scholarly journals Transformation of Undifferentiated Thy-1lo B220+ Thymic Lymphoid Cells by the Abelson Murine Leukemia Virus

2000 ◽  
Vol 8 (1) ◽  
pp. 1-18 ◽  
Author(s):  
Eric Y. Chen ◽  
Bradley J. Swanson ◽  
Steven S. Clark
Keyword(s):  
Murine Leukemia Virus ◽  
Leukemia Virus ◽  
Lymphoid Cells ◽  
Abelson Murine Leukemia Virus ◽  
Murine Leukemia

scholarly journals Nonrandom cytogenetic changes accompany malignant progression in clonal lines abelson virus-infected lymphocytes

Blood ◽  
1994 ◽  
Vol 84 (12) ◽  
pp. 4301-4309 ◽  
Author(s):  
SS Clark ◽  
Y Liang ◽  
CK Reedstrom ◽  
SQ Wu
Keyword(s):  
Tumor Progression ◽  
Murine Leukemia Virus ◽  
Leukemia Virus ◽  
Lymphoid Cells ◽  
Full Transformation ◽  
Cytogenetic Abnormalities ◽  
Cytogenetic Changes ◽  
Abelson Murine Leukemia Virus ◽  
Murine Leukemia ◽  
Over Time

Initially, lymphoid cells transformed by v-abl or BCR/ABL oncogenes are poorly oncogenic but progress to full transformation over time. Although expression of the oncogene is necessary to initiate and maintain transformation, other molecular mechanisms are thought to be required for full transformation. To determine whether tumor progression in ABL oncogene-transformed lymphoid cells has a genetic basis, we examined whether progression of the malignant phenotype of transformed clones correlates with particular cytogenetic abnormalities. A modified in vitro bone marrow transformation model was used to obtain clonal Abelson murine leukemia virus-transformed B lymphoid cells that were poorly oncogenic. Multiple subclones were then derived from each clone and maintained over a marrow-derived stromal cell line for several weeks. Over time, clonally related Abelson murine leukemia virus-transformed subclones progressed asynchronously to full transformation. The data show that tumor progression can occur in the absence of detectable cytogenetic changes but, more importantly, that certain cytogenetic abnormalities appear reproducibly in highly malignant subclones. Therefore, three independent subclones showed deletion in a common region of chromosome 13. Other highly malignant cells carried a common breakpoint in the X chromosome, and, finally, two subclones carried an additional chromosome 5. These results are consistent with the hypothesis that ABL oncogenes are sufficient for the initial transformation of cells but that additional genetic events can drive oncogenic progression. These observations further suggest that diverse genetic mechanisms may be able to drive tumor progression in cells transformed with ABL oncogenes.

scholarly journals Multiple immunoglobulin heavy-chain gene transcripts in Abelson murine leukemia virus-transformed lymphoid cell lines

1982 ◽  
Vol 2 (4) ◽  
pp. 386-400
Author(s):  
F W Alt ◽  
N Rosenberg ◽  
V Enea ◽  
E Siden ◽  
D Baltimore
Keyword(s):  
Heavy Chain ◽  
Lymphoid Cell ◽  
Murine Leukemia Virus ◽  
Leukemia Virus ◽  
Lymphoid Cells ◽  
Chain Gene ◽  
Rna Sequences ◽  
Abelson Murine Leukemia Virus ◽  
Polypeptide Chains ◽  
Murine Leukemia

Lymphoid cells transformed by Abelson murine leukemia virus (A-MuLV) contain three classes of RNA transcripts from immunoglobulin mu genes. P mu-mRNAs (productive) correspond to the normal 2.7-kilobase (kb) membrane (mu m) and 2.4-kb secreted (mu s) mu mRNA species both in size and coding capacity and occur at approximately equal abundance in most mu-positive (pre-B-like) A-MuLV transformants. A mu-mRNAs (aberrant) generally fall into one of two categories--aberrantly small 2.3-kb mu m and 2.0-kb mu s mRNAs which encode aberrantly small mu polypeptide chains, or normal-sized, V H-containing mu RNAs which do not encode immunologically identifiable mu polypeptide chains. In one case, the latter type of A mu-mRNA was demonstrated to result from an in-phase termination codon in the D segment of the mu mRNA. Also, most, if not all, A-MuLV transformants express members of a 3.0 to 1.9-kb set of C mu-containing, but V H-negative S mu-RNAs (for sterile), the expression of which may occur simultaneously with but independently of P mu-mRNAs or A mu-mRNAs. The S mu-RNA sequences do not encode immunologically identifiable mu chains and can be produced by cells with unrearranged heavy-chain alleles, such as T-lymphocytes, although the structure of the S mu-RNAs from T-lymphoid cells appears to be different from that of B-lymphoid cell S mu-RNAs. Certain A-MuLV transformants also express gamma-RNA sequences that are probably analogous to the three different forms of mu RNA. These data support the concept that heavy-chain allelic exclusion, like that of light chains, is not mediated by control at the DNA or RNA levels but is probably a consequence of feedback control from cytoplasmic mu chains.

scholarly journals Multiple immunoglobulin heavy-chain gene transcripts in Abelson murine leukemia virus-transformed lymphoid cell lines.

1982 ◽  
Vol 2 (4) ◽  
pp. 386-400 ◽  
Author(s):  
F W Alt ◽  
N Rosenberg ◽  
V Enea ◽  
E Siden ◽  
D Baltimore
Keyword(s):  
Heavy Chain ◽  
Lymphoid Cell ◽  
Murine Leukemia Virus ◽  
Leukemia Virus ◽  
Lymphoid Cells ◽  
Chain Gene ◽  
Rna Sequences ◽  
Abelson Murine Leukemia Virus ◽  
Polypeptide Chains ◽  
Murine Leukemia

Lymphoid cells transformed by Abelson murine leukemia virus (A-MuLV) contain three classes of RNA transcripts from immunoglobulin mu genes. P mu-mRNAs (productive) correspond to the normal 2.7-kilobase (kb) membrane (mu m) and 2.4-kb secreted (mu s) mu mRNA species both in size and coding capacity and occur at approximately equal abundance in most mu-positive (pre-B-like) A-MuLV transformants. A mu-mRNAs (aberrant) generally fall into one of two categories--aberrantly small 2.3-kb mu m and 2.0-kb mu s mRNAs which encode aberrantly small mu polypeptide chains, or normal-sized, V H-containing mu RNAs which do not encode immunologically identifiable mu polypeptide chains. In one case, the latter type of A mu-mRNA was demonstrated to result from an in-phase termination codon in the D segment of the mu mRNA. Also, most, if not all, A-MuLV transformants express members of a 3.0 to 1.9-kb set of C mu-containing, but V H-negative S mu-RNAs (for sterile), the expression of which may occur simultaneously with but independently of P mu-mRNAs or A mu-mRNAs. The S mu-RNA sequences do not encode immunologically identifiable mu chains and can be produced by cells with unrearranged heavy-chain alleles, such as T-lymphocytes, although the structure of the S mu-RNAs from T-lymphoid cells appears to be different from that of B-lymphoid cell S mu-RNAs. Certain A-MuLV transformants also express gamma-RNA sequences that are probably analogous to the three different forms of mu RNA. These data support the concept that heavy-chain allelic exclusion, like that of light chains, is not mediated by control at the DNA or RNA levels but is probably a consequence of feedback control from cytoplasmic mu chains.

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