Oncogenic role of TOX in CTCL
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE57122 | GEO | 2014/04/29
SECONDARY ACCESSION(S): PRJNA245500
REPOSITORIES: GEO
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Project description:TOX is a nuclear factor essential for the development of CD4+ T cells in the thymus. TOX is found to be aberrantly up-regulated in the skin biopsies and in the blood CD4+ T cells of cutaneous T cell lymphoma. The goal of this study is to identify potential transcriptional targets of TOX in CTCL by comparison between TOX shRNA transfected CTCL cells (Hut78 and HH) and control CTCL cells. Two color experiment. Lentivirus transduced control vector vs. TOX shRNA vectors on Hut78 and HH cell lines. Biological replicates: 3 control replicates, 3 shRNA tansduced replicates for each cell line.
2014-04-29 | E-GEOD-57122 | biostudies-arrayexpress
Project description:IKZF2 is an important nuclear matrix protein and plays a pivotal role in T cell development and differentiation, while its expression and function in Cutaneous T cell lymphoma (CTCL) remain ambiguous. Our study aimed to investigate the expression pattern, biological function of IKZF2 in a large clinical cohort. IKZF2 is specifically over-expressed in malignant T cells with MF tumor-stage. In order to explore the function of IKZF2 in the pathogenesis of CTCL, transcriptome sequencing was performed among Hut78 cells transfected with shRNAs targeting IKZF2 (shIKZF2) and scrambled shRNA(sh0) to investigate genes regulated by IKZF2 in CTCL cells .
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Project description:We examined the function of miR-150 in T-cell lymphomagenesis. We transfected GFP-control or GFP-miR-150 into several T-cell lymphoma lines and sought which genes were regulated by miR-150. To examine the function of miR-150 in T-cell lymphomagenesis, we first transfected GFP-control (Mock) or GFP-miR-150 into several T-cell lymphoma lines (ATN-1, HUT78, My-La, and HH). To detect genes commonly downregulated among these cells, we used the CodeLinkTM Human Whole Genome Bioarray platform with the criterion that the miR-150/GFP-control ratio must be <0.75 in all 3 CTCL lines.
2013-07-30 | E-GEOD-49308 | biostudies-arrayexpress
Project description:Transcriptional profiling of human CTCL cell line H9 comparing cells transfected with vehicle control with ShBCL11B cells. Previous study have shown the involvements of BCL11b/BCL11B in T cell development and hematopoietic malignancies of T-cell origin. Objective was to explore the action of BCL11B in the pathogenesis of cutaneous T-cell lymphoma(CTCL).
2019-12-17 | GSE90616 | GEO
Project description:<p>Mycosis Fungoides (MF) and Sézary Syndrome (Sz) comprise the majority of Cutaneous T-Cell Lymphoma (CTCL) cases and are characterized by clinical heterogeneity. This array of symptoms includes skin patches, plaques and tumors as well as blood involvement and erythroderma. Because the genetic basis of CTCL is still poorly understood, we performed whole-exome sequencing on 11 MF/Sz samples and their matched, normal control DNA. Upon analyzing this data, we distilled a list of an additional 494 genes to be sequenced at depth. The majority of these 494 genes were sequenced in the exons alone, however, for a small subset of these genes we sequenced the entire genomic locus in search of structural variation events. This 494 gene targeted resequencing effort was performed upon 72 patients with MF/Sz and their matched, normal control DNA. An additional 5 MF/Sz and matched, normal DNA samples underwent whole genome amplification (WGA) prior to library preparation, which appears to have introduced mutations into these samples, however we also include them here. We additionally include 10 MF/Sz samples without a matched, normal control samples, 1 of which underwent WGA. In addition to primary disease samples, we also performed targeted resequencing on 4 CTCL cell lines (HH, MyLa, SeAx and Hut78) as well as on H9 cells (a subclone of Hut78 cells) and Jurkat cells, a T-ALL derived cell line that was used as an experimental system for our work. In sum, this data deposition includes exome and/or targeted resequencing from 92 individuals with 192 samples submitted.</p>
| phs000913 | dbGaP
Project description:Cutaneous T cell lymphoma (CTCL) can have clinical and histological features resembling benign inflammatory dermatosis (BID) and can be difficult to diagnose especially at the early stage of CTCL. We used microarrays to detail the global alteration of miRNA transcriptome and generate a diagnosis and prognosis signature.
