Evidence builds for potential new cancer drug target

In a paper published today in the Proceedings of the National Academy of Sciences, Temple University researchers report that one of the functions of the c-myb gene, which leukemia cells depend on for proliferation, is the formation of white blood cells.

“This study is another step in the process of validating the c-myb gene as a potential target for new cancer drugs,” said Prem Reddy, Ph.D., professor and director of the Fels Institute for Cancer Research and Molecular Biology at Temple University School of Medicine.

Knowing that the c-myb gene played a role in the spread of leukemia, the researchers wanted to determine the gene’s normal function. This was accomplished by deleting the c-myb gene in a mouse model. New technology allowed the scientists to delete c-myb from one specific type of tissue in the model rather than from the entire organism. “We removed the c-myb gene from T cells and in the process discovered that c-myb is required for white blood cell formation,” said Reddy. In other research conducted by the team but not yet published, c-myb was deleted from breast tissue. The researchers believe that this gene plays a critical role in breast cancer and want to show the effects of its deletion on breast tumor cell proliferation.

The group’s research is providing detailed genetic explanations of how and why c-myb is essential for the proliferation of white blood cells and breast cells by demonstrating that when it’s removed, cell proliferation is impaired and the risk of developing cancer is reduced. “We hope to develop a drug that blocks the harmful activity of this gene in the near future. This finding was very serendipitous. We used to think c-myb was only associated with the development of leukemia but found that it’s also involved in the development of breast cancer,” said Reddy.

Other researchers on the team include the study’s first author, Yen K. Lieu, Atul Kumar, Anthony G. Pajerowski, and Thomas J. Rogers.