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Blood, 1 December 2000, Vol. 96, No. 12, pp. 3922-3931
NEOPLASIA
Evaluation of Apaf-1 and procaspases-2, -3, -7, -8, and -9 as
potential prognostic markers in acute leukemia
Phyllis A. Svingen,
Judith
E. Karp,
Stan Krajewski,
Peter W. Mesner Jr,
Steven
D. Gore,
Philip J. Burke,
John C. Reed,
Yuri A. Lazebnik, and
Scott H. Kaufmann
From the Division of Oncology Research and Department
of Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic,
Rochester, MN; Greenebaum Cancer Center, University of Maryland,
Baltimore; Burnham Institute, LaJolla, CA; Leukemia Program, Johns
Hopkins Oncology Center, Baltimore, MD; and Cold Spring Harbor
Laboratories, Cold Spring Harbor, NY.
Recent studies have suggested that variations in levels of
caspases, a family of intracellular cysteine proteases, can profoundly affect the ability of cells to undergo apoptosis. In this study, immunoblotting was used to examine levels of apoptotic protease activating factor-1 (Apaf-1) and procaspases-2, -3, -7, -8, and -9 in
bone marrow samples (at least 80% leukemia) harvested before chemotherapy from adults with newly diagnosed acute myelogenous leukemia (AML, 42 patients) and acute lymphocytic leukemia (ALL, 18 patients). Levels of each of these polypeptides varied over a more than
10-fold range between specimens. In AML samples, expression of
procaspase-2 correlated with levels of Apaf-1
(Rs = 0.52, P < .02),
procaspase-3 (Rs = 0.56,
P < .006) and procaspase-8
(Rs = 0.64, P < .002).
In ALL samples, expression of procaspases-7 and -9 was highly
correlated (Rs = 0.90,
P < .003). Levels of these polypeptides did not
correlate with prognostic factors or response to induction
chemotherapy. In further studies, 16 paired samples (13 AML, 3 ALL),
the first harvested before induction therapy and the second harvested
at the time of leukemia regrowth, were also examined. There were no
systematic alterations in levels of Apaf-1 or procaspases at relapse
compared with diagnosis. These results indicate that levels of
initiator caspases vary widely among different leukemia specimens
but cast doubt on the hypothesis that this variation is a major
determinant of drug sensitivity for acute leukemia in the clinical setting.
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