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Integrated multi-modal analysis reveals tumor and immune characteristics that distinguish Epstein-Barr virus-positive and -negative B cell post-transplant lymphoproliferative disorders [Affymetrix]

ABSTRACT: The highly prevalent oncogenic Epstein-Barr virus (EBV) can drive tumorigenesis with disrupted host immunity, causing malignancies including post-transplant lymphoproliferative disorders (PTLD). PTLD can also arise in the absence of EBV but the biological differences underlying EBV(+) and EBV(-) B cell PTLD and the associated host-EBV-tumor interactions remain poorly understood. Here, we reveal the core differences between EBV(+) and EBV(-) PTLD, characterized by increased expression of genes related to immune processes or DNA interactions respectively, and the augmented ability of EBV(+) PTLD B cells to modulate the tumor microenvironment through elaboration of monocyte-attracting cytokines/chemokines. We create a reference resource of proteins distinguishing EBV(+) B lymphoma cells from EBV(-) B lymphoma including the immunomodulatory molecules CD300a and CD24, respectively. Moreover, we show that CD300a is essential for maximal survival of EBV(+) PTLD B lymphoma cells. Our comprehensive multi-modal analyses uncover the biological underpinnings of PTLD and offer opportunities for precision therapies.

ORGANISM(S): Homo sapiens

PROVIDER: GSE279598 | GEO | 2024/11/12

REPOSITORIES: GEO

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Integrated multi-modal analysis reveals tumor and immune characteristics that distinguish Epstein-Barr virus-positive and -negative B cell post-transplant lymphoproliferative disorders [scRNA-seq]

Project description:The highly prevalent oncogenic Epstein-Barr virus (EBV) can drive tumorigenesis with disrupted host immunity, causing malignancies including post-transplant lymphoproliferative disorders (PTLD). PTLD can also arise in the absence of EBV but the biological differences underlying EBV(+) and EBV(-) B cell PTLD and the associated host-EBV-tumor interactions remain poorly understood. Here, we reveal the core differences between EBV(+) and EBV(-) PTLD, characterized by increased expression of genes related to immune processes or DNA interactions respectively, and the augmented ability of EBV(+) PTLD B cells to modulate the tumor microenvironment through elaboration of monocyte-attracting cytokines/chemokines. We create a reference resource of proteins distinguishing EBV(+) B lymphoma cells from EBV(-) B lymphoma including the immunomodulatory molecules CD300a and CD24, respectively. Moreover, we show that CD300a is essential for maximal survival of EBV(+) PTLD B lymphoma cells. Our comprehensive multi-modal analyses uncover the biological underpinnings of PTLD and offer opportunities for precision therapies.

2024-11-12 | GSE279989 | GEO

Expression data from post-transplant lymphoproliferative disorder (PTLD) patient samples

Project description:In this study we focussed on malignant post-transplant lymphomas. Post-transplant lymphoma is strongly associated with Epstein-Barr Virus (EBV) infection in contrast to lymphoma arising in an immunocompetent population. Nevertheless, about 1 in 3 PTLD cases are negative for EBV. We used a microarray to define the gene expression profile of different PTLDs to elucidate the pathogenesis of EBV(+) and EBV(-) PTLD and to define whether EBV(-) PTLD is biologically different from EBV(-) lymphoma arising in an immunocompetent host.

2012-06-23 | GSE38885 | GEO

Expression data from post-transplant lymphoproliferative disorder (PTLD) patient samples

2012-06-22 | E-GEOD-38885 | biostudies-arrayexpress

Unravelling the heterogeneous molecular landscape of pediatric post-transplant lymphoproliferative disorders

Project description:It is unknown whether pediatric monomorphic post-transplant lymphoproliferative disorders (mPTLD) display similar genetic features than the immunocompetent counterpart and if they resemble adult mPTLD. We have investigated 39 pediatric mPTLD, 33 diffuse large B-cell lymphoma (DLBCL) and six Burkitt lymphoma (BL), by an integrated approach, including fluorescence in situ hybridization, cell of origin determination (COO), targeted gene sequencing and copy-number arrays. According to COO, 24/28 DLBCL (86%) were classified as activated B-cell (ABC) and all six BL were germinal center B cell (GCB)-type. Thirty-three out of 37 investigated mPTLD were positive for EBV infection. Overall, PTLD-BL carried mutations in MYC in addition to ID3 and DDX3X, ARID1A or CCND3 and a higher mutational burden than PTLD-DLBCL (12.3 vs 6.2, P = 0.01). CN profile of PTLD-BL was less complex than in IC-BL (1 vs 6.26; P < 0.005). PTLD-DLBCL showed a very heterogeneous genomic profile characterized by a lower number of mutations (2.4 vs 6.5, P=0.01) and less CNA (2.10 vs 4.36 ; P < 0.05) than in IC patients. Pathway enrichment analysis revealed that epigenetic modifiers and Notch pathway (4 cases each) were the most recurrently affected. In conclusion, these findings further unravel for the first time the molecular heterogeneity of pediatric mPTLD and provide new parameters for the design of more effective therapeutic strategies.

