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Gene expression profiles of monocytes derived from chronic lymphocytic leukemia patients and normal controls

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NIAID Data Ecosystem2026-03-10 收录
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https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE35179
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We collected monocytes from peripheral blood of 5 chronic lymphocytic leukemia (CLL) patients and 5 healthy donors and we performed gene expression analysis by microarray. Comparison of gene expression profiles (GEPs) between CLL-derived and normal monocytes was used to discover molecular abnormalities in this nonmalignant immune cellular population in leukemia-bearing patients. Although analysed cells were not part of the malignant clone, in unsupervised hierarchical clustering analysis, GEPs of normal monocytes were clearly distinguishable from those of monocytes obtained from CLL patients. Supervised analysis identified 65 genes significantly up-regulated and 48 genes down-regulated in CLL monocytes compared with monocytes from normal controls (FC=2, p<0.05). Modification of gene expression profile would imply impairment of phagocytosis and production of immunosuppressive mediators in CLL-derived monocytes. The alterations described in our study further contribute to characterize the complexity of factors potentially involved in acquired immune deficiency of CLL patients. Large-scale gene expression profiling (GEP) was performed on total RNA extracted from purified CD14+ monocytes (RNeasy Mini kit Plus, QIAGEN, Valencia, CA, USA) isolated from 5 individual CLL patients and 5 healthy controls by hybridization on 4X44K Whole Human Genome Microarray (Agilent Technologies, Palo alto, CA). Fluorescence data were analysed with Feature Extraction Software v.10.5 (Agilent Technologies) an QC Chart tool v.1.3. Agglomerative two-dimensional clustering analysis and supervised analyses based on t-test were performed using Gene Spring GX (Agilent) software. Genes were defined as differentially expressed between groups at a significant level of p<0.05 and with a fold change cut off ± 2 in all the pair wise comparisons.
创建时间:
2019-01-23
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