Relationship Between Concanavalin A-Induced Agglutinability of Murine Leukemia Cells and Their Propensity To Form Heterotypic Aggregates With Syngeneic Lymphoid Cells234

1981 ◽  
Keyword(s):  
Concanavalin A ◽  
Lymphoid Cells ◽  
Leukemia Cells ◽  
Murine Leukemia

Aryl Maleimides as Apoptosis Inducers on L5178-Y Murine Leukemia Cells (in silico, in vitro and ex vivo Study)

2016 ◽  
Vol 16 (12) ◽  
pp. 1615-1621 ◽  
Author(s):  
Erik Andrade-Jorge ◽  
Marycarmen Godínez-Victoria ◽  
Luvia Enid Sánchez-Torres ◽  
Luis Humberto Fabila-Castillo ◽  
José G. Trujillo-Ferrara
Keyword(s):  
In Silico ◽  
Ex Vivo ◽  
Leukemia Cells ◽  
Ex Vivo Study ◽  
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.

Lymphoid and other tissue-specific phenotypes of polyomavirus enhancer recombinants: positive and negative combinational effects on enhancer specificity and activity

1986 ◽  
Vol 6 (6) ◽  
pp. 2068-2079
Author(s):  
B A Campbell ◽  
L P Villarreal
Keyword(s):  
Cell Lines ◽  
Heavy Chain ◽  
Murine Leukemia Virus ◽  
Tissue Specificity ◽  
Leukemia Virus ◽  
Simian Virus 40 ◽  
Simian Virus ◽  
Lymphoid Cells ◽  
B Lymphoid ◽  
Murine Leukemia

Heterologous enhancer recombinants and deletions of the polyomavirus (Py) noncoding region were constructed and analyzed for tissue specificity of DNA replication and transcription in a number of lymphoid and other cell lines. The simian virus 40 72-base-pair repeat, mouse immunoglobulin heavy-chain enhancer, and Moloney murine leukemia virus enhancer were inserted into the PvuII-D locus (nucleotides 5128 through 5265) of Py. The ability of these recombinants and the parental PvuII-D deletion mutant to replicate in permissive 3T6 cells and MOP-6 cells as well as in nonpermissive mouse B lymphoid, T lymphoid, mastocyte, and embryonal carcinoma cells was determined. Wild-type Py DNA was not permissive for replication in most lymphoid cell lines, except one hybridoma line. Simply deleting the Py PvuII-D region, however, gave Py an expanded host range, allowing high-level replication in some T lymphoid and mastocytoma cell lines, indicating that this element can be a tissue-specific negative as well as positive element. Substitution of the murine leukemia virus enhancer for Py PvuII-D yielded a Py genome which retained the ability to replicate in 3T6 cells but also replicated well in B lymphoid cells. Substitution with the immunoglobulin heavy-chain enhancer allowed replication in B lymphoid cells but interfered with replication in 3T6 cells and mastocytomas. Surprisingly, substitution with the simian virus 40 72-base-pair enhancer repeat gave a recombinant which would not replicate in any cell line tried, including MOP-6 cells, even though other recombinants with this enhancer would replicate. Thus, we observed both cooperation and interference in these combinations between enhancer components and the Py genome and that these combined activities were cell specific. These results are presented as evidence that there may be a positional dependence, or syntax, for the recognition of genetic elements controlling Py tissue specificity.

scholarly journals Differential effect of 4-hydroperoxycyclophosphamide and antimyeloid monoclonal antibodies on T and natural killer cells during bone marrow purging

Blood ◽  
1994 ◽  
Vol 83 (8) ◽  
pp. 2345-2351 ◽  
Author(s):  
RK Zhong ◽  
AD Donnenberg ◽  
J Rubin ◽  
ED Ball
Keyword(s):  
Bone Marrow ◽  
Monoclonal Antibodies ◽  
Natural Killer ◽  
Progenitor Cells ◽  
Interleukin 2 ◽  
Lymphoid Cells ◽  
Hematopoietic Progenitor Cells ◽  
Leukemia Cells ◽  
High Dose ◽  
Hematopoietic Progenitor

