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Tumor dormancy and cell signaling. V. Regrowth of the BCL1 tumor after
dormancy is established
ES Vitetta, TF Tucker, E Racila, YW Huang, R Marches, N Lane, RH Scheuermann, NE Street, T Watanabe and JW Uhr
Cancer Immunobiology Center and Department of Microbiology, University of
Texas Southwestern Medical Center at Dallas, 75235, USA.
The majority of BALB/c mice immunized with the BCL1 lymphoma-derived
idiotype (Id+) IgM and subsequently challenged with BCL1 tumor cells
develop a state of tumor dormancy. The vast majority of dormant lymphoma
cells are in cell cycle arrest, but there are also residual replicating
cells. In the present studies, we attempted to define features of both the
dormant lymphoma cells and the host that lead to escape from dormancy.
Escape from dormancy occurs at a steady rate over a 2-year period,
suggesting that it is a stochastic process. We found that, in the majority
of mice, escape was due to the emergence of genetic variants that were no
longer susceptible to the anti-Id- mediated induction of dormancy. Ten
percent of these variants were Id-; the remainder were Id+ but could grow
in the presence of anti-Id antibodies, suggesting that there were mutations
in molecules involved in one or more mIg-mediated negative-signaling
pathways. In two of five such escapees, alterations in either Syk, HS1,
and/or Lyn were observed. In a small percentage of mice, a low titer of
circulating anti-Id antibody before tumor challenge correlated with a
subsequent, more rapid loss of dormancy.
Volume 89,
Issue 12,
pp. 4425-4436,
06/15/1997
Copyright © 1997 by The American Society of Hematology
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