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Two decades ago, a diagnosis of chronic myelogenous leukemia was a death sentence.

But new drugs introduced in the past six years mean that Toronto Maple Leafs forward Jason Blake and thousands of others with CML can expect to live full and active lives.

In fact, experts say the successes with CML could hold promise as a model for treating other cancers. Because scientists have identified the specific mutation that causes CML, they have developed drugs that target only the cancerous cells — an elusive goal for many cancer researchers.

"There's a lot of hope out there," says Hildy Dillon, the Leukemia and Lymphoma Society's vice-president for patient services and disease programs. "It's a very exciting area in terms of cancer research."

Mr. Blake announced yesterday that he has CML and that he's taking medication for it and doesn't plan to miss any playing time.

About 3,000 Canadians are living with this type of leukemia, according to the CML Society of Canada, and about 460 new cases are diagnosed each year. The early symptoms include tiredness, night sweats, weight loss and fever, while advanced cases have more specific symptoms such as an enlarged spleen and anemia.

Most cases are caught early when a routine blood test shows a high white blood cell count, an indicator of leukemia. If untreated, the disease is fatal within about five years.

But the prognosis for CML patients improved dramatically in 2001, when the U.S. and Canadian health authorities approved a drug called Gleevec, which puts about 80 per cent of CML patients into remission, Ms. Dillon says.

In March of this year, Canada approved use of a second drug, Sprycel, for patients for whom Gleevec causes bad side effects or doesn't work.

"We have basically turned this into a chronic disease," says leukemia expert Jerry Radich, a doctor with the Fred Hutchinson Cancer Research Center in Seattle. While some patients do suffer from side effects such as swelling, gastro-intestinal problems or bone pain, such symptoms are rare, Dr. Radich says.

The combination of drugs "doesn't necessarily cure the disease," Ms. Dillon says, "but it manages the disease well enough that people can live a normal life and go on with their normal activities."

And if your normal activities include fast breaks and being slammed into the boards, experts say, there's no reason for CML to stop that.

Mr. Blake, who practised with the Leafs yesterday, isn't the only CML patient on the ice. Tim Linklater of Burnaby, B.C., who was diagnosed a year ago, played hockey with his neighbourhood league yesterday. His wife, Shalyn Linklater, is active with the CML Society of Canada.

"He's doing amazing," says Ms. Linklater. In the 1980s, one of her cousins died of CML nine months after being diagnosed. By contrast, her husband takes Gleevec daily, snowboards and runs in addition to playing hockey. He keeps up with their three children and never missed a day of work due to CML.

"His quality of life is very good," Ms. Linklater says. The CML Society is sponsoring a wellness retreat in Toronto this November and a fundraising trip to climb Mount Kilimanjaro in February.

One reason CML is so treatable is because the genetic abnormality that causes the cancer was discovered more than 40 years ago, and has been intensely studied ever since.

CML occurs when sections of two chromosomes switch places, creating an extra-short chromosome that's called the Philadelphia chromosome after the city where researchers discovered it.

This mutated gene causes the body to produce too many white blood cells, which eventually build up and crowd out healthy blood cells.

Researchers still don't know why the chromosome switch happens, but they do know what to look for and, more importantly, how to stop it.

The drugs developed for CML target only the cells with the cancer gene, thus avoiding the blitzkrieg approach of many other cancer drugs. That's why patients being treated for CML usually have minimal side effects.

Although it is rare, CML is a well-researched disease because experts hope it will give them clues for fighting other types of cancer in the same targeted way.

"This was the first cancer where we knew what gene was involved," Dr. Radich says. "It's a good model of what we think is going on in all cancers."