In a study presented at the annual meeting of the American Association for Cancer Research (AACR), they found that CML does not "crowd out" normal blood cells in the bone marrow, as has long been thought, but actually kills those healthy cells through use of a unique cell "death factor."

Those destructive proteins, known as lipocalin 24p3, work to promote the development of leukemia by giving the cancer room to grow and spread, making it easier to invade the bone marrow and spleen, say the researchers.

Because they also show in this study that blocking the protein with an antibody in mouse cell experiments will restrain the ability of the cell death protein to kill normal bone marrow cells, the researchers suggest that a therapy that could disable 24p3 might prove useful to CML patients when combined with traditional treatment, such as with Gleevec.

"We don't yet have a therapy that can be tested in humans, but our hope is that this work can lead to development of such a one-two punch," says the study's principal investigator, Ralph Arlinghaus, Ph.D., a professor and chair of the Department of Molecular Pathology.

In the least, the research demonstrates that CML is much craftier than had been suspected, he says. Before this study, no one knew that the 24p3 mouse protein (known in humans as neutrophil gelatinase-associated lipocalin, or NGAL) had any involvement in leukemia, Arlinghaus says.

The protein is a normal component of cells and is believed to have a variety of functions. But the "BCR-ABL oncoprotein (encoded by the Philadelphia chromosome, a translocation of genetic material responsible for most CML) appea
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Contact: Nancy Jensen
nwjensen@mdanderson.org
713-792-0655
University of Texas M. D. Anderson Cancer Center
19-Apr-2005