Winning the War on Cancer (page 2 of 3)

Smart-Bomb Designer Drugs

"Now that we're beginning to understand the process of how a cell grows and spreads, we are beginning to see places where we can intervene," says Dr. von Eschenbach. Traditional treatments like chemotherapy work by killing cancer cells, but they may also be toxic to the body's noncancerous cells. The war on cancer is evolving from the "atomic bomb" approach of wholesale destruction of both cancerous and healthy tissue to the "smart bomb" approach of isolating the target and designing treatments that will home in and destroy only those targets, leaving the healthy cells alone.

Because targeted drugs are so specific, side effects are relatively minimal. Thus, for Doug Jenson, whose hematologist took him off the interferon he was taking to treat his chronic myeloid leukemia (CML) because he said it was "killing you faster than the leukemia," these smart drugs came in the nick of time.

In 1998, Jenson, a 64-year-old father and grandfather, had no other options. "What do you think about going on an experimental drug that no one else has ever taken?" asked Brian Druker, MD, the driving force behind Gleevec, one of the hottest new cancer medications. Gleevec would supposedly attack the enzyme that was fueling the growth of Jenson's leukemia cells. "I was so sick before I went on Gleevec that the most I could do was get up in the morning, go down the stairs, and sit in a big recliner by the window until it was time to go to bed," says Jenson, now 72. "Today I'm as good as I was before I was diagnosed. Since I've been on Gleevec, I've been to Guatemala twice, to New York City for New Year's Eve. I go to the health club; I ride my bike. My leukemia is undetectable."

Before Gleevec came along, the average survival for a patient diagnosed with CML was about four to six years. Interferon, the standard therapy for CML, could prolong survival for another one or two years, if a patient could tolerate it or was among the few who responded well. In the four years since Gleevec has been on the market, only 16 percent of newly diagnosed patients on Gleevec have relapsed. "If those numbers stay on track, the average survival could be in the 15- to 20-year range," notes Dr. Druker, director of Oregon Health & Science University's Center for Hematologic Malignancies. "That's a huge difference." It turns out that because the enzyme that drives the growth of a kind of stomach cancer called gastrointestinal stromal cancer (GIST) is similar to the enzyme at work in CML, Gleevec has also turned the prognosis of that disease around. "Before Gleevec, there was no effective treatment for GIST," says Dr. Druker. If the tumor wasn't operable, or the surgeon couldn't remove the entire tumor, patients lived an average of one to two years after diagnosis. More than half of the GIST patients taking Gleevec show little sign of active disease.

Another exciting advance is the study of angiogenesis, the process by which tumors create new blood vessels, says William W. Li, MD, president and medical director of the Angiogenesis Foundation. Without it, tumors can't grow past the size of a grain of rice. A new therapy called antiangiogenesis cuts off the blood supply necessary for tumor growth. Avastin, the first antiangiogenesis designer drug, improved survival when added to standard chemotherapy in patients with advanced nonsquamous, non-small cell lung cancer (the No. 1 cause of cancer death in the United States) by 30 percent, compared with patients on chemo alone. Approved last year for the treatment of advanced colorectal cancer, Avastin was also found to shrink tumors, and extend life, in metastatic breast cancer patients. "Avastin is the flagship in a fleet of antiangiogenesis drugs that are part of a medical revolution," says Dr. Li, noting that there are 97 such drugs currently undergoing human clinical trials worldwide. Stop the growth of blood vessels, and you should theoretically prevent the spread of cancer.

Pharmaceutical companies are focused on getting new targeted therapies approved and marketed as quickly as possible. And the pace of research surrounding these drugs is staggering. "There are so many exciting discoveries that we had to spend extra time at this year's annual meeting teaching doctors about all the new findings that benefit their patients," says David Johnson, MD, immediate past president of the American Society of Clinical Oncology. "The sense of urgency is there, because the advances we're seeing are really substantive." For example, though the drug Herceptin is now commercially available, it is approved only for women with advanced breast cancer who take it in combination with chemotherapy, or alone if they've already had one or more regimens of chemotherapy. Two recent studies showed that when Herceptin was combined with chemotherapy in women with earlier-stage disease, the recurrence rate decreased by more than 50 percent, compared with those who only had chemo. None of these new therapies is a magic bullet, however: Over time, cancers could become resistant to certain antiangiogenesis drugs, and some genetic-based therapies benefit only patients who have the specific gene mutation being targeted (350 have been identified so far). In fact, the National Cancer Institute will begin work on identifying them all so that diagnosis and treatment eventually may be tailored according to tumor type.

• • Colon Cancer
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