Loss of viral gene expression and retention of tumorigenicity by Abelson lymphoma cells.

Abstract:

:Lymphomas induced by the Abelson murine leukemia virus (A-MuLV) were examined for the expression of biochemical and biological markers associated with A-MuLV transformation before and after in vivo growth in genetically distinguishable host mice. Although all tumors and clonal lines derived from them initially expressed the A-MuLV-encoded gag fusion protein p160, they ceased synthesis of this molecule after several weeks of growth in vivo as ascites tumors. Transplanted clonal lines continued to express the alloantigenic marker H-2b and the isoenzyme marker Gpi-1b of the donor tumor cells, indicating that the cells were of donor and not host origin. Examination of cellular DNA obtained from p160-positive and derivative p160-negative lines indicated that p160-negative clones had lost A-MuLV-specific proviral sequences as detected by hybridization with several probes. Although the clonal lines no longer expressed p160, they retained their malignant phenotype and continued to express the Abelson antigen, a cell surface marker associated with A-MuLV lymphomagenesis. Continued expression of the A-MuLV genome was not required for maintenance of oncogenic potential under these conditions of in vivo tumor growth.

journal_name

J Virol

journal_title

Journal of virology

authors

Grunwald DJ,Dale B,Dudley J,Lamph W,Sugden B,Ozanne B,Risser R

doi

10.1128/JVI.43.1.92-103.1982

subject

Has Abstract

pub_date

1982-07-01 00:00:00

pages

92-103

issue

1

eissn

0022-538X

issn

1098-5514

journal_volume

43

pub_type

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