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 Cloning and analysis of reverse transcript P160 genomes of Abelson murine leukemia virus.

1983 ◽  
Vol 45 (3) ◽  
pp. 1195-1199 ◽  
Author(s):  
S A Latt ◽  
S P Goff ◽  
C J Tabin ◽  
M Paskind ◽  
J Y Wang ◽  
...  
Keyword(s):  
Murine Leukemia Virus ◽  
Leukemia Virus ◽  
Abelson Murine Leukemia Virus ◽  
Reverse Transcript ◽  
Murine Leukemia

Abelson murine leukemia virus induces platelet-derived growth factor-independent fibroblast growth: correlation with kinase activity and dissociation from full morphologic transformation

1989 ◽  
Vol 9 (1) ◽  
pp. 278-287
Author(s):  
R W Rees-Jones ◽  
M Goldfarb ◽  
S P Goff
Keyword(s):  
Growth Factor ◽  
Murine Leukemia Virus ◽  
Kinase Activity ◽  
Cell Transformation ◽  
Leukemia Virus ◽  
Platelet Derived Growth Factor ◽  
Fibroblast Growth ◽  
Morphological Transformation ◽  
Abelson Murine Leukemia Virus ◽  
Murine Leukemia

Abelson murine leukemia virus (A-MuLV) encodes a single protein product, a tyrosine-specific protein kinase, whose activity is necessary for cell transformation by this retrovirus. Using a defined medium culture system, we demonstrate that transformation of NIH 3T3 fibroblasts by A-MuLV abrogates their normal requirement for platelet-derived growth factor (PDGF) for cell growth. Analysis of constructed insertional mutant viruses revealed an absolute correlation between A-MuLV-encoded tyrosine kinase activity and PDGF-independent fibroblast growth. Sequences of the provirus not required for kinase activity appeared unnecessary for abrogating the fibroblast requirement for PDGF. Conversely, sequences required for kinase activity appeared necessary, suggesting that induction of PDGF-independent fibroblast growth, like cell transformation, is a function of this tyrosine kinase. Fibroblasts transformed by a partially transformation-defective mutant demonstrated incomplete morphological transformation but were still independent of PDGF for growth. Thus, the processes of full morphological transformation and growth factor independence can be partially dissociated.

Determinants of Abelson Murine Leukemia Virus Pathogenesis

1986 ◽  
pp. 62-74
Author(s):  
Patrick L. Green ◽  
Gina D. Holland ◽  
Donal Kaehler ◽  
John McKearn ◽  
James McCubrey ◽  
...  
Keyword(s):  
Murine Leukemia Virus ◽  
Leukemia Virus ◽  
Abelson Murine Leukemia Virus ◽  
Murine Leukemia
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