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Regression of experimental Burkitt's lymphoma induced by Epstein-Barr
virus-immortalized human B cells
G Tosato, C Sgadari, K Taga, KD Jones, SE Pike, A Rosenberg, JM Sechler, IT Magrath, LA Love and K Bhatia
Division of Hematologic Products, Center for Biologics Evaluation and
Research, Rockville, MD 20852-1448.
Epstein-Barr virus (EBV)-immortalized human B cells survive only
transiently when injected subcutaneously into athymic mice, whereas
Burkitt's lymphoma cells give rise to progressively growing subcutaneous
tumors. In this study, we tested whether these Burkitt's tumors could be
induced to regress via a bystander effect induced by EBV-immortalized B
cells. Simultaneous inoculation of EBV-immortalized B cells and Burkitt's
lymphoma cells in the same subcutaneous site resulted in tumors that
regressed with necrosis and scarring. Similarly, simultaneous inoculation
of EBV-immortalized B cells and Burkitt's lymphoma cells in separate
subcutaneous sites resulted in regression of a proportion of the Burkitt's
tumors. Furthermore, most of the established human Burkitt's tumors
regressed with necrosis and scarring after intratumor inoculations with
EBV-immortalized B cells. The EBV-immortalized B cells continued to exert
this antitumor effect even when killed with irradiation. The experimental
approach to Burkitt's lymphoma treatment described here exploits the
ability of athymic mice to reject EBV-immortalized B cells to target an
effective antitumor response to malignant cells normally incapable of
eliciting it.
Volume 83,
Issue 3,
pp. 776-784,
02/01/1994
Copyright © 1994 by The American Society of Hematology
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