Differences in gene expression between B-cell chronic lymphocytic leukemia and normal B cells: a meta-analysis of three microarray studies

Wang, J.; Coombes, Kevin R.; Highsmith, W. Edward; Keating, MJ; Abruzzo, Lynne V.

doi:10.1093/bioinformatics/bth381

Cited by 110 publications

(81 citation statements)

References 51 publications

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“…A recent metaanalysis of three microarray studies comparing gene expression between chronic lymphocytic leukemia and normal B cells also found that TNFRSF7 and TNFRSF1B were overexpressed in chronic lymphocytic leukemia, 31 although similar findings have not been reported for follicular lymphoma. TNFRSF7 interacts with CD40 to inhibit apoptosis in B cells.…”

Section: Mcl1 Wasmentioning

confidence: 90%

“…Indeed, this practice is not uncommon in studies using group analysis. 23,31 We recognize that gene expression microarrays provide in vitro data primarily for generation of hypothesis. Thus, we have validated the upregulation of survivin in postchemotherapy chronic lymphocytic leukemia tumor samples with an in vivo method, immunohistochemistry.…”

Section: Mcl1 Wasmentioning

confidence: 99%

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Pathway-specific apoptotic gene expression profiling in chronic lymphocytic leukemia and follicular lymphoma

et al. 2006

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Defects in the apoptotic pathway are pathogenetically important in chronic lymphocytic leukemia and follicular lymphoma. To further understand these defects, we profiled the apoptotic gene expression of these two neoplasms. Oligonucleotide arrays with 112 apoptotic genes were used, and data analysis was performed on seven chronic lymphocytic leukemia and 10 follicular lymphoma frozen tumor samples from six and seven patients, respectively. The overall gene expression pattern was strikingly similar among all 17 samples, regardless of the type of lymphoma and history of chemotherapy exposure. MCL1, TNFRSF1B and TNFRSF7 were highly expressed in most cases. The apoptotic gene expression between the groups of untreated chronic lymphocytic leukemia (n ¼ 3) and untreated follicular lymphoma (n ¼ 6) was also similar (Pearson correlation coefficient, 0.94). Comparison between the groups of untreated chronic lymphocytic leukemia (n ¼ 3) and postchemotherapy chronic lymphocytic leukemia (n ¼ 4) revealed six genes with 42-fold changes, including BIRC5/Survivin that was higher in the postchemotherapy samples. This finding was validated by immunohistochemistry. Similar analysis of follicular lymphoma cases did not identify any significant differences. To conclude, our findings suggest that chronic lymphocytic leukemia and follicular lymphoma share common apoptotic defects, and highlight the importance of MCL1 and the TNF pathway. Upregulation of survivin may be one of the mechanisms by which chronic lymphocytic leukemia becomes desensitized to chemotherapy.

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Section: Mcl1 Wasmentioning

confidence: 90%

Section: Mcl1 Wasmentioning

confidence: 99%

Pathway-specific apoptotic gene expression profiling in chronic lymphocytic leukemia and follicular lymphoma

et al. 2006

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“…Indeed, cancer has been associated with alterations in the epigenetic code leading to abnormal gene expression. 37 In 2004, Wang et al 38 conducted a meta-analysis comparing CLL with normal B-cell gene expression profiles and identified a number of genes that were differentially expressed between CLL and normal samples. Several genes described as overexpressed in CLL (for example, CD5, BCL2, CD23, LCK and PIM1) were downregulated by VPA, whereas genes described as underexpressed in CLL (for example, BCLA1, c-MYC, DUSP2 and PEA15) were upregulated by VPA.…”

Section: Gene Expression Profile Of Vpa-treated Cll B Cells B Stamatomentioning

confidence: 99%

Antileukemic activity of valproic acid in chronic lymphocytic leukemia B cells defined by microarray analysis

et al. 2009

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“…Differential expression was identified to be similar to that described by Wang et al (16). We used Z values (defined below) to assess differentially expressed genes between current and never or former smokers, in whom the magnitude of the Z values is assumed to represent the effect of smoking cessation.…”

Section: Identification Of Differentially Expressed Genesmentioning

confidence: 99%

“…The permutation was done within each of the data sets, but never across the data sets. Note that other than the permutation step, our method is the same as that described by Wang et al (16).…”

Section: Smoking Cessation and Global Gene Expressionmentioning

confidence: 99%

Impact of Smoking Cessation on Global Gene Expression in the Bronchial Epithelium of Chronic Smokers

Zhang

Lee

Tang

et al. 2008

Cancer Prevention Research

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Cigarette smoke is the major cause of lung cancer and can interact in complex ways with drugs for lung cancer prevention or therapy. Molecular genetic research promises to elucidate the biological mechanisms underlying divergent drug effects in smokers versus nonsmokers and to help in developing new approaches for controlling lung cancer. The present study compared global gene expression profiles (determined via Affymetrix microarray measurements in bronchial epithelial cells) between chronic smokers, former smokers, and never smokers. Smoking effects on global gene expression were determined from a combined analysis of three independent data sets. Differential expression between current and never smokers occurred in 591 of 13,902 measured genes (P < 0.01 and >2-fold change; pooled data)-a profound effect. In contrast, differential expression between current and former smokers occurred in only 145 of the measured genes (P < 0.01 and >2-fold change; pooled data). Nine of these 145 genes showed consistent and significant changes in each of the three data sets (P < 0.01 and >2-fold change), with eight being down-regulated in former smokers. Seven of the eight down-regulated genes, including CYP1B1 and three AKR genes, influence the metabolism of carcinogens and/or therapeutic/chemopreventive agents. Our data comparing former and current smokers allowed us to pinpoint the genes involved in smoking-drug interactions in lung cancer prevention and therapy. These findings have important implications for developing new targeted and dosing approaches for prevention and therapy in the lung and other sites, highlighting the importance of monitoring smoking status in patients receiving oncologic drug interventions.

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Differences in gene expression between B-cell chronic lymphocytic leukemia and normal B cells: a meta-analysis of three microarray studies

Cited by 110 publications

References 51 publications

Pathway-specific apoptotic gene expression profiling in chronic lymphocytic leukemia and follicular lymphoma

Pathway-specific apoptotic gene expression profiling in chronic lymphocytic leukemia and follicular lymphoma

Antileukemic activity of valproic acid in chronic lymphocytic leukemia B cells defined by microarray analysis

Impact of Smoking Cessation on Global Gene Expression in the Bronchial Epithelium of Chronic Smokers

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