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 journalArticle

43 Citations (Scopus)

Abstract

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
JournalBlood
Volume89
Issue number12
StatePublished - Jun 15 1997

Fingerprint

Cell signaling
Tumors
Lymphoma
Neoplasm Antibodies
Anti-Idiotypic Antibodies
Random processes
Stochastic Processes
Immunoglobulin M
Neoplasms
Cells
Cell Cycle Checkpoints
Molecules
Antibodies
Mutation

ASJC Scopus subject areas

  • Hematology

Cite this

Vitetta, E. S., Tucker, T. F., Racila, E., Huang, Y. W., Marches, R., Lane, N., ... Uhr, J. W. (1997). Tumor dormancy and cell signaling. V. Regrowth of the BCL1 tumor after dormancy is established. Blood, 89(12), 4425-4436.

Tumor dormancy and cell signaling. V. Regrowth of the BCL1 tumor after dormancy is established. / Vitetta, Ellen S.; Tucker, Thomas F.; Racila, Emilian; Huang, Yi Wu; Marches, Radu; Lane, Nancy; Scheuermann, Richard H.; Street, Nancy E.; Watanabe, Takeshi; Uhr, Jonathan W.

In: Blood, Vol. 89, No. 12, 15.06.1997, p. 4425-4436.

Research output: Contribution to journalArticle

Vitetta, ES, Tucker, TF, Racila, E, Huang, YW, Marches, R, Lane, N, Scheuermann, RH, Street, NE, Watanabe, T & Uhr, JW 1997, 'Tumor dormancy and cell signaling. V. Regrowth of the BCL1 tumor after dormancy is established', Blood, vol. 89, no. 12, pp. 4425-4436.
Vitetta ES, Tucker TF, Racila E, Huang YW, Marches R, Lane N et al. Tumor dormancy and cell signaling. V. Regrowth of the BCL1 tumor after dormancy is established. Blood. 1997 Jun 15;89(12):4425-4436.
Vitetta, Ellen S. ; Tucker, Thomas F. ; Racila, Emilian ; Huang, Yi Wu ; Marches, Radu ; Lane, Nancy ; Scheuermann, Richard H. ; Street, Nancy E. ; Watanabe, Takeshi ; Uhr, Jonathan W. / Tumor dormancy and cell signaling. V. Regrowth of the BCL1 tumor after dormancy is established. In: Blood. 1997 ; Vol. 89, No. 12. pp. 4425-4436.
@article{29f2ac61aaf54b44b4de5c070bd4bded,
title = "Tumor dormancy and cell signaling. V. Regrowth of the BCL1 tumor after dormancy is established",
abstract = "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.",
author = "Vitetta, {Ellen S.} and Tucker, {Thomas F.} and Emilian Racila and Huang, {Yi Wu} and Radu Marches and Nancy Lane and Scheuermann, {Richard H.} and Street, {Nancy E.} and Takeshi Watanabe and Uhr, {Jonathan W.}",
year = "1997",
month = "6",
day = "15",
language = "English (US)",
volume = "89",
pages = "4425--4436",
journal = "Blood",
issn = "0006-4971",
publisher = "American Society of Hematology",
number = "12",

}

TY - JOUR

T1 - Tumor dormancy and cell signaling. V. Regrowth of the BCL1 tumor after dormancy is established

AU - Vitetta, Ellen S.

AU - Tucker, Thomas F.

AU - Racila, Emilian

AU - Huang, Yi Wu

AU - Marches, Radu

AU - Lane, Nancy

AU - Scheuermann, Richard H.

AU - Street, Nancy E.

AU - Watanabe, Takeshi

AU - Uhr, Jonathan W.

PY - 1997/6/15

Y1 - 1997/6/15

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=0030912221&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0030912221&partnerID=8YFLogxK

M3 - Article

C2 - 9192767

AN - SCOPUS:0030912221

VL - 89

SP - 4425

EP - 4436

JO - Blood

JF - Blood

SN - 0006-4971

IS - 12

ER -