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Blood, Vol. 94 No. 8 (October 15), 1999:
pp. 2901-2910
Shiga-Like Toxin-1 Receptor on Human Breast Cancer, Lymphoma, and
Myeloma and Absence From CD34+ Hematopoietic Stem Cells:
Implications for Ex Vivo Tumor Purging and Autologous Stem Cell
Transplantation
E.C. LaCasse,
M.R. Bray,
B. Patterson,
W.-M. Lim,
S. Perampalam,
L. G. Radvanyi,
A. Keating,
A.K. Stewart,
R. Buckstein,
J.S. Sandhu,
N. Miller,
D. Banerjee,
D. Singh,
A.R. Belch,
L.M. Pilarski, and
J. Gariépy
From the Department of Medical Biophysics, University of Toronto and
the Ontario Cancer Institute, Toronto, Ontario, Canada; the Department
of Oncologic Pathology, Princess Margaret Hospital, Toronto, Ontario,
Canada; the Autologous Blood and Marrow Transplantation Program,
University of Toronto and the Toronto Hospital, Toronto, Ontario,
Canada; the Samuel Lunenfeld Research Institute, Mount Sinai Hospital
(Toronto) and the Department of Pathology, Women's College Hospital,
Toronto, Ontario, Canada; and the Department of Oncology, University of
Alberta and the Cross Cancer Institute, Edmonton, Alberta,
Canada.
The ribosome-inactivating protein, Shiga-like toxin-1 (SLT-1),
targets cells that express the glycolipid globotriaosylceramide (CD77) on their surface. CD77 and/or SLT-1 binding was detected by flow
cytometry and immunocytochemistry on lymphoma and breast cancer cells
recovered from biopsies of primary human cancers as well as on B cells
or plasma cells present in blood/bone marrow samples of multiple
myeloma patients. Breast cancer cell lines also expressed receptors for
the toxin and were sensitive to SLT-1. Treatment of primary B lymphoma,
B-cell chronic lymphocytic leukemia, and myeloma B or
plasma cells with SLT-1-depleted malignant B cells by 3- to 28-fold,
as measured by flow cytometry. Depletion of myeloma plasma cells was
confirmed using a cellular limiting dilution assay followed by reverse
transcriptase-polymerase chain reaction analysis of
clonotypic IgH transcripts, which showed a greater than 3 log reduction
in clonotypic myeloma cells after SLT-1 treatment. Receptors for the
toxin were not detected on human CD34+ hematopoietic
progenitor cells (HPC). HPC were pretreated with a concentration of
SLT-1 known to purge primary malignant B cells and cultured for 6 days.
The number of HPC was comparable in toxin-treated and untreated
cultures. HPC were functionally intact as well. Colony-forming units
(CFU) were present at an identical frequency in untreated and SLT-1
pretreated cultures, confirming that CFU escape SLT-1 toxicity. The
results suggest the ex vivo use of SLT-1 in purging SLT-1
receptor-expressing malignant cells from autologous stem cell grafts of
breast cancer, lymphoma, and myeloma patients.
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