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Blood, Vol. 92 No. 10 (November 15), 1998:
pp. 3817-3828
Development of a Model for Evaluating the Interaction Between Human
Pre-B Acute Lymphoblastic Leukemic Cells and the Bone Marrow Stromal
Cell Microenvironment
Nisha Shah,
LeAnn Oseth, and
Tucker W. LeBien
From the Department of Laboratory Medicine/Pathology, Center for
Immunology, and the Cancer Center, University of Minnesota,
Minneapolis, MN.
Clonal expansion of B-cell precursor acute lymphoblastic leukemia
(ALL) is potentially regulated by survival, growth, and death signals
transduced by the bone marrow (BM) microenvironment. Using a human BM
stromal cell culture that supports the growth of normal human B-cell
precursors, we established a pre-B ALL cell line designated BLIN-2.
BLIN-2 has a clonal rearrangement of the Ig heavy chain locus, a
dic(9;20) chromosomal abnormality, and a bi-allelic deletion of the
p16INK4a and p19ARF genes. The
most interesting feature of BLIN-2 is an absolute dependence on
adherent human BM stromal cells for sustained survival and growth.
BLIN-2 cultured in the absence of BM stromal cells undergo apoptosis,
and direct contact with viable BM stromal cells is essential for
optimal growth. BLIN-2 cells also grow on vascular cell adhesion
molecule-1 (VCAM-1)-negative human skin fibroblasts, making it
unlikely that a very late antigen-4 (VLA-4)/VCAM-1
interaction is required for BLIN-2 growth. Western blot analysis of
BLIN-2 cells cultured in the presence or absence of BM stromal cells demonstrates that contact of BLIN-2 with BM stromal cells induces hyperphosphorylation of Rb. In contrast, the pre-B ALL cell line BLIN-1, which has a bi-allelic deletion of p16INK4a
p19ARF but does not require BM stromal cells for growth,
does not undergo Rb phosphorylation after BM stromal cell contact. The
BLIN-2 cell line will facilitate identification of ligand/receptor
interactions at the B-cell precursor/BM stromal cell interface and may
provide new insight into microenvironmental regulation of leukemic cell survival and growth.
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