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introduction
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by clonal expansion of immature myeloblasts, initiating from rare leukemic stem or progenitor cells. In Europe and the USA, the incidence and mortality rates of AML are about 5 to 8/100.000 and 4 to 6/100.000 per year, respectively.>>1<< Despite a high rate of complete remission after treatment with genotoxic agents, the relapse rate remains very high and the prognosis very poor.
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Relapses are caused by malignant cell regrowth initiated by chemoresistant leukemic clones.>>2<<,
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Relapses are caused by malignant cell regrowth initiated by chemoresistant leukemic clones.2, >>3<<
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a robust xenotransplantation model to study primary human AML biology and stem cell function based on the engraftment of primary AML samples into non-obese diabetic (NOD)/LtSz-severe combined immunodeficiency (SCID) IL2Rγcnull (NSG) mice.>>4<<, 5 These highly immunodeficient mice have the advantages of a longer life span and higher levels of engraftment of human AML cells compared with other immunocompromised mouse strains such as SCID, NOD-SCID.
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xenotransplantation model to study primary human AML biology and stem cell function based on the engraftment of primary AML samples into non-obese diabetic (NOD)/LtSz-severe combined immunodeficiency (SCID) IL2Rγcnull (NSG) mice.4, >>5<< These highly immunodeficient mice have the advantages of a longer life span and higher levels of engraftment of human AML cells compared with other immunocompromised mouse strains such as SCID, NOD-SCID.
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(SCID) IL2Rγcnull (NSG) mice.4, 5 These highly immunodeficient mice have the advantages of a longer life span and higher levels of engraftment of human AML cells compared with other immunocompromised mouse strains such as SCID, NOD-SCID.>>4<<, 6, 7 However, this model is based on three-to-six month-long experiments with a large excess of cells and requires access to a biobank of diverse primary AML patient samples.
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IL2Rγcnull (NSG) mice.4, 5 These highly immunodeficient mice have the advantages of a longer life span and higher levels of engraftment of human AML cells compared with other immunocompromised mouse strains such as SCID, NOD-SCID.4, >>6<<, 7 However, this model is based on three-to-six month-long experiments with a large excess of cells and requires access to a biobank of diverse primary AML patient samples.
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IL2Rγcnull (NSG) mice.4, 5 These highly immunodeficient mice have the advantages of a longer life span and higher levels of engraftment of human AML cells compared with other immunocompromised mouse strains such as SCID, NOD-SCID.4, 6, >>7<< However, this model is based on three-to-six month-long experiments with a large excess of cells and requires access to a biobank of diverse primary AML patient samples.
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results and discussion
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of primary human AML or normal CD34+ cells is greatly enhanced if recipients receive a chemical conditioning regimen such as busulfan (a myeloablative alkylating agent, 25–35 mg/kg) or total body irradiation (up to 4 Gy).>>8<<, 9, 10, 11 However, it is not clear whether conditioning improves the engraftment of human AML cell lines especially in the most recently developed NSG mouse model.
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of primary human AML or normal CD34+ cells is greatly enhanced if recipients receive a chemical conditioning regimen such as busulfan (a myeloablative alkylating agent, 25–35 mg/kg) or total body irradiation (up to 4 Gy).8, >>9<<, 10, 11 However, it is not clear whether conditioning improves the engraftment of human AML cell lines especially in the most recently developed NSG mouse model.
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of primary human AML or normal CD34+ cells is greatly enhanced if recipients receive a chemical conditioning regimen such as busulfan (a myeloablative alkylating agent, 25–35 mg/kg) or total body irradiation (up to 4 Gy).8, 9, >>10<<, 11 However, it is not clear whether conditioning improves the engraftment of human AML cell lines especially in the most recently developed NSG mouse model.
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8, 9, 10, >>11<< However, it is not clear whether conditioning improves the engraftment of human AML cell lines especially in the most recently developed NSG mouse model.
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show a diversity of engraftment capacities and aggressiveness in these AML cell lines, as well as a diversity in tissue tropism, consistent with what we observed with AML patient cells transplanted in the same immunodeficient mice strain.>>4<< Engraftment levels, tissue distribution and overall survival are not associated with any clinical features and cytogenetic abnormalities.
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With the sole exception of the CD38 marker, the NSG-based model of AML maintains cell phenotype more consistently than in the NOD-SCID model.>>12<<
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