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Aggressive therapy best for certain AML patients

COLUMBUS , Ohio A new study suggests that acute leukemia patients whose cancer cells show a genetic change that usually predicts a swift return of the disease following remission may remain disease-free longer when given aggressive therapy.

The findings apply to people with acute myeloid leukemia (AML) whose cancer cells have normal-looking chromosomes and a gene mutation called MLL-PTD.

Typically, these AML patients responded poorly following treatment with older standard therapies, often relapsing within a year. Of AML patients with normal chromosomes who lack the mutation, on the other hand, four in 10 are cured.

The new study suggests that treating patients who have the mutation with an aggressive therapy such as an autologous stem cell transplant while they are in remission might significantly extend their disease-free survival.

An autologous transplant uses stem cells taken from the patient's own blood.

The research was led by investigators at the Ohio State University Comprehensive Cancer Center. It is part of a larger study sponsored by the Cancer and Leukemia Group B (CALGB), a clinical cooperative group composed of oncologists from academic medical centers and community hospitals across the nation.

The findings were published in a recent issue of the journal Blood.

Our data is the first to show that AML patients with normal-looking chromosomes and this mutation do as well when treated aggressively as patients who don't have the mutation, says principal investigator Clara D. Bloomfield, professor of internal medicine and an internationally known AML specialist.

About 13,400 new cases of AML are expected this year, and about half will have cancer cells with chromosomes that show distinctive damage. The nature of that damage helps doctors determine a patient's therapy and estimate the patient's prognosis.

The remaining AML cases have cancer cells with normal
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Contact: Eileen Scahill
Eileen.Scahill@osumc.edu
614-293-2092
Ohio State University
1-Aug-2007


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