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Blood, Vol. 94 No. 2 (July 15), 1999:
pp. 754-764
High Frequency of Adhesion Defects in B-Lineage Acute Lymphoblastic
Leukemia
Teunis B.H. Geijtenbeek,
Yvette van Kooyk,
Sandra J. van Vliet,
Maurits H. Renes,
Reinier A.P. Raymakers, and
Carl G. Figdor
From the Departments of Tumor Immunology and Hematology, University
Hospital Nijmegen, Nijmegen, The Netherlands.
Aberrant proliferation, differentiation, and/or migration of
progenitors observed in various hematological malignancies may be
caused by defects in expression and/or function of integrins. In this
study, we have developed a new fluorescent beads adhesion assay that
facilitates flow cytometric investigation of lymphocyte function-associated antigen 1 (LFA-1)- and very late activation antigen-4 (VLA-4)-mediated functional adhesion in B-lineage acute lymphoblastic leukemia (ALL) of both the CD10 and
CD10+ (leukemic) cell population within one blood or bone
marrow sample. Surprisingly, of the 20 B-lineage ALL patients
investigated, 17 contained a leukemic cell population with LFA-1-
and/or VLA-4-mediated adhesion defects. Five patients contained
CD10+ cells that did not exhibit any LFA-1-mediated
adhesion due to the lack of LFA-1 surface expression. The
CD10+ cells from 10 ALL patients expressed LFA-1 that
could not be activated by the phorbol ester phorbol 12-myristate
13-acetate (PMA), whereas the CD10 cells
expressed a functional LFA-1. Seven patients contained CD10+ cells that expressed a PMA-unresponsive form of
VLA-4. The PMA unresponsiveness of the integrins LFA-1 and VLA-4
expressed by the CD10+ cells may be due to mutations in
the integrins itself, in protein kinases, or in other intracellular
molecules involved in integrin adhesion. These data clearly demonstrate
the importance of investigating integrin function in addition to
integrin surface expression. The strikingly high frequency (85%) of
adhesion defects in ALL could suggest a causal relationship between
integrin-mediated adhesion and B-lineage ALL.
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