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ABSTRACT: Hepatosplenic T cell lymphoma

PROVIDER: PRJNA248463 | ENA |

REPOSITORIES: ENA

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Dataset's files

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			Action	DRS
	SRR1186052_1.fastq.gz	Fastqsanger.gz
	SRR1186052_2.fastq.gz	Fastqsanger.gz
	SRR1186053_1.fastq.gz	Fastqsanger.gz
	SRR1186053_2.fastq.gz	Fastqsanger.gz
	SRR1186054_1.fastq.gz	Fastqsanger.gz

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Project description:We report changes in the DNA methylome in a patient with γδ hepatosplenic T-cell lymphoma (HSTCL) who responded to treatment with interferon-α2c. We studied the methylome by 450k methylation array in 5 blood samples taken within a time period of 20 months. During this time period, the WBC counts dropped from 22,300 to 7,200/μl blood, yet the proportion of γδ T cell lymphoma blasts remained around 90%. We observed time-dependent changes in overall DNA methylation and performed an in-depth bioinformatic analysis of the modulated CpG sites associated with disease progression. We identified a CpG site differentially regulating methylation, possibly related to the interferon response during the course of treatment in this particular case. Therefore, the present case report will help to understand the substantial changes in DNA methylation of lymphoma resulting in a survival benefit of this γδ HSTCL patient.

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Project description:Inhibitor of DNA binding proteins (ID), including Id1-4, are transcriptional regulators involved in promoting cell proliferation and survival in various cell types. Although upregulation of Id proteins have been widely reported to be associated with a broad spectrum of tumors, recent studies have identified that Id3 also plays a tumor suppressor role in the development of Burkittâ??s lymphoma in humans and Hepatosplenic T cell lymphomas in mice. However, there is a lack of evidence to suggest the tumor suppressor roles for other Id genes, particularly Id2, which is highly expressed in many T lymphocytes. In this study we report that Id2 plays a tumor suppressive role in collaboration with Id3 in developing T cells in mice. We found that there was rapid lymphoma development in Id2f/fId3f/fLckCre mice caused by unchecked neonatal expansion of invariant Natural Killer T (iNKT) cells and a unique subset of innate-like, CD1d-independent T cells. These tumors also gave rise to lymphomas in Rag-deficient mice, reaffirming the inherent tumorigenic potential of these cells. Microarray analysis revealed a significantly modified program in expanding iNKT cells that ultimately contributed to tumorigenesis. We found chromosome instability and significant upregulation of several different signaling pathways, including pathways for multiple chemokines, cytokines and their receptors, in these tumors. While Id proteins are being considered as potential therapeutic targets in some cancer models, our results highlight the possibility of aggravated tumorigenesis upon suppression of Id2 and Id3. Pre-malignant iNKT (TCRÎ²+CD1dTet+) cells were sorted from three 20 day old L-DKO mice. Lymphoma cells (T cells that are CD1dTet+ or CD1dTet-) were sorted from tissues of 18-37 week old L-DKO mice. Total RNA was extracted, and mRNA profiling was done using GeneChip Mouse Genome 430A 2.0 arrays (GPL8321, Affymetrix)

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ena-DATASET-DAVELAB-22-03-2017-21:30:50:663-38 - samples

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