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An E mu‐v‐abl transgene elicits plasmacytomas in concert with an activated myc gene.
Author(s) -
Rosenbaum H.,
Harris A.W.,
Bath M.L.,
McNeall J.,
Webb E.,
Adams J.M.,
Cory S.
Publication year - 1990
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1002/j.1460-2075.1990.tb08187.x
Subject(s) - biology , murine leukemia virus , immunoglobulin heavy chain , enhancer , transgene , abl , plasmacytoma , microbiology and biotechnology , carcinogenesis , oncogene , gene rearrangement , gene , virus , cancer research , virology , gene expression , genetics , immunology , cell cycle , signal transduction , tyrosine kinase , multiple myeloma
To clarify how the v‐abl oncogene of Abelson murine leukemia virus contributes to lymphoid tumorigenesis, we introduced the gene linked to an immunoglobulin heavy chain enhancer (E mu) into the mouse germline. Although lymphoid development was not detectably affected in young E mu‐v‐abl mice, three transgenic lines shared a high predisposition to develop clonal plasmacytomas that secreted IgA or IgG. The unexpected absence of pre‐B lymphomas suggests that Abelson virus generates such tumors by infecting an early lymphoid progenitor cell that has not yet activated the heavy chain enhancer. Most plasmacytomas bore a rearranged c‐myc gene, apparently as a result of spontaneous translocation to the Igh locus. Moreover, progeny of a cross with analogous E mu‐myc mice rapidly developed oligoclonal plasmacytomas. Thus, the collusion of v‐abl with c‐myc is stage specific, efficiently transforming plasma cells but not pre‐B cells or B cells.