Researchers at Harvard and University of California, San Francisco have developed a model for human leukemia in mice, a breakthrough that may allow scientists to more effectively study human cancers.

The researchers focused on a type of leukemia known as acute myeloid leukemia (AML), a disease largely caused by genetic mutations that increases the production of potentially cancerous proteins known as Ras proteins. The disease is reported to cause roughly 9,000 deaths in the U.S. annually, according to the National Cancer Institute.

The study found that mutations in two genes for different Ras proteins—known as Nras and Kras—induced AML symptoms in mice. But mutations in Nras were found to cause a slower, more benign disease progression.

The study highlights a critical distinction in disease-specific cancer treatments, said Harvard Medical School Assistant Professor of Pathology Kevin M. Haigis, a co-author of the study. He added that the findings reveal how functional differences between genes arise in different disease scenarios.

According to the researchers, the findings hold significant implications.

“For many, many years people thought all the Ras proteins were the same, so if you made a drug that could effectively treat one type of Ras cancer, you could use that for all Ras cancers,” said Haigis. “What we’re beginning to learn now is that not all the Ras genes are the same—Kras is different from Nras, so the therapies for treating these cancers is different.”

Haigis said that the research was founded upon the observation that mutations in these genes are commonly found in instances of human AML.

“While these genes are highly related, human cancer studies suggest that they can be different in their function,” Haigis said.

“In the Kras mice, the disease occurs so fast that it’s hard to study, but in Nras mice, we see a much more indolent, slow-moving disorder,” said Scott C. Kogan ’86, a professor of laboratory medicine at UCSF and co-author of the study.

Kogan said that the work might enable scientists to gain a deeper understanding as to how genetic changes contribute to AML, adding that his team is currently using the model to understand the pathogenesis of the disease.

The researchers mentioned that they are continuing to explore new avenues of focus with their model.

“We’re developing models showing [that] the model mimics human disease, and we plan to use these models to test ideas about treatments.” said Kogan.

The study was published in a recent issue of the hematology journal Blood.

—Staff writer Amy Guan can be reached at guan@fas.harvard.edu.