Acute myelogenous leukemia: Reducing the risk of a relapse

December 10, 2012 | by Roberta Nichols

Although some acute myelogenous leukemia (AML) patients receiving treatment will achieve a complete remission, most adult patients will suffer a relapse within the first two years. And often, the disease is more difficult to treat the second time around.

Researchers at City of Hope have made significant inroads in a new approach that may improve the odds for those patients. The method: Program immune system T cells from either the patient or from a healthy donor to attack AML cells, but leave normal cells alone. 

“In our work to develop a cell-based immune therapy for cancer, we’ve taken T cells from the patients, genetically reprogrammed them to recognize cancer and returned them to the patients to treat B cell lymphoma and pre-B acute lymphocytic leukemia,” said Stephen J. Forman, M.D., chair of the Department of Hematology & Hematopoietic Cell Transplantation at City of Hope, and the Francis and Kathleen McNamara Distinguished Chair in Hematology and Hematopoietic Cell Transplantation. He was the senior author of a study on the new research, presented Tuesday at the American Society of Hematology's annual meeting in Atlanta.

In this study, the scientists took the immune cells from three healthy donors or from AML patients and for the first time genetically re-engineered them to recognize a protein called CD123 (which is abundant on the surface of AML cells).

“In our study, we showed that the engineered T cells can recognize the CD123 on the leukemia cells and immediately destroy them – without harming cells that do not contain CD123,” said first author Armen Mardiros, M.S., a graduate student mentored by Forman in the hematology department at City of Hope.

Forman sees the study as a significant step toward making a powerful new therapy to treat a deadly disease and says it points the way for researchers to develop a clinical trial to treat AML patients using the engineered donor T cells.

The work was funded in part by the National Cancer Institute Lymphoma SPORE (grant numbers P50 CA107399, PO1 CA030206, and MO1 RR0004) and the Tim Nesvig Lymphoma Fellowship and Research Fund.

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