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Direct demonstration that autologous bone marrow transplantation for solid
tumors can return a multiplicity of tumorigenic cells
DR Rill, VM Santana, WM Roberts, T Nilson, LC Bowman, RA Krance, HE Heslop, RC Moen, JN Ihle and MK Brenner
Division of Bone Marrow Transplantation, St Jude Children's Research
Hospital, Memphis, TN 38105.
Patients with solid tumors are increasingly being treated by autologous
bone marrow transplantation (BMT). Although response rates appear to be
increased, disease recurrence is the commonest cause of treatment failure.
Whether relapse is entirely due to residual disease in the patient or
arises also from infiltrating malignant cells contained in the autologous
marrow transplant has not been resolved. If the latter explanation is
correct, then purging would be required as part of the transplantation
procedure. We used retrovirally mediated transfer of the
neomycin-resistance gene to mark BM harvested from eight patients with
neuroblastoma in clinical remission. The marked marrow cells were
subsequently reinfused as part of an autologous BMT. At relapse, we sought
the marker gene in malignant cell populations. Three patients have
relapsed, and in each the marker gene was detected by phenotypic and
genetic analyses of resurgent malignant cells at medullary and
extramedullary sites. Analysis of neuroblast DNA for discrete marker gene
integration sites suggested that at least 200 malignant cells, each capable
of tumor formation, were introduced with the autologous marrow transplant
and contributed to relapse. Thus, autologous BMTs administered to patients
with this solid tumor may contain a multiplicity of malignant cells that
subsequently contribute to relapse. The marker-gene technique we describe
should permit evaluation of the mechanisms of relapse and the efficacy of
purging in patients receiving autologous marrow transplantation for other
solid tumors that infiltrate the marrow.
Volume 84,
Issue 2,
pp. 380-383,
07/15/1994
Copyright © 1994 by The American Society of Hematology
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