Genome-wide gene expression profile analysis of MCL1 over-expressing B-NHL cells
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE8834 | GEO | 2007/08/23
SECONDARY ACCESSION(S): PRJNA102169
REPOSITORIES: GEO
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Project description:To get insight into the mechanisms of MCL1-induced survival and transformation, we screened 41,000 human genes in a genome-wide gene expression profile analysis of MCL1 over-expressing B-NHL cells. Experiment Overall Design: Two-color (Cy5-CTP/ Cy3-CTP) microarray-based gene expression formats presenting high-density oligonucleotide probes printed on a single glass slide were used (Agilent technologies, Cat No# G4112A whole human genome 41K). Total RNAs from MCL1 over-expressing RAMOS RA-1 and Z-138 B-cells were labeled with Cy5-CTP, whereas RNAs from references (empty vector/ RAMOS RA-1 and empty vector/ Z-138 B-cells) were labeled with Cy3-CTP. After competitive hybridization [RNA-Cy5 from MCL1 over-expressing RAMOS RA-1 or MCL1 over-expressing Z-138 versus RNA-Cy3 from either empty vector/ RAMOS RA-1 or empty vector/ Z-138 respectively] gene expression data were pre-processed using Feature Extraction software and GEPAS tools (http://gepas.bioinfo.cipf.es/).
2008-06-16 | E-GEOD-8834 | biostudies-arrayexpress
Project description:MCL1 is an anti-apoptotic member of the BCL2 family that is deregulated in various solid and hematological malignancies. However, its role in the molecular pathogenesis of diffuse large B-cell lymphoma (DLBCL) is unclear. We analyzed gene expression profiling data from 350 DLBCL patient samples and detected that activated B-cell-like (ABC) DLBCLs express MCL1 at significantly higher levels compared to germinal center B-cell-like (GCB) DLBCL patient samples (p=2.7 x 10(-10)) [PMID 23257783]. Immunohistochemistry confirmed high MCL1 protein expression predominantly in ABC DLBCL in an independent patient cohort (n=249; p=0.001). To elucidate molecular mechanisms leading to aberrant MCL1 expression, we analyzed array comparative genomic hybridization (aCGH) data of 203 DLBCL samples [GSE11318] and identified recurrent chromosomal gains/amplifications of the MCL1 locus that occurred in 26% of ABC DLBCLs. In addition, aberrant STAT3 signaling contributed to high MCL1 expression in this subtype. Knockdown of MCL1 as well as treatment with the BH3-mimetic obatoclax induced apoptotic cell death in MCL1 positive DLBCL cell lines. In summary, MCL1 is deregulated in a significant fraction of ABC DLBCLs and contributes to therapy resistance. These data suggest that specific inhibition of MCL1 might be utilized therapeutically in a subset of DLBCLs. This GEO dataset is comprised of aCGH measurements for DLBCL cell lines, which are used in the above-mentioned paper. Cell lines were measured against the DNA of a healthy male donor who in turn was measured against a pool of healthy DNAs to correct for individual CNVs of the donor.
2013-01-04 | E-GEOD-43272 | biostudies-arrayexpress
Project description:MCL1 is an anti-apoptotic member of the BCL2 family that is deregulated in various solid and hematological malignancies. However, its role in the molecular pathogenesis of diffuse large B-cell lymphoma (DLBCL) is unclear. We analyzed gene expression profiling data from 350 DLBCL patient samples and detected that activated B-cell-like (ABC) DLBCLs express MCL1 at significantly higher levels compared to germinal center B-cell-like (GCB) DLBCL patient samples (p=2.7 x 10(-10)) [PMID 23257783]. Immunohistochemistry confirmed high MCL1 protein expression predominantly in ABC DLBCL in an independent patient cohort (n=249; p=0.001). To elucidate molecular mechanisms leading to aberrant MCL1 expression, we analyzed array comparative genomic hybridization (aCGH) data of 203 DLBCL samples [GSE11318] and identified recurrent chromosomal gains/amplifications of the MCL1 locus that occurred in 26% of ABC DLBCLs. In addition, aberrant STAT3 signaling contributed to high MCL1 expression in this subtype. Knockdown of MCL1 as well as treatment with the BH3-mimetic obatoclax induced apoptotic cell death in MCL1 positive DLBCL cell lines. In summary, MCL1 is deregulated in a significant fraction of ABC DLBCLs and contributes to therapy resistance. These data suggest that specific inhibition of MCL1 might be utilized therapeutically in a subset of DLBCLs.
2013-01-04 | GSE43272 | GEO
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