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Transcription profiling of human nephroblastoma

ABSTRACT: A ""Cartes d'Identite des Tumeurs"" (CIT) project from the french Ligue Nationale Contre le Cancer (http://cit.ligue-cancer.net). 73 samples (60 tumoral, 6 normal kidneys (NK), 3 fetal kidneys (FK) and 4 cell lines (L)), hybridized on Affymetrix HG-U133A GeneChips.Tumor classification based on a characterization of WT1 and Betacatenin. Identification of major differences between two categories of Wilms' Tumors defined according to WT1 and CTNNB1 genomic and expression features. First large scale study based on post-chemotherapy resected tumors, according to the SIOP protocoles.

ORGANISM(S): Homo sapiens

DISEASE(S): Wilms' tumor

SUBMITTER: Funda Vilmaz

PROVIDER: E-TABM-53 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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WNT/beta-catenin pathway activation in Wilms tumors: a unifying mechanism with multiple entries?

Corbin Marie M de Reyniès Aurélien A Rickman David S DS Berrebi Dominique D Boccon-Gibod Liliane L Cohen-Gogo Sarah S Fabre Monique M Jaubert Francis F Faussillon Marine M Yilmaz Funda F Sarnacki Sabine S Landman-Parker Judith J Patte Catherine C Schleiermacher Gudrun G Antignac Corinne C Jeanpierre Cécile C

Genes, chromosomes & cancer 20090901 9

Based on characterization of both genomic and expression status of WT1 and CTNNB1 (beta-catenin) in a series of 60 Wilms tumor samples, combined with genome-wide expression profiling of these tumors, normal mature and fetal kidney controls, we show that WT1/beta-catenin expression was a better classifier than WT1/CTNNB1 mutations. We present molecular data supporting that the WNT pathway is involved in both tumor classes, with and without WT1/beta-catenin alterations. In the tumor class with WT1 ...[more]

PMID: 19530245

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Transcription profiling by array of human adrenocortical tumors to identify molecular predictors of diagnosis and prognosis

Project description:A ""Cartes d'Identite des Tumeurs"" (CIT) project from the french Ligue Nationale Contre le Cancer (http://cit.ligue-cancer.net). 92 samples on Affymetrix HG-U133 Plus 2.0 GeneChips arrays for 92 patients with Adrenocortical Tumors (ACT). 4 normal adrenal samples from the same batch are also included. 10 ACTH-independant Macronodular Adrenal Hyperplasia (AIMAH) from the same batch are also included.

2009-01-15 | E-TABM-311 | biostudies-arrayexpress

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2013-01-15 | E-MTAB-951 | biostudies-arrayexpress

Transcription profiling of advanced human breast cancers treated with a dose-intense epirubicin /cyclophosphamide regimen followed by mastectomy

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2007-03-26 | E-TABM-43 | biostudies-arrayexpress

MESO-JD

Project description:A Cartes dM-^RIdentite des Tumeurs (CIT) project from the french Ligue Nationale Contre le Cancer (http://cit.ligue-cancer.net/) | Affymetrix HG-U133 Plus 2.0 : 43 samples. Characteristics[OS.event] means the survival status (0: dead/1:alive). Characteristics[OS_delay] means the survival delay form diagnosis to the last follow up. Characteristics[Asbestos.Exposure] : exposure history to the asbestos (E: Exposed, PE: probably exposed, NE: not exposed). BAP1.Gene.mutation: (M: mutated, WT: wild type). Characteristics[CDKN2B.Gene.mutation]: (M: mutated, WT: wild type) . Characteristics[CTNNB1.Gene.mutation]: (M: mutated, WT: wild type). Characteristics[NF2.Gene.mutation]: (M: mutated, WT: wild type). Characteristics[P14ARF.Gene.mutation]: (M: mutated, WT: wild type). Characteristics[P16INKa.Gene.mutation]: (M: mutated, WT: wild type). Characteristics[TP53.Gene.mutation]: (M: mutated, WT: wild type). Characteristics[molecular.subgroup]: the clusters identified by the unsupervised analyses of gene expression. NOTE: This experiment was updated on 10th April 2014. The following changes were made: 5 samples (MPM39, MPM40, MPM41, MPM42, MPM430) and their associated data files were removed. Histology values were updated and the column headings regarding gene mutations were modified.

