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Individualized intervention guided by BCR-ABL transcript levels after HLA-identical sibling donor transplantation improves HSCT outcomes for subjects with chronic myeloid leukemia.

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The online version of this article has a Supplementary Appendix. BackgroundTo understand how myelodysplastic syndrome cells evolve from normal stem cells and gain competitive advantages over normal hematopoiesis, we established a murine xenograft model harboring bone marrow cells from patients with myelodysplastic syndromes or acute myeloid leukemia with myelodysplasia-related changes. Design and Methods Bone marrow CD34+ cells obtained from patients were injected, with or without human mesenchymal stem cells, into the bone marrow of non-obese diabetic/severe combined immunodeficient/IL2Rγ null hosts. Engraftment and differentiation of cells derived from the patients were investigated by flow cytometry and immunohistochemical analysis. ResultsCo-injection of patients' cells and human mesenchymal stem cells led to successful engraftment of patient-derived cells that maintained the immunophenotypes and genomic abnormalities of the original patients. Myelodysplastic syndrome-originated clones differentiated into mature neutrophils, megakaryocytes, and erythroblasts. Two of the samples derived from patients with acute myeloid leukemia with myelodysplasia-related changes were able to sustain neoplastic growth into the next generation while these cells had limited differentiation ability in the murine host. The hematopoiesis of mice engrafted with patients' cells was significantly suppressed even when human cells accounted for less than 1% of total marrow mononuclear cells. Histological studies revealed invasion of the endosteal surface by patient-derived CD34 + cells and disruption of extracellular matrix architecture, which probably caused inhibition of murine hematopoiesis. ConclusionsWe established murine models of human myelodysplastic syndromes using cells obtained from patients: the presence of neoplastic cells was associated with the suppression of normal host hematopoiesis. The efficiency of engraftment was related to the presence of an abnormality in chromosome 7.Key words: xenograft, MDS, NOG mouse, niche, MSC. syndromes. Haematologica 2011;96(4):543-551. doi:10.3324/haematol.2010 This is an open-access paper. Citation: Muguruma Y, Matsushita H, Yahata T, Yumino S, Tanaka Y, Miyachi H, Ogawa Y, Kawada H, Ito M, and Ando K. Establishment of a xenograft model of human myelodysplastic Establishment of a xenograft model of human myelodysplastic syndromes

The platelet counting performance of the PLT-F channel of the XN Series had improved accuracy and precision in the low range and in abnormal samples, avoiding the interference by nonplatelet particles.