Taking Aim at Relapse of Leukemia in Kids

June 18 -- WEDNESDAY, June 17 (HealthDay News) -- Scientists have identified molecules that enable tumor cells to invade the nervous system of patients with a blood-borne childhood cancer, a finding that may lead to the development of drugs that block these molecules and prevent relapse.

In T-cell acute lymphoblastic leukemia (T-ALL), which primarily strikes children and adolescents, the bone marrow makes too many white blood cells.

"In general, [T-ALL] is treatable with basic chemotherapy and radiation, so close to 80 percent of kids can be cured," study leader Ioannis Aifantis, an associate professor of pathology and co-director of the Cancer Stem Cell Program at the New York University Cancer Institute, said in a university news release. "But you have a very high rate of relapse. And after the relapse, it is not treatable because the cancer occurs in tricky places, like the central nervous system."

In research with mice, Aifantis and colleagues found that a protein receptor (CCR7) embedded on the outer surface of leukemic cells enables the cancer cells to infiltrate the brain and spinal cord.

"What we have found is that leukemic cells over-express this receptor," Aifantis said. "If you knock out this receptor, these cells will not go to the brain under any circumstances."

The researchers also found that a protein called CCL21 acts as a "come-hither" signal for CCR7 protein receptors. CCL21 was found in tiny veins of the brain near infiltrating tumor cells.

"Perhaps there are antibodies or small molecules that can block the interaction between these two proteins to reduce their interactions and, hopefully, that could be used as a type of prophylactic treatment to prevent a relapse in the central nervous system among patients who have already been treated for leukemia," Aifantis said.

The study is in the June 18 issue of the journal Nature.

More information

The American Cancer Society has more about childhood leukemia.

SOURCE: NYU Langone Medical Center, news release, June 17, 2009