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1 od parameters, leukocyte depletion, and bone marrow hypoplasia.
2 asia, extramedullary hematopoiesis, and bone marrow hypoplasia.
3 y reduced BCNU-induced mortality due to bone marrow hypoplasia.
4 characterized by peripheral pancytopenia and marrow hypoplasia.
5 eded the development of neutropenia and bone-marrow hypoplasia.
6  a food additive (Rux-chow), attenuated bone marrow hypoplasia, ameliorated peripheral blood pancytop
7  (F1) recipients failed to induce the severe marrow hypoplasia and fatal pancytopenia that is produce
8    Here, histology and flow cytometry reveal marrow hypoplasia and impaired hematopoiesis in all coll
9 gnificant thrombocytopenia secondary to both marrow hypoplasia and increased PLT destruction.
10 letion of both PTPN1 and PTPN2 leads to bone marrow hypoplasia and lethality, while inducible deletio
11  factor, and MDS/AML usually manifested with marrow hypoplasia and monosomy 7, but the somatic mutati
12 ich is characterized by immune-mediated bone marrow hypoplasia and pancytopenia, can be treated effec
13 o, including red blood cell deficiency, bone marrow hypoplasia, and defective thymopoiesis.
14 t in the production of red blood cells, bone marrow hypoplasia, and runting.
15  one of six trials required documentation of marrow hypoplasia before CSF use.
16 M oligoclonal T-cell infiltration and severe marrow hypoplasia indicated by approximately 10-fold dec
17                                              Marrow hypoplasia occurred between days 14 and 28 in 12
18                                              Marrow hypoplasia occurred between days 14 and 28 in 73%
19 cells per kg dose (prolonged cytopenias with marrow hypoplasia; severe cytokine release syndrome) led
20 res with the development of pancytopenia and marrow hypoplasia, validating a major role for the Fas/F
21                    Overall, postchemotherapy marrow hypoplasia was achieved in 33 patients.
22 hether leukemia response or documentation of marrow hypoplasia was required before cytokine use, and