(RxWiki News) The computational power available to researchers has grown exponentially over the years, allowing broad analysis of genetics involved in cancer to get new ideas for exploring new methods of therapy.
New research on acute myeloid leukemia has laid the groundwork for testing even more effective treatments than are currently available.
In a study observing the role of a certain gene commonly involved in acute myeloid leukemia (AML) that grows resistant to cancer drugs, a team of researchers performed a broad, genome-wide computational analysis on AML cells.
Researchers found that activating a gene known as WEE1 could single-handedly cause widespread cellular death specific to this form of leukemia.
The study utilized a new technique pioneered by the CU Cancer Center Functional Genomics Shared Resource from the the University of Colorado in Boulder. The analysis tested every gene one by one, comparing the effects of each available pharmaceutical treatment for AML on the individual cells.
The abstract does not disclose the specific pharmaceutical WEE1 inhibition therapy utilized. However, researchers believe that this method, in conjunction with the commonly used chemotherapy agent, cytarabine, is ready for further testing.
"I'm optimistic that this will eventually lead to a therapeutic regimen that allows us to target AML cells that have escaped conventional therapies," says Christopher Porter, M.D., investigator at the University of Colorado Cancer Center. Initial results, according to Dr. Porter, are "extremely promising."
"In light of these data, we are already early in the clinical trial planning process," Dr. Porter says.
While the effects of the treatment were certainly impressive, and the team believes they have found a treatment to specifically inhibit WEE1, it is worth remembering that historically the implementation of gene-based therapy has been a rocky road. Deactivating a single gene in a cancer cell is far easier said than done outside of a laboratory environment.
Findings were published in the journal Leukemia.
The authors of this study did not disclose any financial conflict of interest.
