Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

50 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

IGR_CamaraClayette_MCL

ABSTRACT: We designed a gene profiling experiment to identify genes involved in secondary drug resistance in mantle cell lymphomas (MCL). We obtained paired tissue samples collected before treatment and after relapse or progression. Variations in gene expression between the 2 samples were estimated for 5 patients. For each gene, the mean variation was estimated for patients with a refractory primary tumor and for responders who developed secondary drug resistance. Nine genes of interest were selected on the basis of the magnitude and statistical significance of the variation of expression in responders and non-responders. BMP7 was the only one with significantly increased expression at relapse in patients who developed secondary resistance. Validation of BMP7 as a key gene involved in secondary resistance was performed using cultures of cell line. Incubation of BMP7 with MCL cell lines increased their resistance to Bortezomib and Cytarabine, while inhibition of BMP7 expression by siRNA correlated with increased cell death linked to drug application.

ORGANISM(S): Homo sapiens

SUBMITTER: Guillaume Meurice

PROVIDER: E-MTAB-1090 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Transcription profiling of non-small cell lung carcinoma cell line H1975 treated with cisplatin or BMS-69014 a novel panHER/VEGFR inhibitor

Project description:Non-small cell lung cancer (NSCLC) with activating mutations in the epidermal growth factor receptor (EGFR) responds to EGFR tyrosine kinase inhibitors such as erlotinib. However, secondary somatic EGFR mutations (e.g. T790M) confer resistance to erlotinib. BMS-690514, a novel panHER/VEGFR inhibitor described here, exerted antiproliferative and pro-apoptotic effects on NSCLC cell lines, with prominent efficacy on H1975 cells expressing the T790M mutation. In this model, BMS-690514 induced a G1 cell cycle arrest, as well as ultrastructural hallmarks of apoptosis, mitochondrial release of cytochrome c, and activation of caspases involved in the intrinsic (e.g. caspase -2, -3, -7 and -9), but not in the extrinsic (e.g. caspase-8) pathway. Caspase inhibition conferred partial protection against BMS-690514 cytotoxicity, pointing to the involvement of both caspase-dependent and -independent effector mechanisms. Transcriptome analyses revealed the upregulation of pro-apoptotic (e.g. Bim, Puma) and cell cycle inhibitory (e.g. p27Kip1, p57Kip2) factors, as well as the downregulation of anti-apoptotic (e.g. Mcl1), heat shock (e.g. HSP40, HSP70, HSP90) and cell cycle promoting (e.g. cyclins B1, D1 and D3, CDK1, MCM family proteins, PCNA) proteins. BMS-690514-induced death of H1975 cells was modified in a unique fashion by a panel of siRNAs targeting apoptosis modulators. Downregulation of components of the NF-kappaB survival pathway (e.g. p65, Nemo/IKK, TAB2) sensitized cells to BMS-690514, whereas knockdown of pro-apoptotic factors (e.g. Puma, Bax, Bak, caspase-2, etc) and DNA damage-related proteins (e.g. ERCC1, hTERT) exerted cytoprotective effects. BMS-690514 is a new pan-HER/VEGFR inhibitor that may become an alternative to erlotinib for the treatment of NSCLC.

2007-07-24 | E-TABM-239 | biostudies-arrayexpress

Transcription profiling of human T cell lines isolated from tumor infiltrating lymphocytes or peripheral blood lymphocytes of a patient with large cell carcinoma of the lung

Project description:The IGR-Heu tumor cell line was established from patient Heu suffering from large cell carcinoma of the lung. Heu171 T cell clones were isolated from autologous tumor infiltrating lymphocytes. H32-22 clone was isolated from autologous peripheral blood lymphocytes after stimulation with IGR-Heu and sorting with peptide-MHC tetramers. T cells were grown in the presence of irradiated autologous tumor and lymphoblastoid cell lines in complete media supplemented with rIL-2 and conditioned medium from phytohemagglutinin-activated lymphocytes for 3 weeks. Then, for microarray assays, RNA was extracted from the different cells

2007-03-02 | E-TABM-207 | biostudies-arrayexpress

Transcription profiling of human cell lines treated with cytochalasin D and nocodazole with the aim of characterising tetraploid clones

Project description:During the oncogenic process, tetraploidy is a candidate intermediate stage leading from diploidy to aneuploidy. The aim of our experiment was to establish tetraploid clones and to characterize their transcriptome.

