Long-term marrow culture of cells from patients with acute myelogenous leukemia. Selection in favor of normal phenotypes in some but not all cases.

Persistence of dormant leukemic progenitors during interferon-induced remission in chronic myelogenous leukemia. Analysis by polymerase chain reaction of individual colonies.

“…However, with this treatment, the normal hemopoiesis is restored by donor bone marrow. Evidence for persistent, albeit suppressed normal progenitors in patients with CML comes from long-term bone marrow cultures, and clinically complete restoration of normal hemopoiesis can be obtained with intensive chemotherapeutic treatments (2,3). However, the remissions induced by the latter are of short duration.…”

In AML t(8;21) colony growth of both leukemic and residual normal progenitors is restricted to the CD34+, lineage-negative fraction

“…Interestingly, these authors concluded from their data that in some AML precursors are non-clonal, without speculating about residual normal colonies. Coulombel et al 20 and Iland et al 21 reported overgrowth of normal BM cells over leukemic cells in long-term bone marrow culture. Coulombel et al 20 concluded that long-term marrow culture selected in favor of residual normal progenitors.…”

“…Coulombel et al 20 and Iland et al 21 reported overgrowth of normal BM cells over leukemic cells in long-term bone marrow culture. Coulombel et al 20 concluded that long-term marrow culture selected in favor of residual normal progenitors. However, their data also fit with our observations that the residual normal progenitors show growth and differentiation for a longer period (up to 4 weeks) compared with the leukemic progenitors.…”

“…Residual normal colonies have been observed in full-blown AML bone marrow samples by other investigators. [19][20][21] Bernstein et al 19 separated the more differentiated and more primitive cells by labeling with CD34 and CD33. The CD34 + /CD33 − fraction in AML (in contrast with CML) produced colonies that were non-clonal using G6PD as a clonality marker.…”

Large scale recovery and characterization of stromal cell-associated primitive haemopoietic progenitor cells from filter-retained human bone marrow

“…Failure may be due to insufficient grafted HSCs, [2][3][4][5] an acute graftversus-host reaction and graft rejection, 6,7 too many residual malignant cells 8 or severe opportunistic infection. Defective stromal cell function may also contribute to graft failure, because the stromal cell compartment in the host BM was not replaced by donor derived cells following transplantation, 9 and persistent, not yet fully defined abnormalities of the stromal cells have been described before treatment in patients with malignant haemopathies, [10][11][12][13][14] and following intensive chemotherapy or radiation. 15 The development of optimal conditioning regimens, 16 the use of selective cytotoxic agents to purge the BM of malignant cells, 17 the use of recombinant haemopoietic growth factors (rHGFs) to accelerate BM regeneration, 18 and most recently, the use of peripheral stem cells, 19 purified CD34 + or CD34 + CD38 − cells 20 and umbilical cord blood cells 21,22 have all considerably improved the efficacy of HSCT technology and have opened up new perspectives.…”