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Gene expression profile of circulating CD34(+) cells and granulocytes in chronic myeloid leukemia.

Authors: Cokic, Vladan P  Mojsilovic, Slavko  Jaukovic, Aleksandra  Kraguljac-Kurtovic, Nada  Mojsilovic, Sonja  Šefer, Dijana  Mitrovic Ajtic, Olivera  Miloševic, Violeta  Bogdanovic, Andrija  Ðikic, Dragoslava  Milenkovic, Pavle  Puri, Raj K 
Citation: Cokic VP, etal., Blood Cells Mol Dis. 2015 Dec;55(4):373-81. doi: 10.1016/j.bcmd.2015.08.002. Epub 2015 Aug 7.
Pubmed: (View Article at PubMed) PMID:26460262
DOI: Full-text: DOI:10.1016/j.bcmd.2015.08.002


PURPOSE: We compared the gene expression profile of peripheral blood CD34(+) cells and granulocytes in subjects with chronic myeloid leukemia (CML), with the accent on signaling pathways affected by BCR-ABL oncogene.
METHODS: The microarray analyses have been performed in circulating CD34(+) cells and granulocytes from peripheral blood of 7 subjects with CML and 7 healthy donors. All studied BCR-ABL positive CML patients were in chronic phase, with a mean value of 2012±SD of CD34(+)cells/µl in peripheral blood.
RESULTS: The gene expression profile was more prominent in CML CD34(+) cells (3553 genes) compared to granulocytes (2701 genes). The 41 and 39 genes were significantly upregulated in CML CD34(+) cells (HINT1, TXN, SERBP1) and granulocytes, respectively. BCR-ABL oncogene activated PI3K/AKT and MAPK signaling through significant upregulation of PTPN11, CDK4/6, and MYC and reduction of E2F1, KRAS, and NFKBIA gene expression in CD34(+) cells. Among genes linked to the inhibition of cellular proliferation by BCR-ABL inhibitor Imatinib, the FOS and STAT1 demonstrated significantly decreased expression in CML.
CONCLUSION: The presence of BCR-ABL fusion gene doubled the expression quantity of genes involved in the regulation of cell cycle, proliferation and apoptosis of CD34(+) cells. These results determined the modified genes in PI3K/AKT and MAPK signaling of CML subjects.

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CRRD Object Information
CRRD ID: 13674165
Created: 2018-07-10
Species: All species
Last Modified: 2018-07-10
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.