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Despite maturation arrest, blast cells in acute myeloid leukemia (AML) are often capable of expressing lineage-restricted (granulomonocytic or myelomastocytic) differentiation antigens. Tryptases are lineage-associated serine proteases primarily expressed in mast cells, and less abundantly in blood basophils. We have recently shown that myeloblasts in a group of patients with AML (approximately 40%) produce significant amounts of tryptase(s). In these patients, serum tryptase levels are elevated (> 15 ng/ml) and reflect the total burden of leukemic cells. In most cases, myeloblasts express alpha-tryptase mRNA in excess over beta-tryptase mRNA, and secrete the respective protein (= pro-alpha-tryptase) in a constitutive manner. It was also found that these AML blasts frequentlyco-express tryptase with additional mast cell lineage- and/or basophil-related differentiation antigens including KIT (CD117), histamine, and 2D7. We hypothesize that tryptase-positive AMLs arise from a leukemic progenitor that exhibits a limited potential to differentiate into mast cells and/or basophils.
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Sperr et al. (2002) studied this question.
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