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Pediatric post-transplant lymphoproliferative disorders

ABSTRACT: Unravelling the heterogenous molecular landscape of pediatric post-transplant lymphoproliferative disorders

PROVIDER: PRJEB50295 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR9792320_1.fastq.gz	Fastqsanger.gz
	ERR9792320_2.fastq.gz	Fastqsanger.gz
	ERR9792330_1.fastq.gz	Fastqsanger.gz
	ERR9792330_2.fastq.gz	Fastqsanger.gz
	ERR9792340_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

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

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

| PRJNA814282 | ENA

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

Ganciclovir Plus Arginine Butyrate in Treating Patients With Cancer or Lymphoproliferative Disorders Associated With the Epstein Barr Virus

Project description:RATIONALE: The Epstein Barr virus can cause cancer and lymphoproliferative disorders. Ganciclovir is an antiviral drug that acts against the Epstein Barr virus. Arginine butyrate may make virus cells more sensitive to ganciclovir. Combining ganciclovir and arginine butyrate may kill more Epstein Barr virus cells and tumor cells. PURPOSE: Phase I trial to study the effectiveness of arginine butyrate plus ganciclovir in treating patients who have cancer or lymphoproliferative disorders that are associated with the Epstein Barr virus.

| 2005372 | ecrin-mdr-crc

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

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 | GSE279598 | GEO

Linking the KIR phenotype with STAT3 and TET2 mutations to identify chronic lymphoproliferative disorders of NK cells

Project description:We report two transcriptomic profile for Chronic lymphoproliferative disorders of NK cells: STAT3-like and AITL-like

2021-02-02 | GSE163093 | GEO

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]

2024-11-12 | GSE279989 | GEO

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

Gene Expression Profiling of Cutaneous CD30+ Lymphoproliferative Disorders by RNA-seq

Project description:Gene Expression Profiling of Cutaneous CD30+ Lymphoproliferative Disorders by RNA-seq

| PRJNA431541 | ENA

Hepatitis C virus up-regulates B-cell receptor signaling: a novel mechanism for HCV-associated B-cell lymphoproliferative disorders

Project description:B-cell receptor (BCR) signaling is essential for the development of B-cells and plays a critical role in B-cell neoplasia. Increasing evidence indicates an association between chronic hepatitis C virus (HCV) infection and B-cell lymphoma, however, the mechanisms by which HCV causes B-cell lymphoproliferative disorder are still unclear. Herein, we demonstrate the expression of HCV viral proteins in B-cells of HCV-infected patients and show that HCV up-regulates BCR signaling in human primary B-cells. HCV nonstructural protein NS3/4A interacts with CHK2 and down-regulates its activity, modulating HuR posttranscriptional regulation of a network of target mRNAs associated with B-cell lymphoproliferative disorders. Interestingly, the BCR signaling pathway was found to have the largest number of transcripts with increased association with HuR and was up-regulated by NS3/4A. Our study reveals a previously unidentified role of NS3/4A in regulation of host BCR signaling during HCV infection, contributing to a better understanding of the molecular mechanisms underlying HCV-associated B-cell lymphoproliferative disorders.

2015-10-14 | GSE71757 | GEO

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