Yehia Daaka’s team at UF studies ways prostate cancer cells get around current treatments.

Seventy years ago, scientists were still looking for the silver bullet cure for cancer: a single treatment that would eliminate the dreaded disease.

Researchers thought they had found it with prostate cancer. They identified a link between prostate cancer cells and testosterone and showed that the hormone acted like a fuel for the hungry, growing cancer. Eliminate the testosterone and starve the cancer, they thought.

It worked — for a while. Prostate cancer proved itself far more complex and too good at adapting to fall for a single cure.

Yehia Daaka is one of the leading prostate cancer scientists in the world today. He is engaged in groundbreaking work inside the University of Florida's Cancer Genetics Research Complex on Mowry Road.

But he, like other scientists, no longer looks for silver bullets. The 51-year-old Daaka is looking to solve just a sliver of all the various ways prostate cancer cells adapt and change to stay alive with the invariable result of killing many of its hosts.

Daaka and his team look upon the war against prostate cancer as a series of battles. Gaining ground in the laboratory is measured in modest inches.

The team's research focuses on biological roadblocks: ways to block some of the avenues prostate cancer cells take to get around current treatments. It's not the kind of research that often gets headlines, but if the work is successful in shutting off even some of these avenues, it could save thousands of lives every year.

The work is slow-going.

"It takes time. It takes patience," said Daaka, a specialist in biochemistry and pharmacology. "You're never going to find instant gratification in the work we do."

The work Daaka faces is daunting because the same ways healthy prostate cells adapt to survive under environmental stresses, so do cancer cells. They share the same biological arsenal, and the arsenal is awesome. Or as Daaka likes to describe it admiringly: a well-greased machine.

The essentials

The research Daaka is doing is complex, but the essentials are simple.

Healthy prostate gland cells have growth factor receptors on their membranes that attach to growth hormones called androgens. The growth factor receptors function like radio towers capturing radio waves that tell a car radio what music to play.

One such growth factor is testosterone, important in sperm health and the formation of other male characteristics. The hormone is also important in getting healthy cells to divide, replacing themselves and repairing the prostate.

In healthy prostate cells, those receptors send signals to structures inside the cell called androgen receptors. Once the androgen receptors get the signal, they then slip into the cell's nucleus, where genetic DNA is stored. Together, they tell the cell to divide.

In cancer cells, the mechanism that tells the cell to divide at a healthy rate is broken and keeps dividing, like a copy machine run amok.

The tactic scientists have taken to find a cure is trying to interfere with the way the androgen receptor gets its signal and is told to go into the nucleus. The thinking behind the strategy: shut off the fuel, stop the machine.

But in the case of prostate cancer cells, once they have a taste for growth factors, there's almost no stopping them, Daaka said. That was also seen 70 years ago, when chemical castration and stopping the flow of testosterone didn't stop prostate cancer. Instead, the cancer went away for a year or so only to come back, and usually with a vengeance.

Three strategies

Prostate cancer cells typically follow three strategies when confronted with treatments that shut off the testosterone pipeline.

About a third of cancer cells simply grow more growth factor receptors to absorb what testosterone is still made throughout the male body. It's equivalent to building more radio towers to pick up fewer and weaker radio signals.

Another third mutate their growth factor receptors to pluck growth factors other than testosterone from their environment. In the radio analogy, it's as if the radio towers can't pick up FM signals anymore so a repairman scuttles up the tower and makes a few changes to capture AM waves instead. The radio never knows the difference.

The last third of prostate cancer cells adapt by drafting receptors along the cell membranes that normally never interact with androgen receptors. The cancer cells use those new receptors to now grab whatever growth factors are floating by. The drafted receptors then send androgen receptors the signal to head to the cell's nucleus and start replicating unabated.

That last third is where Daaka comes in.

He and his team have identified a whole family of hijacked receptors, until now unknown to scientists, as being taken over by cancer cells.

That might not seem like much to most laypeople, but to experienced researchers it's like identifying a cell of terrorists helping to make a bomb.

The next step is to determine how it gets that bomb to the person who sets it off. In the language of prostate cancer cell research, Daaka is trying to find out how those hijacked receptors are sending their signals to the androgen receptor.

If he can figure that out, the next step is to block the signal. If the signal is blocked, it shuts down one more set of ways prostate cancer cells dodge treatment bullets.

But identifying how growth factor receptors talk with androgen receptors won't take decades, at least not in this Internet age, Daaka said.

Because researchers have easy Internet access to what other cancer colleagues are doing in their fields, there's a lot of information sharing, he said. That means that once he identifies one of his signals, another researcher may already know how to block it.

It's a team effort, Daaka said, with the end goal of saving lives.

Daaka said his work won't mean an end for all prostate cancers; it's more about cutting off one more escape route, the same way police set up road blocks to stop a bank robber.

Daaka said that by cutting off ways for prostate cancer cells to adapt, it also keeps their unbridled growth in check. For every dead end researchers can lay in the cancers' path, the more time doctors can buy for their patients.

In the meantime, Daaka said he'll continue fighting the prostate cancer battle for inches, coming to the lab during weekends and holidays to work for a little more ground.

"It's like a drug," he said, describing his research and finding something no one else has before him. "And we believe we will get somewhere."

Reach Fred Hiers at and 352-867-4157.