A New Chapter Begins With CML

Hope is growing for patients who are living with CML. 
At first, Kelly Starling just felt numb. When the 46-year-old heard on August 23, 2012, that she had chronic myeloid leukemia (CML), her biggest concern was that her three adolescent children would have to watch her go through the trials of chemotherapy, lose her hair and suffer the awful side effects. But then, like so many other patients diagnosed with CML, she was told, “If you’re going to have leukemia, this is the very best kind to have.”

This isn’t always the most comforting follow-up to a cancer diagnosis, but it refers to the fact that CML is a very treatable leukemia that rarely causes death — that wasn’t always the case.

Chronic myeloid leukemia develops when certain bone marrow cells acquire a mutation that causes white blood cells to grow out of control. Until 2001, scientists had no way to stop the cells with mutations from taking over. Interferon could extend a patient’s life up to five or 10 years, but the only cure was and remains a stem cell transplant. This involves high doses of chemotherapy to kill the leukemia cells, but this also damages normal bone marrow cells. A stem cell transplant can then take place. The most common is an allogeneic transplant, where the stem cells come from a donor.

However, when the new drug Gleevec (imatinib) was approved in May 2001 by the Food and Drug Administration (FDA), it exceeded everyone’s expectations and permanently changed the landscape of CML treatment. Gleevec converted an almost certain death sentence into a normal life span, usually with a reasonably good quality of life. But there was a catch: Those living with CML would need to take an increasingly expensive medication daily for the rest of their lives. Now, new evidence suggests that edict is changing.

Gleevec is a tyrosine kinase inhibitor (TKI), a drug that targets the protein in CML that directs white cells to multiply uncontrollably, and thereby, prevent other bone marrow cells from properly developing. This protein, which produces the enzyme tyrosine kinase, is itself produced by the fusion of two genes, the ABL gene on chromosome 9 and the BCR gene on chromosome 22. Their fusion, which is due to a chromosomal breakage and reconnection known as a translocation, creates the “Philadelphia chromosome” that characterizes CML.

Five FDA-approved TKIs inhibit this errant protein’s signal: Gleevec, Sprycel (dasatinib), Tasigna (nilotinib), Bosulif (bosutinib) and Iclusig (ponatinib). Gleevec was the first TKI, but second-generation drugs Sprycel and Tasigna have joined it as first-line treatments and may induce a stronger response than Gleevec. Bosulif and Iclusig are currently only used in patients who develop resistance or intolerance to the three first-line TKIs or develop a mutation, such as the T315I mutation.

Starling had become one of the more than 8,000 people newly diagnosed with CML in the United States each year. Soon she would become one of more than 70,000 people in the U.S. who live with it daily. And just over three years later, she would be among a few thousand or so to experience treatment-free remission.

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