Enhancement by conditioned medium of stretched calvarial bone cells of the osteoclast-like cell formation induced by parathyroid hormone in mouse bone marrow cultures

1997 ◽  
Vol 42 (3) ◽  
pp. 205-211 ◽  
Author(s):  
S. Soma ◽  
S. Matsumoto ◽  
T. Takano-Yamamoto
Endocrinology ◽  
1988 ◽  
Vol 122 (4) ◽  
pp. 1373-1382 ◽  
Author(s):  
NAOYUKI TAKAHASHI ◽  
HIROMI YAMANA ◽  
SHUSAKU YOSHIKI ◽  
G. DAVID ROODMAN ◽  
GREGORY R. MUNDY ◽  
...  

1992 ◽  
Vol 17 ◽  
pp. 189
Author(s):  
K. Kasono ◽  
K. Sato ◽  
Ya. Sato ◽  
K. Shizume ◽  
H. Demura

1994 ◽  
Vol 263 (1-2) ◽  
pp. 181-185 ◽  
Author(s):  
Yasuhiro Akiyama ◽  
Kuniko Hara ◽  
Tetsuya Tajima ◽  
Sei-itsu Murota ◽  
Ikuo Morita

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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