Genetic variation in CD33 influences how AML patients' leukemic cell responds to GO

Published on February 26, 2013 at 11:47 PM · No Comments

Researchers from the College of Pharmacy and Medical School working within the Masonic Cancer Center, University of Minnesota, have partnered to identify genetic variations that may help signal which acute myeloid leukemia (AML) patients will benefit or not benefit from one of the newest antileukemic agents.

Their study is published today in Clinical Cancer Research.

In the latest study, U of M researchers evaluated how inherited genetic polymorphisms in CD33, a protein that naturally occurs in most leukemia cells, could affect clinical outcomes of patients treated with an existing chemotherapy drug, gemtuzumab ozogamicin (GO), an immuno-conjugate between anti-CD33 antibody and a cytotoxin known as calicheamicin, which binds to CD33 on leukemic cells. As GO is internalized by leukemia cells, the cytotoxin is released, causing DNA damage and generating leukemic cell death.

In recent clinical trials GO has been shown to induce remission and improve survival in subset of patients with AML, however there is wide inter-patient variation in response.

Jatinder Lamba, Ph.D., and colleagues identified and evaluated three genetic variations of CD33 in two groups of patients with pediatric AML - one group that received the drug GO, and one group that did not. They found that specific genetic variation in CD33 that significantly affected the clinical outcome of AML patients who received GO based chemotherapy.

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