Tumor dormancy and cell signaling. V. Regrowth of the BCL1 tumor after dormancy is established

Ellen S. Vitetta, Thomas F. Tucker, Emilian Racila, Yi Wu Huang, Radu Marches, Nancy Lane, Richard H. Scheuermann, Nancy E. Street, Takeshi Watanabe, Jonathan W. Uhr

Research output: Contribution to journalArticlepeer-review

45 Scopus citations


The majority of BALB/c mice immunized with the BCL1 lymphoma-derived idiotype (Id+) IgM and subsequently challenged with BCL1 tumor calls develop a state of tumor dormancy. The vest 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 s 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, mere rapid loss of dormancy.

Original languageEnglish (US)
Pages (from-to)4425-4436
Number of pages12
Issue number12
StatePublished - Jun 15 1997


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