The kinetics of granulopoiesis in long-term mouse bone marrow culture. Part I.

1984 ◽  
Vol 2 (6) ◽  
pp. 394-407 ◽  
Author(s):  
Ursula Reincke ◽  
Markus Loeffler ◽  
H. Erich Wichmann ◽  
Bettina Harrison

1984 ◽  
Vol 2 (6) ◽  
pp. 408-424 ◽  
Author(s):  
H. Erich Wichmann ◽  
Markus Loeffler ◽  
Ursula Reincke




2014 ◽  
Vol 182 (1) ◽  
pp. 92 ◽  
Author(s):  
Isabelle R. Miousse ◽  
Lijian Shao ◽  
Jianhui Chang ◽  
Wei Feng ◽  
Yingying Wang ◽  
...  


1986 ◽  
Vol 10 (6) ◽  
pp. 659-663 ◽  
Author(s):  
J.L. Chertkov ◽  
Nina J. Drize ◽  
Olga A. Gurevitch ◽  
G.A. Udalov


1989 ◽  
Vol 9 (9) ◽  
pp. 3973-3981 ◽  
Author(s):  
G V Borzillo ◽  
C J Sherr

Murine long-term bone marrow cultures that support B-lymphoid-cell development were infected with a helper-free retrovirus containing the v-fms oncogene. Infection of B-lymphoid cultures resulted in the rapid clonal outgrowth of early pre-B cells, which grew to high cell densities on stromal cell feeder layers, expressed v-fms-coded glycoproteins, and underwent immunoglobulin heavy-chain gene rearrangements. Late-passage cultures gave rise to factor-independent variants that proliferated in the absence of feeder layers, developed resistance to hydrocortisone, and became tumorigenic in syngeneic mice. The v-fms oncogene therefore recapitulates known effects of the v-abl and bcr-abl oncogenes on B-lineage cells. The ability of v-fms to induce transformation of early pre-B cells in vitro underscores the capacity of oncogenic mutants of the colony-stimulating factor-1 receptor to function outside the mononuclear phagocyte lineage.



1996 ◽  
Vol 93 (1) ◽  
pp. 30-37 ◽  
Author(s):  
Vikki Gill ◽  
Robin J. Shattock ◽  
Andrew R. Freedman ◽  
Grant Robinson ◽  
George E. Griffin ◽  
...  


2012 ◽  
Vol 4 (10) ◽  
pp. 1215 ◽  
Author(s):  
Masayoshi Yamaguchi ◽  
M. Neale Weitzmann ◽  
Clifton A. Baile ◽  
Tomiyasu Murata


1989 ◽  
Vol 9 (9) ◽  
pp. 3973-3981
Author(s):  
G V Borzillo ◽  
C J Sherr

Murine long-term bone marrow cultures that support B-lymphoid-cell development were infected with a helper-free retrovirus containing the v-fms oncogene. Infection of B-lymphoid cultures resulted in the rapid clonal outgrowth of early pre-B cells, which grew to high cell densities on stromal cell feeder layers, expressed v-fms-coded glycoproteins, and underwent immunoglobulin heavy-chain gene rearrangements. Late-passage cultures gave rise to factor-independent variants that proliferated in the absence of feeder layers, developed resistance to hydrocortisone, and became tumorigenic in syngeneic mice. The v-fms oncogene therefore recapitulates known effects of the v-abl and bcr-abl oncogenes on B-lineage cells. The ability of v-fms to induce transformation of early pre-B cells in vitro underscores the capacity of oncogenic mutants of the colony-stimulating factor-1 receptor to function outside the mononuclear phagocyte lineage.



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