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Erin Ahn, Ph.D., points to a bar graph showing various forms of the SON protein, some longer than others
“We screened leukemia patients and found an abundance of SON, but not the full-length form,” said Dr. Ahn, assistant professor of oncologic sciences at USA Mitchell Cancer Institute. “These were shorter than normal.”
Dr. Ahn’s discovery -- that a shortened form of the SON protein is linked to leukemia – was published in an article in Molecular Cell on Thursday, March 17. To a scientist, being published in a prominent, high-impact journal like Molecular Cell is akin to a basketball player making it to the Final Four, said Laurie Owen, Ph.D., associate director for basic and translational research at MCI.
Dr. Ahn's work could have big implications for understanding and treating leukemia, Dr. Owen said. “This research points toward a critical role for the SON protein in turning on genes associated with leukemia and provides a potential strategic platform to detect and treat acute myeloid leukemia,” she said.
The SON protein is a large, DNA- and RNA-interacting protein encoded by the SON gene. SON had been the subject of Dr. Ahn’s work since she joined MCI in 2012. She and her team had studied the protein’s function in various cancers and knew that it was overexpressed – the scientist’s term for “found in abundance” -- in leukemia cells.
She began collaborating with medical oncologist Dr. Thomas Butler of MCI, who specializes in blood cancers. They examined the blood of consenting patients with leukemia and compared it to healthy samples, and to blood and bone marrow samples obtained from the University of Pennsylvania.
Dr. Ahn and her team isolated white blood cells called “mononuclear cells” from the patients’ blood and bone marrow, where the SON protein is found. Their patient sample screening work continued for more than two years.
Ultimately, their findings provided new insight into the differences in SON proteins. They discovered that shortened version of the protein is the real culprit, activating several genes that cause acute myeloid leukemia and myelodysplastic syndrome, which is a leukemia precursor.
“We learned that the short form (of SON) blocks the normal SON function, and we also figured out how the ‘short SON’ affects the on and off status of multiple genes in blood cells,” she said.
What could this mean for patients? One way to take the scientific discovery "from the bench to the bedside" of patients would be to find a way to maintain the right level of gene expression – a balance between the long and short forms of SON, said Dr. Ahn.
In late 2015, Dr. Ahn was awarded a $1.7 million five-year R01 grant from the National Cancer Institute at the National Institutes of Health to study the role of the SON protein in leukemia.
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