scholarly journals Identification of a new common provirus integration site in gross passage A murine leukemia virus-induced mouse thymoma DNA.

1987 ◽  
Vol 7 (1) ◽  
pp. 512-522 ◽  
Author(s):  
R Villemur ◽  
Y Monczak ◽  
E Rassart ◽  
C Kozak ◽  
P Jolicoeur
Keyword(s):  
T Cell ◽  
Murine Leukemia Virus ◽  
Cell Transformation ◽  
Integration Site ◽  
Leukemia Virus ◽  
Tumor Development ◽  
Mouse Strains ◽  
Mouse Tumor ◽  
Provirus Integration ◽  
Murine Leukemia

The Gross passage A murine leukemia virus (MuLV) induced T-cell leukemia of clonal (or oligoclonal) origin in inoculated mice. To study the role of the integrated proviruses in these tumor cells, we cloned several newly integrated proviruses (with their flanking cellular sequences) from a single tumor in procaryotic vectors. With each of the five clones obtained, a probe was prepared from the cellular sequences flanking the provirus. With one such probe (SS8), we screened several Gross passage A MuLV-induced SIM.S mouse tumor DNAs and found that, in 11 of 40 tumors, a provirus was integrated into a common region designated Gin-1. A 26-kilobase-pair sequence of Gin-1 was cloned from two lambda libraries, and a restriction map was derived. All proviruses were integrated as a cluster in the same orientation within a 5-kilobase-pair region of Gin-1, and most of them had a recombinant structure of the mink cell focus-forming virus type. The frequency of Gin-1 occupancy by provirus was much lower in thymoma induced by other strains of MuLV in other mouse strains. Using somatic-cell hybrid DNAs, we mapped Gin-1 on mouse chromosome 19. Gin-1 was not homologous to 16 known oncogenes and was distinct from the other common regions for provirus integration previously described. Therefore, Gin-1 appears to represent a new common provirus integration region. The integration of a provirus within Gin-1 might be an important event leading to T-cell transformation, and the Gin-1 region might harbor sequences which are involved in tumor development.

Identification of a new common provirus integration site in gross passage A murine leukemia virus-induced mouse thymoma DNA

1987 ◽  
Vol 7 (1) ◽  
pp. 512-522 ◽  
Author(s):  
R Villemur ◽  
Y Monczak ◽  
E Rassart ◽  
C Kozak ◽  
P Jolicoeur
Keyword(s):  
T Cell ◽  
Murine Leukemia Virus ◽  
Cell Transformation ◽  
Integration Site ◽  
Leukemia Virus ◽  
Tumor Development ◽  
Mouse Strains ◽  
Mouse Tumor ◽  
Provirus Integration ◽  
Murine Leukemia

The Gross passage A murine leukemia virus (MuLV) induced T-cell leukemia of clonal (or oligoclonal) origin in inoculated mice. To study the role of the integrated proviruses in these tumor cells, we cloned several newly integrated proviruses (with their flanking cellular sequences) from a single tumor in procaryotic vectors. With each of the five clones obtained, a probe was prepared from the cellular sequences flanking the provirus. With one such probe (SS8), we screened several Gross passage A MuLV-induced SIM.S mouse tumor DNAs and found that, in 11 of 40 tumors, a provirus was integrated into a common region designated Gin-1. A 26-kilobase-pair sequence of Gin-1 was cloned from two lambda libraries, and a restriction map was derived. All proviruses were integrated as a cluster in the same orientation within a 5-kilobase-pair region of Gin-1, and most of them had a recombinant structure of the mink cell focus-forming virus type. The frequency of Gin-1 occupancy by provirus was much lower in thymoma induced by other strains of MuLV in other mouse strains. Using somatic-cell hybrid DNAs, we mapped Gin-1 on mouse chromosome 19. Gin-1 was not homologous to 16 known oncogenes and was distinct from the other common regions for provirus integration previously described. Therefore, Gin-1 appears to represent a new common provirus integration region. The integration of a provirus within Gin-1 might be an important event leading to T-cell transformation, and the Gin-1 region might harbor sequences which are involved in tumor development.

Tumor progression in murine leukemia virus-induced T-cell lymphomas: monitoring clonal selections with viral and cellular probes.

1986 ◽  
Vol 60 (1) ◽  
pp. 230-241 ◽  
Author(s):  
H T Cuypers ◽  
G C Selten ◽  
M Zijlstra ◽  
R E de Goede ◽  
C J Melief ◽  
...  
Keyword(s):  
T Cell ◽  
Tumor Progression ◽  
Murine Leukemia Virus ◽  
Leukemia Virus ◽  
T Cell Lymphomas ◽  
Cellular Probes ◽  
Murine Leukemia

scholarly journals Mutation of All Runx (AML1/Core) Sites in the Enhancer of T-Lymphomagenic SL3-3 Murine Leukemia Virus Unmasks a Significant Potential for Myeloid Leukemia Induction and Favors Enhancer Evolution toward Induction of Other Disease Patterns

2004 ◽  
Vol 78 (23) ◽  
pp. 13216-13231 ◽  
Author(s):  
Karina Dalsgaard Sørensen ◽  
Leticia Quintanilla-Martinez ◽  
Sandra Kunder ◽  
Jörg Schmidt ◽  
Finn Skou Pedersen
Keyword(s):  
T Cell ◽  
Murine Leukemia Virus ◽  
Myeloid Leukemia ◽  
Leukemia Virus ◽  
Color Flow ◽  
Potent Inducer ◽  
Induced Tumors ◽  
Myeloid Leukemias ◽  
T Lymphomas ◽  
Murine Leukemia

ABSTRACT SL3-3 murine leukemia virus is a potent inducer of T-lymphomas in mice. Using inbred NMRI mice, it was previously reported that a mutant of SL3-3 with all enhancer Runx (AML1/core) sites disrupted by 3-bp mutations (SL3-3dm) induces predominantly non-T-cell tumors with severely extended latency (S. Ethelberg, J. Lovmand, J. Schmidt, A. Luz, and F. S. Pedersen, J. Virol. 71:7273-7280, 1997). By use of three-color flow cytometry and molecular and histopathological analyses, we have now performed a detailed phenotypic characterization of SL3-3- and SL3-3dm-induced tumors in this mouse strain. All wild-type induced tumors had clonal T-cell receptor β rearrangements, and the vast majority were CD3+ CD4+ CD8− T-lymphomas. Such a consistent phenotypic pattern is unusual for murine leukemia virus-induced T-lymphomas. The mutant virus induced malignancies of four distinct hematopoietic lineages: myeloid, T lymphoid, B lymphoid, and erythroid. The most common disease was myeloid leukemia with maturation. Thus, mutation of all Runx motifs in the enhancer of SL3-3 severely impedes viral T-lymphomagenicity and thereby discloses a considerable and formerly unappreciated potential of this virus for myeloid leukemia induction. Proviral enhancers with complex structural alterations (deletions, insertions, and/or duplications) were found in most SL3-3dm-induced T-lymphoid tumors and immature myeloid leukemias but not in any cases of myeloid leukemia with maturation, mature B-lymphoma, or erythroleukemia. Altogether, our results indicate that the SL3-3dm enhancer in itself promotes induction of myeloid leukemia with maturation but that structural changes may arise in vivo and redirect viral disease specificity to induction of T-lymphoid or immature myeloid leukemias, which typically develop with moderately shorter latencies.

Sign in / Sign up

Export Citation Format

Share Document