2023-12-19 | GSE198253 | GEO

Comparative whole genome profiling of post-transplant lymphoproliferative disorders and diffuse large B-cell lymphomas.

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. Keywords: Genomic DNA on Affymetrix 10K SNP array

2007-06-15 | GSE8123 | GEO

EBV Modulates Host Cell microRNA-194 to Promote IL-10 Production and B Lymphoma Cell Survival

2014-09-10 | GSE61283 | GEO

Expression of EBV miRNAs in numerous EBV-positive cell lines

2008-12-01 | GSE12014 | GEO

EBV Modulates Host Cell microRNA-194 to Promote IL-10 Production and B Lymphoma Cell Survival

Project description:The purpose of this study was to investigate the effect of EBV infection on host cell miR and to characterize the miRNome in EBV+ B cell lymphomas from patients with PTLD. A qPCR array was used to measure the expression level of 377 previously identified miRs from RNA isolated from three sources: total B cells isolated from healthy individuals (n=4), lymphoblastoid cell lines (LCL) generated by transformation of normal B cell with the B95-8 lab strain of EBV (n=4) and EBV+ B cell lines isolated from patients with PTLD (n=6). miRNA expression was assayed in total B cells samples (n = 4, in duplicate), in lymphoblastoid cell lines (n = 4, in duplicate) and in spontaneous lymphoblastoid cell lines derived from PTLD patients with EBV+ B cell lymphomas (n = 6 in duplicate). The expression of miRNA in the B cell samples was used as a control.

2014-09-10 | E-GEOD-61283 | biostudies-arrayexpress

Expression of EBV miRNAs in numerous EBV-positive cell lines

Project description:EBV-positive cell lines were assayed for expression of EBV miRNAs. The names of the miRNAs are from miRBase from Fall 2007. Microarray probes are tandem complements of the mature miRNA sequence. We assayed Burkitt's lymphoma (BL), Nasopharyngeal carcinoma, post-transplant lymphoproliferative disease (PTLD), primary effusion lymphoma, and lymphoblastoid cell lines. We also assayed primary B cells that were infected with the B95-8 strain of EBV, which was found to express EBV miRNAs as early as 20 hours post infection. We have found PTLD and BLs from HIV-positive donors both express EBV miRNAs. These types of cell lines have not previously been found to express viral miRNAs. We have found that cells that support type I and type II latency express only the BART miRNAs, whereas cells that support type III latency express BART and BHRF1 miRNAs. Furthermore, BL cell lines that spontaneously lose EBV express levels of the viral miRNAs that are at least 5-fold lower than cell lines that do not lose EBV. In total, 48 samples have been assayed and included in this study. EBV-negative control samples are not included in this data set, but raw and processed data may be requested from the contributors. These EBV-negative cell lines include the Burkitt's lymphoma cell lines, BJAB and Akata-negative, the gastric carcinoma cell line, AGS, and uninfected primary B cells. Of the 48 samples, we have assayed 22 different EBV-positive cell lines and 4 different time points after infection of primary B cells with EBV. Replicates of the majority of cell lines is included in this data set. Replicates are from independent RNA isolations that were then hybridized to individual microarrays.

2008-11-30 | E-GEOD-12014 | biostudies-arrayexpress

Tabelecleucel for Solid Organ or Allogeneic Hematopoietic Cell Transplant Participants With Epstein-Barr Virus-Associated Post-Transplant Lymphoproliferative Disease (EBV+ PTLD) After Failure of Rituximab or Rituximab and Chemotherapy

Project description:The purpose of this study is to determine the clinical benefit and characterize the safety profile of tabelecleucel for the treatment of Epstein-Barr virus-associated post-transplant lymphoproliferative disease (EBV+ PTLD) in the setting of (1) solid organ transplant (SOT) after failure of rituximab and rituximab plus chemotherapy or (2) allogeneic hematopoietic cell transplant (HCT) after failure of rituximab.

| 2262897 | ecrin-mdr-crc

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