2017-11-08 | GSE106645 | GEO
Project description:Cutaneous T cell lymphoma (CTCL) can have clinical and histological features resembling benign inflammatory dermatosis (BID) and can be difficult to diagnose especially at the early stage of CTCL. We used microarrays to detail the global alteration of miRNA transcriptome and generate a diagnosis and prognosis signature.
2017-11-08 | GSE106644 | GEO
Project description:AHI-1 is an oncogene often targeted by provirus insertional mutagenesis in murine leukemias and lymphomas. Aberrant expression of human AHI-1 occurs in cutaneous T-cell lymphoma (CTCL) cells and in CD4+CD7- Sezary cells from patients with Sezary syndrome (SS). Stable knockdown of AHI-1 using retroviral-mediated RNA interference in CTCL cells inhibits their transforming activity in vitro and in vivo. To identify genes involved in AHI-1-mediated transformation, microarray analysis was performed to identify differentially expressed genes in AHI-1 suppressed CTCL cells. Fifteen up-regulated and six down-regulated genes were identified and confirmed by Q-RT-PCR. Seven were further confirmed in a microarray analysis of CD4+CD7- Sezary cells from SS patients. HCK and BIN1 emerged as new candidate cooperative genes, with differential protein expression which correlates with observed transcript changes. Interestingly, changes in HCK phosphorylation and biological response to its inhibitor, dasatinib, were observed in AHI-1 suppressed or overexpressed cells. The tumor suppressor BIN1 physically interacts with MYC in CTCL cells, which also exhibit differential MYC protein expression. In addition, aberrant expression of alternative splicing forms of BIN1 was observed in primary and transformed CTCL cells. These findings indicate that HCK and BIN1 may play critical roles in AHI-1-mediated leukemic transformation of human CTCL cells. Keywords: Cell type comparison
2009-02-07 | GSE14746 | GEO
Project description:Mycosis fungoides (MF), the most common subtype of cutaneous T-cell lymphoma (CTCL), may undergo large-cell transformation (LCT), which is related to aggressive clinical courses and resistance to conventional treatments. However, the mechanisms of LCT remain largely unknown.We performed RNA-seq on biopsied specimens isolated from 26 MF-LCT patients and 23 MF-NLCT patients to decipher the mechanisms underlying LCT. We found PEG10 was overexpressed in MF-LCT compared with MF -NLCT cases. In order to explore the function of PEG10 in the pathogenesis of MF, transcriptome sequencing was performed among HH cells transfected with shRNAs targeting PEG10 (shPEG10) and scrambled shRNA(sh0) , Myla cells transfected with empty vetors(vec) and PEG10 expression vectors ( RF1b, RF1b/2, RF1b/2+CNF) to investigate genes regulated by PEG10 in CTCL cells .
2021-12-25 | GSE168508 | GEO
Project description:<p>Sezary syndrome is a leukemic and aggressive form of cutaneous T-cell lymphoma (CTCL) resulting from the malignant transformation of skin-homing central memory CD4+ T cells. To identify new genetic alterations involved in Sezary syndrome and CTCL transformation we performed whole-exome sequencing of tumor-normal sample pairs from 26 Sezary syndrome and 16 CTCL patients. These analyses revealed a distinctive pattern of somatic copy number alterations in Sezary syndrome including highly prevalent recurrent chromosomal deletions involving the TP53, RB1, PTEN, DNMT3A, and CDKN1B tumor suppressor genes. Mutation analysis identified a broad spectrum of somatic mutations involving key genes involved in epigenetic regulation (TET2, CREBBP, MLL3, BRD9, SMARCA4 and CHD3) and signaling, including mutations in MAPK1, BRAF, CARD11 and PRKG1 driving increased MAPK, NFKB and NFAT activity upon T-cell receptor stimulation. Collectively, our findings provide new insights into the genetics of Sezary syndrome and CTCL and support the development of personalized therapies targeting key oncogenically activated signaling pathways for the treatment of these diseases.</p>
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