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D Grander, M Heyman, K Brondum-Nielsen, Y Liu, E Lundgren, S Soderhall and S Einhorn
Division of Experimental Oncology, Radiumhemmet, Stockholm, Sweden.
Various aspects of the interferon (IFN) system were studied in malignant
cells from 37 unselected patients with acute lymphocytic leukemia (ALL). It
was found that leukemic cells from two of 37 patients had a complete loss
of alpha- and beta-IFN genes, whereas cells from four of 37 had lost one of
the alpha-/beta-IFN alleles. In 25 cases, viable cells were also available
for functional studies. Cell clones with loss of one of the alpha-/beta-IFN
alleles produced low amounts of IFN after virus induction in vitro. Some
clones with an apparently normal set of IFN genes were unable to produce
detectable amounts of IFN. All clones studied were found to carry
high-affinity alpha-IFN receptors. In clones carrying deletions of IFN
genes, the cells were sensitive to IFN in vitro as measured by
alpha-IFN-induced enhancement of 2',5'-oligoadenylate synthetase (2',5'-A
synthetase). Cells from four patients with an apparently normal set of IFN
genes were insensitive to this effect of IFN. We conclude that of the 17
patients in which IFN genes, IFN production, alpha-IFN receptors, and
IFN-induced enhancement of 2',5'-A synthetase were studied, nine (53%)
showed some abnormality in their IFN system. This finding may add some
support to the hypothesis that defects in the IFN system could be a step on
the path to malignant transformation in ALL. Moreover, patients whose
malignant cells carry IFN gene deletions or other defects in their
IFN-producing capacity, but are still sensitive to exogenous IFN, could
represent a subgroup of ALL with a greater likelihood of responding to IFN
therapy.
This article has been cited by other articles:
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| Copyright © 1992 by American Society of Hematology Online ISSN: 1528-0020 | |||||||||