Abstract Autologous bone marrow (BM) transplantation after high dose therapy is widely used to treat acute leukemia, lymphoma, and selected solid tumors. In studies of BM purging with chemical agents, monoclonal antibodies (MoAbs), or other agents, the emphasis has been on the efficacy of tumor cell removal and sparing of hematopoietic progenitor cells. Two commonly used methods of BM purging for patients with acute myeloid leukemia have been the drug 4-hydroperoxycyclophosphamide (4- HC) and (MoAbs) directed to myeloid antigens such as CD14, CD15, and CD33. Although both methods of BM purging have potent activity against leukemia cells, 4-HC is also quite toxic to normal hematopoietic progenitor cells in the same concentrations that are used to deplete leukemia cells. To further characterize the cellular composition of BM after purging, we examined the effects of MoAbs plus complement and 4- HC on cells of the lymphoid lineage in the BM. 4-HC exerted a concentration-dependent cytotoxicity on clonogenic T lymphocytes, natural killer (NK) cells, and lymphokine (interleukin-2)-activated killer (LAK) cells, whereas the anti-CD14 and anti-CD15 MoAbs had little effect. At a concentration of 4-HC commonly used for BM purging (60 micrograms/mL), there were 4 to 5 logs of T-cell depletion and almost complete elimination of NK- and LAK-cell activity. In contrast, 4-HC at low concentrations (eg, 3 micrograms/mL) spared the majority of lymphoid cells suggesting that low concentration 4-HC combined with MoAb purging may be a desirable alternative to higher concentration 4- HC. These data indicate that purging with antimyeloid MoAbs, but not with 4-HC, spares the function of mature graft lymphocytes. Infusion of viable lymphocytes may be important for the transfer of immune memory against microbial and neoplastic antigens and may hasten immune reconstitution. In addition, mature graft lymphocytes may also be selectively activated and expanded in conjunction with interleukin-2 administration after BM transplantation.

scholarly journals Solanum lyratumExtracts Induce Extrinsic and Intrinsic Pathways of Apoptosis in WEHI-3 Murine Leukemia Cells and Inhibit Allograft Tumor

2012 ◽  
Vol 2012 ◽  
pp. 1-13 ◽  
Author(s):  
Jai-Sing Yang ◽  
Chia-Chun Wu ◽  
Chao-Lin Kuo ◽  
Yu-Hsuan Lan ◽  
Chin-Chung Yeh ◽  
...  
Keyword(s):  
Antitumor Activity ◽  
Molecular Mechanisms ◽  
Fas Ligand ◽  
Leukemia Cells ◽  
Cycle Arrest ◽  
Phase Arrest ◽  
Apoptotic Pathways ◽  
Murine Leukemia

We investigated the molecular mechanisms of cell cycle arrest and apoptotic death induced bySolanum lyratumextracts (SLE) or diosgenin in WEHI-3 murine leukemia cellsin vitroand antitumor activityin vivo. Diosgenin is one of the components of SLE. Our study showed that SLE and diosgenin decreased the viable WEHI-3 cells and inducedG0/G1phase arrest and apoptosis in concentration- or time-dependent manners. Both reagents increased the levels of ROS production and decreased the mitochondrial membrane potential (ΔΨm). SLE- and diosgenin-triggered apoptosis is mediated through modulating the extrinsic and intrinsic signaling pathways. Intriguingly, the p53 inhibitor (pifithrin-α), anti-Fas ligand (FasL) mAb, and specific inhibitors of caspase-8 (z-IETD-fmk), caspase-9 (z-LEHD-fmk), and caspase-3 (z-DEVD-fmk) blocked SLE- and diosgenin-reduced cell viability of WEHI-3 cells. Thein vivostudy demonstrated that SLE has marked antitumor efficacy against tumors in the WEHI-3 cell allograft model. In conclusion, SLE- and diosgenin-inducedG0/G1phase arrest and triggered extrinsic and intrinsic apoptotic pathways via p53 activation in WEHI-3 cells. SLE also exhibited antitumor activityin vivo. Our findings showed that SLE may be potentially efficacious in the treatment of leukemia in the future.

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