Skip to main content

New Study Sheds Light on Origins of Leukemia

Kristine Willis

Kristine Willis of Georgetown's biology department says the more scientists understand the DNA reading process “the better we’ll be able to do with developing treatments not just for cancer, but all kinds of human sickness.”

November 15, 2011 – A new study led by Kristine Willis in Georgetown’s biology department has discovered important new information about a DNA misreading process that can lead to leukemia and other cancers.

Previous studies have shown how the nuclear pore (proteins that surround a “hole” in the nuclear membrane) helps determine what gets read and copied from our DNA.

Willis’ study, published today in the online journal PLoS ONE, shows that the mutation of certain proteins in the pore can cause them to lose their interaction with a DNA binding protein, resulting in inappropriate copying of information from some genes.

This type of misreading, Willis says, can lead to acute myeloid leukemia.

Exciting Results

“My group is very excited about these results, because specific mutations in nuclear pores have been observed in cases of acute myeloid leukemia that are highly resistant to current chemotherapeutic treatments,” says Willis, an assistant research professor in the biology department.

The research was funded by a grant from the National Institute of General Medical Sciences (NIGMS).

“Normally, certain genes get copied and that information in those genes gets sent out [side of the nucleus] into the cytoplasm of the cell,” she says. “When you mutate these nuclear pore proteins in a certain way, it changes the way the genes get copied.”

New Treatments

“Our results provide new insight into how nuclear pores control gene activity,” Willis notes,  “and should ultimately help to identify new treatments for this particular type of cancer.”

The researchers studied what happens to a set of genes that’s regulated by a protein called Mig1.

They found that the nuclear pore itself helps Mig1 with its main function, which is to bind to the DNA and shut off certain genes. When the researchers mutated the nuclear pore in a particular way, Mig1 no longer shut the genes off.

The researchers used yeast cells rather than human cells for their study because the former are easy to manipulate and have most of the same functions.

 Next Steps

Willis says a possible next step from this research is to use yeast as a tool to screen cancer treatment drugs.

“Because yeast cells are very similar to human cells, and they’re easy to grow and you can handle them very easily, it’s very easy to screen tens of thousands or hundreds of thousands of compounds at once,” Willis explains.  “So you can use your yeast cells as a screen for compounds that will then change how changes in gene expression occur. That’s a project that we’d like to do going forward.”

Willis says basic research is really the key to understanding all kinds of human disease – many of which are caused by changes in the way information in our DNA gets read.

“The better we understand that reading process and how the cell regulates that reading process,” she explains, “the better we’ll be able to do with developing treatments not just for cancer, but all kinds of human sickness.”

Related Information

Georgetown University37th and O Streets, N.W., Washington D.C. 20057(202) 687.0100

Connect with us via: