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High Level Engraftment of NOD/SCID Mice by Primitive Normal and
Leukemic Hematopoietic Cells From Patients With Chronic Myeloid
Leukemia in Chronic Phase
J.C.Y. Wang,
T. Lapidot,
J.D. Cashman,
M. Doedens,
L. Addy,
D.R. Sutherland,
R. Nayar,
P. Laraya,
M. Minden,
A. Keating,
A.C. Eaves,
C.J. Eaves, and
J.E. Dick
From the Department of Genetics, Research Institute, Hospital for
Sick Children; the Department of Molecular and Medical Genetics,
University of Toronto; the Department of Medicine, Princess Margaret
Hospital; the Department of Hematology/Oncology, the Toronto Hospital,
Toronto, Ontario; and the Terry Fox Laboratory, British Columbia Cancer
Agency, Vancouver, British Columbia, Canada.
We have previously shown that intravenously injected peripheral
blood (PB) or bone marrow (BM) cells from newly diagnosed chronic
myeloid leukemia (CML) patients can engraft the BM of sublethally
irradiated severe combined immunodeficient (SCID) mice. We now report
engraftment results for chronic phase CML cells in nonobese diabetic
(NOD)/SCID recipients which show the superiority of this latter model.
Transplantation of NOD/SCID mice with 7 to 10 × 107 patient PB or BM cells resulted in the continuing
presence of human cells in the BM of the mice for up to 7 months, and
primitive human CD34+ cells, including those detectable
as colony-forming cells (CFC), as long-term culture-initiating cells,
or by their coexpression of Thy-1, were found in a higher proportion of
the NOD/SCID recipients analyzed, and at higher levels than were seen
previously in SCID recipients. The human CFC and total human cells
present in the BM of the NOD/SCID mice transplanted with CML cells also
contained higher proportions of leukemic cells than were obtained in
the SCID model, and NOD/SCID mice could be repopulated with transplants of enriched CD34+ cells from patients with CML. These
results suggest that the NOD/SCID mouse may allow greater engraftment
and amplification of both normal and leukemic (Ph+)
cells sufficient for the quantitation and characterization of the
normal and leukemic stem cells present in patients with CML. In
addition, this model should make practical the investigation of
mechanisms underlying progression of the disease and the development of
more effective in vivo therapies.
Blood, Vol. 91 No. 7 (April 1), 1998:
pp. 2406-2414
© 1998 by The American Society of Hematology.
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