PMID: 9450806Feb 5, 1998Paper

Long-term bone marrow cultured stromal cells regulate myeloma tumour growth in vitro: studies with primary tumour cells and LTBMC-dependent cell lines

British Journal of Haematology
A C BloemH M Lokhorst

Abstract

Long-term bone marrow cultured stromal cells (LTBMC) produce IL-6 after contact with tumour cells from multiple myeloma patients. We found that LTBMC could substitute for exogenous IL-6 in the stimulation of bone marrow plasma cells from myeloma patients with active disease in short-term cultures. In addition, tumour cells of some patients with inactive disease, which were unresponsive to exogenous IL-6, were induced to IL-6-dependent growth after LTBMC co-culture. To study the role of LTBMC in myeloma tumour growth in vitro, plasma cell lines UM-2 and UM-3 were selected. UM-2 and UM-3 grew in contact with LTBMC and proliferation was blocked by antibodies against IL-6, IL-6 receptor (IL-6R, gp80, CD126) or the common signal transducing unit, gp130 (CD130). Culture with IL-6 alone or combined with GM-CSF resulted in cell death via apoptosis. The combination of IL-6 with soluble gp80, however, maintained in vitro proliferation of UM-2 and UM-3 cells. These data imply that LTBMC regulate myeloma growth in vitro via production of IL-6, possibly via induction of a functional IL-6 receptor on the tumour cells.

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Citations

May 2, 2001·Journal of Interferon & Cytokine Research : the Official Journal of the International Society for Interferon and Cytokine Research·H S JunejaP J Davies
Apr 26, 2008·Blood·Xin LiShmuel Yaccoby
Mar 21, 2009·Hematology·Dulce Marta SchimieguelJosé Salvador Rodrigues de Oliveira
Feb 4, 2003·Clinical and Experimental Immunology·P A HollowayH M Lokhorst
Mar 23, 2004·Biochemical and Biophysical Research Communications·Hélène LiboubanDaniel Chappard
Jan 8, 2000·Hematology/oncology Clinics of North America·N N Sjak-ShieJ R Berenson
Mar 18, 2004·Cancer Research·Shmuel YaccobyJoshua Epstein

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Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis