作者: PD Emanuel , LJ Bates , RP Castleberry , RJ Gualtieri , KS Zuckerman
DOI: 10.1182/BLOOD.V77.5.925.925
关键词: Biology 、 Hematopoietic growth factor 、 Progenitor cell 、 Juvenile myelomonocytic leukemia 、 Leukemia 、 Myeloid leukemia 、 Haematopoiesis 、 Granulocyte macrophage colony-stimulating factor 、 Myeloproliferation 、 Immunology
摘要: Juvenile chronic myelogenous leukemia (JCML) is a good model for the study of myeloproliferation because JCML hematopoietic progenitor cells grow in vitro at very low cell densities without addition exogenous stimulus. Previous studies have demonstrated that this proliferation dependent on granulocyte-macrophage colony-stimulating factor (GM-CSF), and removal monocytes from population before culture eliminates "spontaneous" myeloproliferation, suggesting paracrine role monocyte stimulation. However, subsequent shown increased GM-CSF production not consistent finding therefore plausible sole mechanism. In examining growth dose-response curves, both GM erythroid nonadherent populations displayed marked selective hypersensitivity to GM-CSF. Responses interleukin-3 G-CSF were identical control curves. This first demonstration myeloid which specific appears be involved pathogenesis disease.