Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

NPMâ??ALK permits the survival of thymic T cells with aberrant T cell receptor rearrangements enabling thymic escape and tumor development

ABSTRACT: We present evidence to support a new model of Anaplastic Large Cell Lymphoma (ALCL) pathogenesis in which the malignancy is initiated in early thymocytes, prior to TCR rearrangement which is bypassed in NPMâ??ALK transgenic mice following Notch1 expression. In support, we show that T cell receptor (TCR) rearrangements are aberrant in some human ALCL, yielding events that would not normally be permissive for survival during T cell development. However, a TCR is required for thymic egress and subsequent development of peripheral tumors in mice yet this TCR must be downâ??regulated for Tâ??cell lymphomagenesis. Children affected by ALCL may thus harbor lymphoma-initiating cells in the thymocyte population that seeds relapse after chemotherapy. comparative genomic hybridization data from 43 human Anaplastic Large Cell Lymphoma (ALCL) samples and control samples

ORGANISM(S): Homo sapiens

SUBMITTER: Mohamed BELHOCINE

PROVIDER: E-GEOD-67131 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

NPM‐ALK permits the survival of thymic T cells with aberrant T cell receptor rearrangements enabling thymic escape and tumor development

Project description:We present evidence to support a new model of Anaplastic Large Cell Lymphoma (ALCL) pathogenesis in which the malignancy is initiated in early thymocytes, prior to TCR rearrangement which is bypassed in NPM‐ALK transgenic mice following Notch1 expression. In support, we show that T cell receptor (TCR) rearrangements are aberrant in some human ALCL, yielding events that would not normally be permissive for survival during T cell development. However, a TCR is required for thymic egress and subsequent development of peripheral tumors in mice yet this TCR must be down‐regulated for T‐cell lymphomagenesis. Children affected by ALCL may thus harbor lymphoma-initiating cells in the thymocyte population that seeds relapse after chemotherapy.

2016-01-05 | GSE67131 | GEO

Transcription profiling of 32 human Anaplastic Large Cell Lymphomas (ALCL) and 5 ALCL cell lines to investigate differences between tumors expressing/not-expressing Anaplastic Lymphoma kinkase

Project description:A "Cartes d'Identite des Tumeurs" (CIT) project from the french Ligue Nationale Contre le Cancer (http://cit.ligue-cancer.net). Affymetrix UU133A gene expression data for a series of 32 cases of systemic Anaplastic Large Cell Lymphoma (ALCL) and 5 ALCL cell lines; used to (1) confirm that tumors expressing Anaplastic Lymphoma Kinase (ALK+ ALCL) and ALK- ALCLs are different entities, (2) identify most significantly differentially expressed genes between ALK+ and ALK- samples, (3) generate a molecular signature of ALK- ALCL, (4) perform unsupervised analysis classifying ALCL in sub-groups related to morphology and clinical variables (e.g. disease stage and enrichment with 'early relapse' patients). Principal Investigator: Dr Georges DELSOL-- Centre de Physiopathologie Toulouse-Purpan CHU-Purpan -- Toulouse -- France -- Email: delsol.g@chu-toulouse.fr Programme "Cartes d'identite des Tumeurs" (CIT) of the "Ligue Nationale Contre le Cancer" (LNCC) Submitter: Fabien PETEL (petelf@ligue-cancer.net)

2007-05-05 | E-TABM-117 | biostudies-arrayexpress

Genomic profiling of Anaplastic Large Cell Lymphoma

Project description:Anaplastic Large Cell Lymphoma (ALCL) is a mature T-cell lymphoma that can present as a systemic or primary cutaneous disease. Systemic ALCL represents 2-5% of adult lymphoma but up to 30% of all pediatric cases. Two subtypes of systemic ALCL are currently recognized on the basis of the presence of a translocation involving the Anaplastic Lymphoma Kinase ALK gene. Despite considerable progress, several questions remain open regarding the pathogenesis of both ALCL subtypes. To investigate the molecular pathogenesis and to assess the relationship between the ALK(+) and ALK(-)ALCL subtypes, we performed a genome-wide DNA profiling using high density, single nucleotide polymorphism (SNP) arrays (SNP-array) on a series of 63 cases and seven cell lines. The commonest lesions were losses at 17p13 and at 6q21, encompassing the TP53 and PRDM1 genes respectively. The latter gene, coding for BLIMP1, was inactivated by multiple mechanisms, more frequently, but not exclusively, in ALK(-)ALCL. In vitro and in vivo experiments showed that that PRDM1 is a tumor suppressor gene in ALCL models, likely acting as an anti-apoptotic agent. Losses of TP53 and/or PRDM1 were present in 52% of ALK(-)ALCL, and in 29% of all ALCL cases with a clinical implication. Genomic profiling of Anaplastic Large Cell Lymphoma

2013-09-20 | E-GEOD-50253 | biostudies-arrayexpress

The DNA-helicase HELLS drives ALK- ALCL proliferation by the transcriptional control of a cytokinesis-related program

