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Hard-to-Treat Leukemia Cell Subtype Identified
Date:1/14/2009

Discovery suggests new treatments for aggressive form of childhood disease, study says

WEDNESDAY, Jan. 14 (HealthDay News) -- Researchers say they may have identified a subtype of T-lymphoblastic leukemia (T-ALL) in children that does not respond to standard intensive chemotherapy.

Approximately 20 percent of children with T-ALL fair poorly on the same chemotherapy treatments that cure others with the disease, and doctors had been unable to explain why and which patients were least likely to improve.

Reporting online Jan. 14 and in the February edition of The Lancet Oncology, a team at St. Jude Children's Research Hospital in Memphis, Tenn., found that those who didn't respond to treatment had early T-cell precursors (ETPs). Believed to be recent migrants from the bone marrow to the thymus, they are substantially different to the lymphoid cells that standard chemotherapy normally attacks and may be resistant to it, the researchers said.

In a U.S.-based group of study participants, nearly three-quarters of those with ETP-ALL suffered a relapse within a decade, compared with only 10 percent of typical T-ALL patients. In an Italian group of participants, 57 percent of ETP-ALL patients had a relapse within two years, compared with only 14 percent of typical T-ALL patients.

"The high risk of remission failure or subsequent relapse for patients with ETP-ALL, if treated with standard intensive chemotherapy, indicates the need for alternative approaches to treatment," Dr. Dario Campana of St. Jude's department of oncology, said in a news release issued by the journal.

Campana and his team suggested trying alternate treatments for ETP-ALL, such as myeloablative therapy (high-dose chemotherapy) followed by haemopoietic stem-cell transplantation in first remission while other therapies are investigated.

More information

The U.S. National Cancer Institute has more about childhood leukemia.



-- Kevin McKeever



SOURCE: The Lancet Oncology, news release, Jan. 14, 2009


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