| pubmed-article:3472017 | pubmed:abstractText | During the invasion of leukemic cells of the rat acute myelocytic leukemia model BNML in the bone marrow, the number of normal bone marrow stem cells (CFU-S) decreased while simultaneously an increase of CFU-S in the leukemic spleen was observed. A small reduction in the tumor load by low dose cyclophosphamide treatment (10 mg/kg) caused a temporary CFU-S recovery in the bone marrow. After a therapeutic dose of cyclophosphamide (100 mg/kg), the CFU-S numbers in femur and spleen decreased to low levels but they rapidly increased immediately thereafter. In the spleen, however, the CFU-S increase halted when femoral CFU-S numbers reached normal levels. Splenectomy following cyclophosphamide treatment revealed that the splenic CFU-S population does not play a role in regeneration of hemopoiesis. During the subsequent leukemia relapse, CFU-S in the femur decreased again while spleen CFU-S tended to rise. It is concluded that the bone marrow CFU-S, which survive both the leukemia and the remission-induction treatment, and not the migrated, extramedullary localized stem cells are the major source for the restoration of normal hemopoiesis. | lld:pubmed |