Project description:Deregulation of chromatin modifiers, including DNA helicases, are emerging as one of the mechanism underlying the transformation of anaplastic lymphoma kinase negative (ALK−) anaplastic large cell lymphoma (ALCL). We recently identified the DNA helicase HELLS as central for proficient ALK-ALCL proliferation and progression. By performing RNA-sequencing profiling coupled with bioinformatic prediction, we demonstrated that HELLS contributes to an appropriate cytokinesis via the transcriptional regulation of genes involved in cleavage furrow regulation in ALK- anaplastic large cell lymphoma

2022-12-15 | E-MTAB-9918 | biostudies-arrayexpress

Dissection of acetylomic profiles in T cell lymphoma following histone deacetylases inhibition

Project description:The aim was to dissect molecular changes in histone and non-histone protein acetylation dynamics following the genetic or pharmacological inhibition of HDAC activity in a model of Anaplastic Large Cell Lymphoma (ALCL), a T cell non-Hodgkin lymphoma, predominantly found in children and adolescents.

2022-10-14 | PXD030503 | Pride

Genomic profiling of Anaplastic Large Cell Lymphoma

2013-09-20 | GSE50253 | GEO

Transcription profiling of Hodgkin Lymphoma- and Anaplastic Large Cell Lymphoma-derived cell lines

Project description:To identify genes and pathways involved in the pathogenesis of Hodgkin Lymphoma (HL) and Anaplastic Large Cell Lymphoma (ALCL) , we used the Ontario Cancer Institute (OCI) Human 27k arrays (UNH Homo sapiens 19K8 array), to study the expression profiling in pairs of HL-derived cell lines (KMH2 and L428) and ALCL-derived cell lines (DEL and SR-786).

2009-03-31 | E-MEXP-1132 | biostudies-arrayexpress

Gene expression study of anaplastic large cell lymphomas: cellular origin, pathogenesis and relation to Hodgkin lymphoma

Project description:Anaplastic large cell lymphoma (ALCL) is a main type of T cell lymphomas and comprises three distinct entities: systemic ALK+, systemic ALK- and cutaneous ALK- ALCL. Little is known about their pathogenesis and their cellular origin, and morphological and immunophenotypical overlap exists between ALK- ALCL and classical Hodgkin lymphoma (cHL). We conducted gene expression profiling of microdissected lymphoma cells of ALK+ and ALK- systemic ALCL, cutaneous ALCL and cHL, and of eight subsets of normal T and NK cells. The analysis supports a derivation of ALCL from activated T cells, but the lymphoma cells acquired a gene expression pattern hampering an assignment to a CD4+, CD8+ or CD30+ T cell origin. Indeed, ALCL display a general down-modulation of T cell characteristic molecules. All ALCL types show significant expression of NFκB target genes and upregulation of genes involved in oncogenesis (e.g. EZH2). Surprisingly few genes are differentially expressed between systemic and cutaneous ALK- ALCL despite their different clinical behaviour, and between ALK- ALCL and cHL despite their different cellular origin. ALK+ ALCL are characterized by expression of genes regulated by pathways constitutively activated by ALK. This study provides multiple novel insights into the molecular biology and pathogenesis of ALCL.

2009-11-16 | GSE14879 | GEO

Characterisation of Anaplastic Large Cell Lymphoma Stem Cells

Project description:Anaplastic Large Cell Lymphoma (ALCL) is propagated by cancer stem cells which are identified by their ability to efflux dye and hence reside in the side population (SP) on FACS analysis. In order to understand the origins of these ALCL SP cells we purified SP and main population (MP; SP-depleted) cell from the ALCL cell line SUDHL-1. On comparison of the gene expression signatures derived from these 2 cellular populations distinct branches dividing the SP and MP populations present indicating that they are distinct subsets within the bulk tumour. We sought to obtain pure populations of SP and MP cells from human SUDHL-1 Anaplastic Large Cell Lymphoma (ALCL) cell line. SUDHL-1 cells were stained with Hoechst 33342 dye, analysed using MoFlo Cell Sorter with UV lasers. The cells were then sorted in triplicates and subjected to RNA extraction. The extracted RNA was subjected to gene expression microarray using the Affymetrix Human Gene 1.0 ST Array.

2012-06-24 | E-GEOD-38906 | biostudies-arrayexpress

Molecular characterization of a series of 22 NF1-associated plexiform neurofibromas

Project description:22 plexiform neurofibromas from 18 unrelated neurofibromatosis-type 1 patients were screened with a high resolution array-CGH. Each PNF DNA (somatic tumor DNA) was individually hybridized on Agilent whole human genome 244K microarrays (Platform GPL4091) using the matched genomic constitutional DNA (lymphocytes DNA) from the corresponding patient as reference, in order to detect tumor-specific aberrations. NF1-associated plexiform neurofibromas DNA vs. constitutional DNA

2011-09-29 | E-GEOD-24328 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data