(RxWiki News) Since the advent of targeted therapies, chronic myeloid leukemia (CML) has become easier to treat. And while the drugs usually put people into remission, the disease can return with full fury.
Using a combination of Gleevec (imatinib) and another targeted therapy, researchers have discovered a way to halt CML in mice. If this work translates to humans, CML may be wiped out totally.
"Stay on top of your CML; it requires regular and ongoing monitoring."
Leukemia stem cells are at the heart of why existing CML therapies can eventually fail. These immature cancer cells hang on for dear life and can bring CML back to life in the process.
Scott A. Armstrong, M.D., Ph.D., of the Harvard Medical School, directed this research which focused on mechanisms that are important in blood stem cells during development but not in adulthood.
This suggests that, at least in mice, leukemia stem cells go back to this early mechanism or pathway.
With this knowledge, researchers learned that these leukemia stem cells responded to Gleevec when this so-called β-catenin pathway was blocked or inhibited with a drug that targeted it.
In other words, when β-catenin inhibitors were given to mice, the leukemia stem cells disappeared. A pain medication currently available also reduced β-catenin levels.
This means that a combination therapy using Gleevec plus a β-catenin inhibitor could keep CML from returning, and that would be a huge advancement.
More work is necessary to make sure the β-catenin blockers work the same in humans as in mice.
If that's the case, CML patients and many others will benefit from a new treatment regimen, according to Dr. Armstrong.
"It will take time because people with CML already do pretty well," Dr. Armstrong says.
"But β-catenin inhibitors might be just what the doctor ordered in the case of some other, harder-to-treat forms of leukemia, in colon cancer, or perhaps in patients who have entered an acute stage of CML," Dr. Armstrong concluded.
This study was published in the April, 2012 issue of Cell Stem Cell, a Cell Press publication.
No financial disclosure information was readily available.
