherapy: Sawyers' MDV3100 was in clinical trials, and Foley qualified to be one of the first patients to try it. He joined the trial—a dose escalation trial in which patients are put on increasing doses of the drug and checked for side effects.
Between February 8 and 15, 2008, thanks to MDV3100, Foley's PSA dropped from 22 to 12. In the next month it dropped to 2 and then a month later to less than 1. It's been undetectable since, and his lymph node tumors have all but disappeared. He'll continue on the drug until it stops working, Foley says, which he hopes is many years away.
“When you first get those high numbers, you never think you'll see low numbers again,” says Foley. “But it just dropped like a rock. I was blown away.”
Not all prostate cancers are the same. In the clinical trial that Foley attributes with giving him a second life, some patients didn't see such dramatic improvements. Sawyers is collaborating with Haber to determine whether there are different markers in the CTCs of patients helped by the drug versus those who saw less improvement. They want to develop a rapid screening test to show who the drug might benefit.
To complicate matters, there may be variety within a single patient's cancer. “One individual might have multiple distinct cancers within the prostate gland that are independently arising,” says Todd Golub, an HHMI investigator at the Dana-Farber Cancer Institute. Instead of one tumor that spreads, he hypothesizes, a cancer-ridden prostate could often have separate tumors, each genetically distinct.
“So if you sample one of these tumors,” Golub says, “it's not necessarily going to be predictive of how the other ones are going to behave. The tumor you die of may not be the tumor that was biopsied and genetically analyzed.”
It's a vexing problem—to analyze all these potentially different tumors in the prostate, the whole gland would need to be removed, and then there would be no measure of which tumors grew. This situation is, in part, leading to dead ends in prostate cancer research, Golub believes. He's collaborating with a group of researchers in Sweden, where the wait-and-see approach is used much more often than in the United States. Golub's Swedish collaborators have followed a large cohort of prostate cancer patients from early diagnosis to see whether their tumors worsen—this approach is more difficult in U.S. cohorts as the prostate is more often removed. To identify differences between prostate cancers, Golub is using DNA chips to quantify the genetics of bits of biopsied tumors.
He's also working—as many researchers are—to create drugs to target the fusion gene identified by Chinnaiyan.