In the past few years, the breakthrough drug imatinib has changed chronic myeloid leukemia from a death sentence to a treatable disease. But 17 percent of patients taking the drug, also called Gleevec, become resistant to its protective effects over 5 years, and their cancer recurs.
Now, two experimental drugs pick up where imatinib leaves off. In many patients with chronic myeloid leukemia (CML) that's impervious to imatinib, the new compounds suppress the malignancy, two studies show.
"In the 1990s, when we saw a patient with CML, we gave them the bad news that they were going to live 3 to 5 years," says hematologist-oncologist Hagop Kantarjian of the M.D. Anderson Cancer Center in Houston, who coauthored both studies. With imatinib and the new drugs, most CML patients may live a normal life. "And with some refinements, these drugs might cure most patients," Kantarjian adds.
The new drugs, called dasatinib and nilotinib, target the same protein that imatinib does (SN: 1/1/05, p. 14: Available to subscribers at http://www.sciencenews.org/articles/20050101/note22.asp). Called Bcr-Abl, this abnormal protein causes the leukemia by disconnecting the brakes on cells' replication machinery. Like imatinib, both nilotinib and dasatinib bind to Bcr-Abl, thereby killing the cancerous cells that harbor it.
However, the new drugs bind tightly even after the gene that encodes Bcr-Abl has mutated such that imatinib can no longer bind to the altered protein.
Kantarjian and his colleagues tested nilotinib and dasatinib in 180 patients with CML and 23 with a related leukemia. All were resistant to or couldn't tolerate imatinib. Patients received nilotinib for 2 to 9 months or dasatinib for 2 to 19 months.
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