Acute myeloid leukemia (AML) is a devastating blood cancer that occurs more often in elderly people. Although not common, AML is fatal within five years to 75% of people who are diagnosed with the disease.

Now, a researcher at Baylor College of Medicine has potentially found a new way to treat AML, by starving the cancer cells of the energy they need to survive. Daisuke Nakada was recruited in 2011 to the Department of Molecular and Human Genetics, from the University of Michigan, where he was a postdoctoral fellow. He was recruited with the help of a First-Time Tenure-Track Award from CPRIT.

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Acute myeloid leukemia (AML) is a devastating blood cancer that occurs more often in elderly people. Although not common, AML is fatal within five years to 75% of people who are diagnosed with the disease.

Now, a researcher at Baylor College of Medicine has potentially found a new way to treat AML, by starving the cancer cells of the energy they need to survive. Daisuke Nakada was recruited in 2011 to the Department of Molecular and Human Genetics, from the University of Michigan, where he was a postdoctoral fellow. He was recruited with the help of a First-Time Tenure-Track Award from CPRIT.

All cells must take up nutrients and metabolize them in order to survive and grow. But Nakada has found that the metabolism of cancer cells is different from normal cells, in a way that might make it possible to target a leukemia cell’s specific metabolism without affecting normal cells.

“We think this could be a way to target leukemia cells without any, or many, side effects in normal cells,” Nakada says.

He’s specifically looking at an enzyme inside all cells that is essential for energy metabolism. Nakada may have found a way to starve cancer cells of energy without harming normal cells. Leukemia cells are completely dependent on this one enzyme, called AMPK, to supply their energy needs, while normal cells have backup systems.

His strategy will be to figure out a way to knock out the AMPK enzyme. He’s found that in animal models, the leukemia cells collapse without it. Even cancer stem cells, which many scientists believe are at the root of recurrent disease, become severely compromised and are unable to grow. If such a drug could be found to work in humans, it may have little or no side effects in normal cells.

Currently Nakada is investigating a research-grade drug that he says can’t be used in clinical trials. But he’s noticed some synergistic effects with a drug that is currently in clinical trials as an epigenetic cancer drug. Abnormal epigenetic changes—modifications to the genome that turn genes on and off—are crucial for the onset and unrestrained growth of cancer cells. Blocking the AMPK enzyme also slows down epigenetics, because some of the necessary building blocks become depleted. He’s hopeful that someday drugs targeting both epigenetics and AMPK could be administered together to enhance their cancer-targeting effects.

“The funding I received from CPRIT was tremendously helpful,” Nakada says. “Having extra funds that allowed a lot of flexibility was a tremendous help in hiring staff and equipping my lab.”

Although Nakada’s initial CPRIT award has ended, he received nearly $2.7 million in follow-on funding for his research from the National Cancer Institute and private foundations. These include Gabrielle’s Angels, a foundation created in memory of 27-year-old actress, Gabrielle Rich Aouad, who died from AML in 1996; and the Edward P. Evans Foundation, founded by the philanthropist who died in 2010 from AML. Nakada also received an additional research award from CPRIT.

Nakada received his undergraduate and graduate training in biological science at Nagoya University in Japan, where he was awarded his Ph.D., prior to becoming a research fellow at Michigan’s Center for Stem Cell Biology in 2006.

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