New Therapy Eliminates Deadly Leukemia Stem Cells
Reported July 03, 2009
(Ivanhoe Newswire) A recent study describes a novel therapeutic approach which significantly advances the fight against the deadly human acute myeloid leukemia (AML), a notoriously treatment-resistant blood cancer.
AML is a cancer of the white blood cells that has an extremely poor prognosis and does not respond well to conventional chemotherapy. “The cellular and molecular basis for this dismal picture is unclear,” senior study author Associate Professor Richard Lock from the Children’s Cancer Institute Australia and the University of New South Wales is quoted as saying. However, previous research has suggested that leukemia stem cells (LSCs) may lie at the heart of post-treatment relapse and chemoresistance.”
Associate Professor Lock and colleagues exploited the fact that the molecule CD123 is expressed at very high levels on LSCs but not on normal blood cells. The researchers created a therapeutic antibody called 7G3 that recognized and bound to CD123, hoping this antibody would selectively interfere with AML-LSC survival.
When AML-LSCs from human patients were transplanted into mice treated with the 7G3 antibody, signaling for growth and proliferation in the tumor cells was blocked. Further, the antibody impaired migration of the AML-LSCs to bone marrow and activated the innate immune system of the host mouse to destroy the AML-LSCs. Overall, treatment with 7G3 antibody substantially improved mouse survival when compared with control groups.
The researchers go on to report that a CD123-targeting antibody is currently being used in phase 1 clinical trials of advanced AML and that there are no signs of treatment-related toxicity. These results hold great promise for future cancer therapeutics.
Associate Professor Lock concluded, “The recent characterization of defined populations of cancer stem cells in a range of human malignancies, as well as their relative resistance to conventional chemotherapy and radiotherapy, supports the broad applicability of our approach and provides rationale for the progression . . . from preclinical evaluation to clinical trials.”
SOURCE: Cell Stem Cell, July 2, 2009
