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Moffitt helps put lung cancer drug on fast track

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Moffitt Cancer Center is part of a national study of a lung cancer drug that is proving to be so effective, it's on a fast track for government approval.

Called crizotinib, it's part of the growing practice of "personalized medicine," in which drugs target specific cancer-causing genes found in patients' tumors.

"This is really promising," said Moffitt doctor Eric Haura, director of Moffitt's Lung Comprehensive Research Center.

"We're able to find these genes and offer therapy that's different from traditional chemotherapy."

He expects the drug to be approved within a year.

Crizotinib, a Pfizer drug, shrank the tumors of patients with a type of lung cancer that strikes about 50,000 people a year worldwide. Compared to standard treatment, it appeared to sharply increase their chances of survival.

Cancer specialists presented their crizotinib results at the recent American Society of Clinical Oncology conference in Chicago.

They expected to see results in only about 10 percent of the 82 initial patients in the study, all of whom were in advanced stages of the disease. Instead, about 90 percent responded.

Nearly three fourths of the patients were still alive after a year; more than half were alive after two years.

Doug Trucks, who's 56, is one of those patients.

The type of cancer that responds to crizotinib typically strikes younger people who have never smoked. Trucks was at stage four when he was diagnosed three years ago.

"They tell you the odds and you go through chemotherapy, knowing it is just to prolong things by a measure of months," Trucks said from his office in Orlando. He helps manage hotel room renovation for the Walt Disney World Resort.

After two years, the chemo became ineffective. Then he learned about the crizotinib trials. He found out Moffitt, on the University of South Florida campus, was enrolling patients, and early last year he was accepted into the study.

"You can imagine, it was like getting a lifeline," he said.

So far, it seems to have stopped his tumors from growing.

"Based on where I started and the amount of previous treatment I had, being stable is probably the best I can hope for," he said. He knows his tumors could become immune to the drug and start growing again, as they have with previous treatments.

"But I've learned to just hold on for that next treatment that may be out there."

And compared to the chemotherapy regimen he endured, taking one crizotinib pill twice a day is easy.

"I remember the hair loss and I remember the nausea and my finger nails falling off and the neuropathy in my feet," he said. "I have some balance issues now, but compared to the chemotherapy it's nothing."

What makes crizotinib different from standard chemotherapy is that it targets only the gene that causes the cancer.

Trucks' type of lung cancer starts when one protein in a cell fuses with another, known as ALK. That activates the ALK protein, which begins telling the cell to proliferate, initiating the cancer growth.

Crizotinib turns off the ALK protein.

Immediately the cancer cells begin to die, said Guiseppe Giaccone, head of the thoracic oncology section of the National Cancer Institute. "It's a very rapid thing. In a week, two weeks, you see this."

The sad thing about the trials now under way is that the patients aren't likely to be cured, he said. They were chosen partly because other treatments had already been tried and failed.

But researchers believe the drug could cure patients in the early stages of the disease, before it's had a chance to grow and spread. "We envision giving this to people immediately after surgery" in combination with other drugs, Giaccone said.

The other limitation is that crizotinib works only for people with the ALK gene, about five percent of all lung cancer patients.

But this isn't the only drug that offers hope, Haura said.

Moffitt is one of 14 centers across the country, the only one in Florida, in the Lung Cancer Mutation Consortium. It's recruiting patients to study several drugs that target other genetic changes that cause lung cancer.

"You can't cure cancers unless you understand the molecular basis of them," Haura said. "Now we're getting close, where we can read out all the genes and proteins.

"Imagine what a circuit look like. Now we can actually see what a cancer circuit looks like. And when you understand the circuitry and master regulators, that tells you what to aim for."

For more information about the Lung Cancer Mutation Consortium trials, go to www.golcmc.com.

http://www2.tbo.com/news/breaking-news/ ... ar-236518/

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Fascinating concept that there is an idea that early use of crizotinib post surgery might actually be a cure! I assume they are only looking at that in early stage disease since surgery is not usually an option in late stage lc.

I know of a couple of women who were given Tarceva post surgery, with no tumor burden remaining. One stopped after 6 months, the other after two years - and both continue to be NED. The question remains as to whether they would be NED without having taken Tarceva - did surgery complete the job? Same would be true with this agent. But it does make a larger sales base for the maker.

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