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Blood, 1 April 2001, Vol. 97, No. 7, pp. 2177-2179
BRIEF REPORT
Expression of tumor-suppressor genes interferon regulatory factor
1 and death-associated protein kinase in primitive acute myelogenous
leukemia cells
Monica L. Guzman,
Donna Upchurch,
Barry Grimes,
Dianna S. Howard,
David A. Rizzieri,
Selina M. Luger,
Gordon L. Phillips, and
Craig T. Jordan
From the Blood and Marrow Transplant Program, Markey
Cancer Center, Division of Hematology/Oncology, University of Kentucky
Medical Center, Lexington Division of Oncology and Bone Marrow
Transplantation, Duke University Medical Center, Durham, NC; and the
Department of Hematology/Oncology, University of Pennsylvania,
Philadelphia, PA.
Previous studies indicate that human acute myelogenous leukemia
(AML) arises from a rare population of leukemic stem
cells. Cells of this nature can initiate and maintain
leukemic cell growth in both long-term cultures and nonobese
diabetic/severe combined immune-deficient mice. To characterize the
biology of primitive AML cells, gene expression screens were
performed with 7 primary AML and 3 normal specimens. For each
sample, stem cell populations (CD34+/CD38 )
were isolated and used to synthesize radiolabeled complementary DNA
(cDNA). AML vs normal probes were then hybridized to cDNA arrays
containing genes related to cancer and apoptosis. Of approximately 1400 genes analyzed, 2 tumor-suppressor genes were identified that were
overexpressed in all 7 of the AML CD34+/CD38
cell populations: death-associated protein kinase and interferon regulatory factor 1. Expression of each gene was confirmed by reverse-transcription polymerase chain reaction and immunoblot analysis. It is proposed that tumor-suppressor proteins play a role in the biology of primitive AML cells.
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