Ningxuan Wang, Xiangan Li, Chenyang She, Jun Zhang
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引用次数: 0
Abstract
Leukemia is a malignant clonal disease originating from hematopoietic stem cells. Its pathogenesis is associated with multiple factors, including biological, physical, chemical, genetic, and other hematological diseases. Previous studies have shown that a high mutation rate (>80%) of colony-stimulating factor receptor 3 (CSF3R) is observed in chronic neutrophilic leukemia (CNL) patients, and these mutations activate downstream signaling pathways, leading to the proliferation of neutrophils. In-depth research on the CSF3R genes and their related mechanisms will help further reveal the mechanisms of leukemia development and provide potential targets for treatment. Therefore, this paper mainly focuses on the roles of colony-stimulating factor 3 (CSF3R) in hematopoiesis and the occurrence of leukemia, with particular attention to the roles of CSF3R in the JAK-STAT, PI3K-AKT, and MAPK-ERK signaling pathways.
期刊介绍:
Cancer Cell International publishes articles on all aspects of cancer cell biology, originating largely from, but not limited to, work using cell culture techniques.
The journal focuses on novel cancer studies reporting data from biological experiments performed on cells grown in vitro, in two- or three-dimensional systems, and/or in vivo (animal experiments). These types of experiments have provided crucial data in many fields, from cell proliferation and transformation, to epithelial-mesenchymal interaction, to apoptosis, and host immune response to tumors.
Cancer Cell International also considers articles that focus on novel technologies or novel pathways in molecular analysis and on epidemiological studies that may affect patient care, as well as articles reporting translational cancer research studies where in vitro discoveries are bridged to the clinic. As such, the journal is interested in laboratory and animal studies reporting on novel biomarkers of tumor progression and response to therapy and on their applicability to human cancers.