Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Human miRNA expression in EBV+ and EBV- PTLD tumor tissue sections

ABSTRACT: Expression of human miRNAs was analyzed in 150 ng of total RNA from nine post-transplant lymphoproliferative disorder (PTLD) patient samples, categorized as Epstein-Barr virus-positive (EBV+ , n = 4) or EBV- (n = 5) PTLD by hybridization on Affymetrix’s GeneChip miR Array 4.0 (Stanford Functional Genomics Facility, Stanford, CA). The Bioconductor ‘oligo’ package was used to perform array background subtraction, quantile normalization, and summarization by median polish. The normalized gene expression dataset was annotated with the ‘pd.mirna.4.0’ annotation library package in R (R Core Team). The expression data was fit to a linear model using the ‘stats’ package in R (R Core Team). Moderated t-statistics and log-odds of differential expression were calculated using the empirical Bayes method. False discovery rate (FDR) tests were performed with the Benjamini-Hochberg procedure for multiple testing correction in R (R Core Team).

ORGANISM(S): Homo sapiens

SUBMITTER: Ayantika Sen

PROVIDER: E-MTAB-12201 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Post-transplant lymphoproliferative disorders (PTLD) are a major complication of solid organ transplantation and represent a cause of severe morbidity and mortality among transplanted patients. Apart from EBV infection, knowledge of the pathogenesis of monoclonal PTLD is limited. Powerful analysis techniques, such as whole genomic DNA profiling (arrayCGH), can improve our understanding of PTLD pathogenesis. Toward this aim, we obtained the whole genome profiling using the Affymetrix GeneChip Human Mapping 10k 2.0 from 20 cases of PTLD and we compared them with those assessed in 25 cases of DLBCL from immunocompetent patients, as a control group. Recurrent lesions were detected among all the samples. Chromosome 18q, 7q, 3q and 12 were the most common gains in DLBCL of immunocompetent hosts. Chromosomes 5p and 11p were commonly gained in PTLD-DLBCL. The latter had frequent losses of 6q, 17p, 1p, and 9p. Chromosome 12p was the most frequent target of deletions among PTLD-DLBCL. The LOH pattern was characterized by involvement of chromosomes 13q and 17p in DLBCL and 10, 1q, 9p and 11q among PTLD-DLBCL. Interestingly, LOH did not always match the DNA loss. In particular, chromosome 10 seemes to be targeted by uniparental disomy in PTLD. Small deletions and gains, involving both known (BCL2 and PAX5) and unknown genes (ZDHHC14), have been identified. Our data suggest that PTLD share, at a lower frequency, common genetic aberrations with DLBCL from immunocompetent patients. The demonstration of 9p13 amplification indicates the importance of PAX5 in PTLD. The combination of DNA copy number and LOH assessment lead to the hypothesis that uniparental disomy may be a potential mechanism in B-cell lymphomagenesis. Twenty specimens of monoclonal B-cell PTLD, collected from 20 solid organ transplant recipients. Experiment Overall Design: 20 PTLD samples. No technical replications. Experiment Overall Design: 25 DLBCL samples (20 patient + 5 cell lines). No technical replications.

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Human miRNA expression in EBV+ and EBV- PTLD tumor tissue sections

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