作者: T. Pietsch , U. Kyas , W.-D. Ludwig , K. Welte
DOI: 10.1007/978-3-642-48715-6_23
关键词: Progenitor cell 、 Cancer research 、 Hematopoietic growth factor 、 Haematopoiesis 、 Myeloid leukemia 、 Leukemia inhibitory factor 、 Chemistry 、 Myeloid 、 Lymphopoiesis 、 Stem cell factor
摘要: Recently the ligand of myeloid surface receptor encoded by proto-oncogene c-kit [11, 13] was identified to be a novel hematopoietic growth factor that stimulates primitive progenitor cells [12, 14]. This stem cell (SCF) is multipotent colony-stimulating (CSF) acting on early progenitors different lineages. The complementary DNA (cDNA) for human SCF has been cloned and expressed in mammalian recombinant purified homogeneity [7, Whereas itself only low capacity induce colony formation assays vitro (colony-forming unit-granulocyte-macrophage, CFU-GM; burst-forming unit-erythroid, BFU-E; CFU-granulocyte-erythroid-monocyte-megakaryocyte, CFU-GEMM; CFU-lymphoid, CFU-L) normal bone marrow cells, it strong synergistic activities with other factors. It synergizes granulocyte (G-CSF), granulocyte-macrophage CSF (GM-CSF), interleukin-3 (IL-3) myelopoiesis [8]. Synergistic were also reported erythropoietin erythropoiesis [8], IL-6 megakaryopoiesis, IL-7 lymphopoiesis [9], IL-3 mast [10]. (SCFR) expression detected not but acute leukemia (AML) blasts fluorescence-activated sorter (FACS) staining [2] binding studies [4]. In this study we investigated mitogenic potential alone or synergy (rh) G-CSF, rhGM-CSF, rhIL-3 leukemic from patients SCFR+ AML.