Unknown,Transcriptomics,Genomics,Proteomics

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MYC-negative BL frequent in posttransplant patients (cytogenetic)

ABSTRACT: We performed genomic and transcriptomic analysis of seven cases of molecular Burkitt lymphoma (mBL) developed in immunosuppressed patients who underwent solid organ transplantation. Interestingly, three cases (43%) were MYC-translocation-negative and revealed the 11q-gain/loss aberration recently identified in 3% of mBL developed in immunocompetent hosts.1 Based on array CGH data, minimal gain and loss regions of 11q (MGR/~4Mb and MLR/~13.5Mb, respectively) were defined and integrative genomic and transcriptomic analysis identified 35 differentially expressed genes, when compared with classic BL. All 16 MGR-dysregulated genes were upregulated, including cancer related USP2, CBL and PAFAH1B2. As expected, all 19 MGL-dysregulated genes were downregulated and two of them, TBRG1 and EI24, are potential tumor suppressor genes. Interestingly, the vast majority of dysregulated 11q23-q25 genes are involved in the MYC and TP53 networks. We hypothesize that the 11q-gain/loss aberration represents a “molecular variant” of t(8q24/MYC) and affects the same pathological pathways as the MYC oncogene. Seven cases of PTLD with BL features were selected from a cohort of 174 posttransplant patients diagnosed with PTLD between 1989 and 2012 at the University Hospitals of KU Leuven (Leuven, Belgium). In addition, five classic BL cases were selected as immunocompetent controls (IC-BL). Morphologic, immunophenotypic, clinical and cytogenetic characteristics of the selected cases were reviewed.

ORGANISM(S): Homo sapiens

SUBMITTER: Julio Finalet

PROVIDER: E-GEOD-64083 | 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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MYC-negative BL frequent in posttransplant patients (cytogenetic)

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