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Department of Medicine, Division of Oncology, University of Rochester School of Medicine [W. D. D. W. J. M. M.], Strong Memorial Hospital [W. D. D. W.], and Rochester General Hospital [W. D. D. W.], Rochester, New York 14642
Previous studies have suggested that the adverse effects of a tumor may limit host recovery after treatment with cyclophosphamide. In the present study the effect of a tumor on the hematopoietic system after cyclophosphamide treatment was assessed by measuring the dose response of marrow colony-forming units (CFU); by following serially the recovery of marrow CFU, marrow cellularity, and peripheral blood counts; and by bioassaying the marrow for metastases. The dose response measured 24 hr after cyclophosphamide showed equal degrees of marrow sensitivity in normal and tumor-bearing mice. In serial measurements of marrow recovery, a delay in the regrowth of CFU was observed in tumor-bearing mice. This delay in CFU regrowth resulted in a more pronounced depression of marrow cellularity and a lower nadir of peripheral blood counts in tumor-bearing mice. The lower nadir of peripheral blood counts in tumor-bearing mice could be correlated with drug-related mortality in treated mice. Marrow bioassay excluded marrow metastases as a factor in this delayed recovery.
These observations suggest that a tumor may have systemic inhibitory effects on the proliferation of marrow stem cells. This distant effect of cancer may reflect a deficiency state or an elaboration of an inhibitory tumor by-product or may be mediated through alteration in humoral factors controlling marrow stem cell proliferation.
1 Supported by Grants CA-08112 and CA-1198, National Cancer Institute, and a grant from the Monroe County Cancer and Leukemia Association.
2 Junior Faculty Fellow of the American Cancer Society. Address correspondence to Dr. DeWys, Section of Medical Oncology, Department of Medicine, Northwestern University Medical School, 303 East Chicago Avenue, Chicago, Ill. 60611.
Received 5/ 4/73. Accepted 7/17/73.
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