2014-04-04 | E-MTAB-1719 | biostudies-arrayexpress

Transcription profiling by array of human non anaplastic T-cell lymphoma biopsies and cell lines

Project description:A Cartes d'Identite des Tumeurs (CIT) project from the french Ligue Nationale Contre le Cancer (http://cit.ligue-cancer.net) | Affymetrix HG-U133 Plus 2.0 : 7 NKTCL biopsies, 2 NKTCL cell lines (SNK6, SNT8), 16 PTCL NOS biopsies, 2 NK cells samples | Biopsies and cell lines of NK/T-cell lymphoma, nasal-type (NKTCL) were subject to combined gene expression profiling and array-based comparative genomic hybridization analyses. Compared to PTCL, NOS, NKTCL had higher transcript levels for NK-cell markers and cytotoxic molecules, especially granzyme H, a novel sensitive biomarker of NKTCL. Compared to normal NK cells, tumors were closer to activated than resting cells and overexpressed several genes related to vascular biology, EBV-induced genes and PDGFRA. Notably, PDGFR? and its phosphorylated form were confirmed at the protein level, and in vitro the MEC04 NKTCL-cell line was sensitive to imatinib. Deregulation of the AKT, JAKSTAT and NF-?B pathways suggested by bioinformatical analysis, was corroborated by nuclear expression of phosphorylated AKT, STAT3 and RelA in NKTCL, and several deregulated genes in these pathways mapped to regions of recurrent copy number aberrations (AKT3 (1q44), IL6R (1q21.3), CCL2 (17q12), TNFRSF21 (6p12.3)). Several features of NKTCL uncovered by this analysis (overexpression of VEGFA and its receptor KDR by the tumor cells, overexpression of MET-HGF) suggest deregulation of angiogenic pathways. Integrative analysis also identified a novel putative tumor suppressor HACE1 in the frequently deleted 6q21 region. This study highlights emerging oncogenic pathways in NKTCL and identifies novel diagnostic and therapeutic targets. | Submitter : Aurelien de Reynies <reyniesa@ligue-cancer.fr> | Project leader : Philippe Gaulard <philippe.gaulard@hmn.aphp.fr>

2009-12-31 | E-TABM-702 | biostudies-arrayexpress

Human benign adrenocortical tumors expression profile

Project description:Gene expression was generated using HG-U133_Plus_2.0 expression arrays (Affymetrix). All samples were normalized using the RMA (Robust Multi-array Average) algorithm from the Bioconductor “affy” package.Unsupervised classification of samples was performed using ConsensusClusterPlus R package v1.40, with hierarchical clustering method and euclidean distance, based on the top 1000 variable transcripts, according to their standard deviation. The optimal number of groups was chosen according to the relative change of area under CDF curve criterion.

2020-08-12 | E-MTAB-6552 | biostudies-arrayexpress

Transcription profiling of pheochromocytomas and paragangliomas (188 tumor samples)

Project description:A Cartes d'Identité des Tumeurs (CIT) project from the french Ligue Nationale Contre le Cancer (http://cit.ligue-cancer.net) | Affymetrix HG-U133 Plus 2.0 : 188 tumor samples |Pheochromocytomas and paragangliomas are neuroendocrine tumors occuring in the context of inherited cancer syndromes in approximately 30% of cases, linked to germline mutations in VHL, RET, NF1, SDHA, SDHB, SDHC, SDHD, SDHAF2 or TMEM127 genes. Although progress has been made with regard to tumorigenesis mechanisms in pheochromocytoma/paraganglioma thanks to genome-wide expression studies, the question of a putative molecular distinction between VHL- and SDHx- on one hand, and RET- and NF1-related tumors on the other hand, remained to be addressed as well as the characterization of genetic events in sporadic tumors. With this purpose, 202 pheochromocytomas/paragangliomas, including 75 hereditary tumors, were investigated by expression profiling, array CGH and somatic mutation screening. The systematic characterization of somatic genetic events associated with tumor suppressor gene germline mutations in tumor tissues reveals a majority of loss of heterozygosity (LOH) but also point mutations and copy neutral LOH. Gene-expression signature defined the hereditary tumors according to their genotype. Especially, a complete sub-separation between SDHx- and VHL-related tumors was observed. Moreover, guided by the transcriptome classification and the LOH profile, somatic mutations in VHL or RET genes were identified in 14% of sporadic pheochromocytomas/paragangliomas. A genetic cause was found in 45.5% (92/202) of the large series of pheochromocytomas/paragangliomas analyzed. Regarding mutated genes, specific molecular pathways involved in tumorigenesis mechanisms are showed. Altogether, these new findings suggest that somatic mutation analysis would give important clues for personalized molecular target therapies.

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