Unknown,Transcriptomics,Genomics,Proteomics

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Reciprocal leukemia-stroma VCAM-1/VLA-4-dependent activation 1 of NF-κB mediates chemoresistance


ABSTRACT: Bone marrow (BM) mesenchymal stromal cells (BM-MSC) upregulate their NF-κB signaling to protect leukemia cells from chemotherapy-induced apoptosis. To elucidate molecular mechanisms by which leukemia-stroma interactions within the BM microenvironment could confer chemoresistance to leukemia cells, we used genome-wide gene expression profiling (GEP) to examine human normal BM-MSC that had been co-cultured with the pre-B ALL REH cells and then separated by flow cytometry (FACS). GEP results for co-cultured cells of each type were compared to GEP results for cells of the corresponding type cultured alone, and taken through the same FACS purification procedure, to identify changes in gene expression profiles caused by co-culture.

ORGANISM(S): Homo sapiens

SUBMITTER: Wencai Ma 

PROVIDER: E-GEOD-55533 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications


Leukemia cells are protected from chemotherapy-induced apoptosis by their interactions with bone marrow mesenchymal stromal cells (BM-MSCs). Yet the underlying mechanisms associated with this protective effect remain unclear. Genome-wide gene expression profiling of BM-MSCs revealed that coculture with leukemia cells upregulated the transcription of genes associated with nuclear factor (NF)-κB signaling. Moreover, primary BM-MSCs from leukemia patients expressed NF-κB target genes at higher leve  ...[more]

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