Lymphoproliferative disease in human peripheral-blood-mononuclear-cell-injected scid mice. II. Role of host and donor factors in tumor generation

1994 ◽  
Vol 59 (5) ◽  
pp. 676-683 ◽  
Author(s):  
Arianna Veronesi ◽  
Vincenzo Coppola ◽  
Maria Luisa Veronese ◽  
Chiara Menin ◽  
Laura Bruni ◽  
...  
1992 ◽  
Vol 176 (6) ◽  
pp. 1763-1767 ◽  
Author(s):  
M L Veronese ◽  
A Veronesi ◽  
E D'Andrea ◽  
A Del Mistro ◽  
S Indraccolo ◽  
...  

Mechanisms of tumor development were studied in SCID mice injected with human lymphoid cells from Epstein-Barr virus-positive (EBV+) donors. About 80% of peripheral blood mononuclear cell (PBMC)-injected animals developed a lymphoproliferative disease associated with oligoclonal EBV+ tumors of human B cell origin. No change in tumor development rate occurred when monocyte-depleted PBMC were inoculated. No tumors developed when purified B cells were injected. B cell lymphoproliferative disease was also prevented in most cases when PBMC-injected animals were treated with agents that prevent T cell activation, such as cyclosporin A. Both CD4+ and CD8+ T cell subpopulations were able to provide putative factor(s) necessary for EBV+ B cell expansion and progression to tumors. These data suggest that the transfer alone of potentially tumorigenic human cells into an immunodeficient environment, such as the SCID mouse, might not be sufficient for cell progression to tumor, and raise the possibility that chronic activation events could play a major role in the pathogenesis of some EBV+ lymphomas in the immunocompromised host.


Virology ◽  
1997 ◽  
Vol 238 (1) ◽  
pp. 22-29 ◽  
Author(s):  
Gastón R. Picchio ◽  
Rebecca E. Sabbe ◽  
Richard J. Gulizia ◽  
Michael McGrath ◽  
Brian G. Herndier ◽  
...  

2016 ◽  
Vol 25 (1) ◽  
pp. 19-24
Author(s):  
Cicia Firakania ◽  
Indra G. Mansur ◽  
Sri W.A. Jusman ◽  
Mohamad Sadikin

Background: Cell proliferation occurs not only in normal but also in cancer cells. Most of cell proliferation inhibition can be done by inhibiting the DNA synthesis, notably by intervening the formation of purine or pyrimidine. In purine de novo synthesis, it was assumed that biotin plays a role as a coenzyme in carboxylation reaction, one of the pivotal steps in the purine de novo pathways. The aim of this study was to see the avidin potency to bind biotin and inhibit mitosis.Methods: Peripheral blood mononuclear cell (PBMC) was cultured in RPMI-1640 medium and stimulated by phytohemagglutinin (PHA) in the presence or absence of interleukin-2 (IL-2), with or without avidin. The effect of avidin addition was observed at 24, 48, and 72 hours for cell proliferation, viability, and cell cycle. Statistical analysis was done by one-way ANOVA.Results: Avidin inhibited cell proliferation and viability in culture under stimulation by PHA with and without IL-2. Cell cycle analysis showed that avidin arrested the progression of PBMC after 72 hours of culture. Most cells were found in G0/G1 phase.Conclusion: Inhibition of biotin utilization by avidin binding can halt cell proliferation.


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