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

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

PROVIDER: PRJNA431541 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6510910_1.fastq.gz	Fastqsanger.gz
	SRR6510910_2.fastq.gz	Fastqsanger.gz
	SRR6510911_1.fastq.gz	Fastqsanger.gz
	SRR6510911_2.fastq.gz	Fastqsanger.gz
	SRR6510912_1.fastq.gz	Fastqsanger.gz

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

Project description:Cutaneous CD30+ lymphoproliferative disorder (CD30+LPDs), including lymphomatoid papulosis (LyP) and primary cutaneous anaplastic large-cell lymphoma (PCALCL), comprises the second most common group of cutaneous T cell lymphoma. Previously, we reported that special AT-rich sequence-binding protein1 (SATB1), a thymocyte specific chromatin organizer, was over-expressed and promoted malignant T-cell proliferation in a portion of CD30+LPDs, whereas other CD30+LPDs didn't express SATB1 at all. To elucidate the underlying molecular events in CD30+LPDs with differential SATB1 expression, we subjected 4 SATB1+ and 3 SATB1- CD30+LPDs skin biopsies to second-generation RNA-sequencing (RNA-seq). These data provide a significant resource for studies of CD30+LPDs.

2019-01-25 | GSE109620 | GEO

Genomic Analysis of Cutaneous CD30-Positive Lymphoproliferative Disorders.

Project description:Primary cutaneous CD30+ T-cell lymphoproliferative disorders are the second most common cutaneous lymphomas. According to the World Health Organization, CD30+ T-cell lymphoproliferative disorders include primary cutaneous anaplastic large cell lymphoma (C-ALCL) and lymphomatoid papulosis (LyP) as well as borderline lesions. C-ALCL and LyP are thought to represent two ends of a spectrum of diseases that have different clinical presentations, clinical courses, and prognoses in their classic forms but share the same histology of medium to large CD30+ atypical lymphoid cell infiltrates. Because the behavior of these entities is different clinically and prognostically, we aim to search for oncogenic genomic variants using whole-exome sequencing that drive the development of LyP and C-ALCL. Clinical information, pathology, immunohistochemistry, and T-cell rearrangements on six cases of LyP and five cases of C-ALCL were reviewed to confirm the rendered diagnosis before whole-exome sequencing of all specimens. Both LyP and C-ALCL had recurrent alterations in epigenetic modifying genes affecting histone methylation and acetylation (SETD2, KMT2A, KMT2D, and CREBBP). However, they also harbor unique differences with mutations in signal transducer and activator of transcription gene STAT3 of the Jak/signal transducer and activator of transcription pathway and EOMES, a transcription factor involved in lymphocyte development, only noted in C-ALCL specimens. Genomic characterization of LyP and C-ALCL in this series confirms the role of multiple pathways involved in the biology and development of these lymphomatous processes. The identification of similar aberrations within the epigenetic modifying genes emphasizes common potential development mechanisms of lymphomagenesis within lymphoproliferative disorders being shared between LyP and C-ALCL; however, the presence of differences may account for the differences in clinical course.

| S-EPMC8688881 | biostudies-literature

Pediatric post-transplant lymphoproliferative disorders

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

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CD30-positive primary cutaneous lymphoproliferative disorders: molecular alterations and targeted therapies.

Project description:Primary cutaneous CD30-positive T-cell lymphoproliferative disorders are the second most common subgroup of cutaneous T-cell lymphomas. They include two clinically different entities with some overlapping features and borderline cases: lymphomatoid papulosis and primary cutaneous anaplastic large cell lymphoma. Molecular studies of primary cutaneous anaplastic large cell lymphoma reveal an increasing level of heterogeneity that is associated with histological and immunophenotypic features of the cases and their response to specific therapies. Here, we review the most significant genetic, epigenetic and molecular alterations described to date in primary cutaneous CD30-positive T-cell lymphoproliferative disorders, and their potential as therapeutic targets.

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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

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

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

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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

Single-cell profiling of cutaneous T-cell lymphoma after treatment with vorinostat and photophoresis.

Project description:Cutaneous T cell lymphomas (CTCL), encompassing a spectrum of T-cell lymphoproliferative disorders involving the skin, have collectively increased in incidence over the last 40 years. Sézary syndrome (SS) is an aggressive form of CTCL characterized by significant presence of malignant cells in both the blood and skin. The guarded prognosis for SS reflects a lack of reliably effective therapy, due in part to an incomplete understanding of disease pathogenesis. Using single-cell sequencing of RNA at the induction of vorinostat and photopherisis treatment (GSE122703) and at the progression on therapy. We identifed thea decrease conventional SS cell markers on therapy and an increase in the number of cells expressing FOXP3+.

2019-06-25 | GSE124898 | GEO

GATA-3 is a proto-oncogene in T-cell lymphoproliferative neoplasms [ChIP-seq]

Project description:In order to identify GATA-3 target genes in T-cell lymphoproliferative neoplasms, we performed GATA-3 ChIP-seq on 3 cutaneous T-cell lymphoma (CTCL) and 4 T-cell acute lymphoblastic leukemia (T-ALL). We have also established cell lines in which GATA-3 was knocked down by shRNA.

2022-04-30 | GSE201743 | GEO

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