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Lymphoma regression induced by monoclonal anti-idiotypic antibodies
correlates with their ability to induce Ig signal transduction and is not
prevented by tumor expression of high levels of bcl-2 protein
WM Vuist, R Levy and DG Maloney
Department of Medicine, Stanford University Medical Center, CA 94305- 5306.
Custom-made monoclonal anti-idiotype antibodies (anti-Id MoAbs) have been
tested as a treatment modality in 34 non-Hodgkin's lymphoma (NHL) patients.
Partial or complete tumor remissions have been induced with this treatment
in 68% of these patients. One mechanism by which anti- idiotype antibodies
may have induced these tumor responses is via a direct antiproliferative
effect on the tumor cells, resulting in apoptosis. Primary NHL cells do not
proliferate well enough in vitro to test this hypothesis directly.
Therefore, we studied the effect of anti- idiotype antibodies on signal
transduction through the surface Ig receptor as measured by the induction
of cellular protein tyrosine phosphorylation. To assess whether bcl-2
protein could protect lymphoma cells from death induced by anti-Id MoAb, we
also measured the level of bcl-2 protein in the same tumor cells. We found
a strong correlation between the ability of an anti-Id MoAb to induce an
increase in tyrosine phosphorylation in vitro and its ability to induce a
tumor regression in the patient. By contrast, the level of bcl-2 expressed
by the tumor cells was not correlated with clinical response to anti-Id
MoAb treatment.
Volume 83,
Issue 4,
pp. 899-906,
02/15/1994
Copyright © 1994 by The American Society of Hematology
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