2006-03-01 | E-TABM-70 | biostudies-arrayexpress

Transcription profiling of cohort of human cutaneous primary melanomas associated with a distant metastasis free survival

Project description:Identification of genomic characteristics in a cohorte of human cutaneous primary melanoma associated with a distant metastasis free survival.

2007-04-01 | E-TABM-1 | biostudies-arrayexpress

Transcription profiling of human cutaneous primary melanomas in an independent population of 17 patients

Project description:Validation of genomics characteristics of human cutaneous primary melanoma in an independnat population of 17 patients.

2007-04-01 | E-TABM-2 | biostudies-arrayexpress

Comparative genomic hybridization of 23 human nevi with a pool of primary cutaneous melanoma

Project description:Genomic profiles comparing 23 nevi with a pool of primary cutaneous melanoma

2009-04-16 | E-TABM-3 | biostudies-arrayexpress

Transcription profiling of 9 pairs of human metastasis/primary melanoma (each from the same patient)

Project description:Study by dye-swap of 9 pairs of metastasis/primary melanoma (each from the same patient)

2007-04-01 | E-TABM-4 | biostudies-arrayexpress

Transcription profiling of response to tamoxifen in human ERa-positive postmenopausal breast tumor patients

Project description:Identification of HRPAP20 and TIMELESS as outstanding candidate markers to predict the response to tamoxifen in ERa-positive postmenopausal breast tumor patients

2007-10-09 | E-TABM-72 | biostudies-arrayexpress

Transcription profiling of human nevoid basal cell carcinoma syndrome primary fibroblasts with non-sense or miss-sense mutations in the tumor supressor gene PTCH1

Project description:Mutations in the tumor suppressor gene PTCH1 are responsible for Gorlin syndrome, or nevoid basal cell carcinoma syndrome (NBCCS). NBCCS causes predisposition to basal cell carcinoma (BCC), the commonest cancer in adult human. In the general population BCC develop almost exclusively in sun-exposed area of the skin (Buettner PG, Raasch BA (1998) Int J Cancer 78: 587-593). In contrast, and, intriguingly, NBCCS BCCs are observed in both sun-protected and sun-exposed areas. Interestingly, our previous studies have shown that both fibroblasts and keratinocytes from NBCCS patients exhibit normal nucleotide excision repair of UVB-induced DNA lesions and survival capacities following a single UVB irradiation (Brellier F, Valin A, et al. (2008) Br J Dermatol.). These data suggest that sun UV are far from being the only etiologic factor of BCC in NBCCS patients. In this study we aimed at documenting the possible role of NBCCS fibroblasts in BCC development in NBCCS patients. Thus, the genome expression of NBCCS primary fibroblasts cultured in a dermal equivalent was compared to the one of control fibroblasts under the same circumstances.

2009-03-19 | E-TABM-549 | biostudies-arrayexpress

Transcription profiling of human CD34+ cells from familial platelet disorder

Project description:Characterize the genes deregulated in CD34 positive cells from peripheral blood of FPD/AML patients harbouring two different RUNX1 mutations. RUNX1 (also called AML1), a DNA-binding subunit of the CBF transcription factor family, is a master regulatory gene in hematopoiesis and acts as a tumour suppressor. Heterozygous germ line alterations in RUNX1 lead to a familial platelet disorder with a propensity to develop acute myeloid leukemia (FPD/AML). Although RUNX1 abnormalities per se are not sufficient to induce full-blown leukemia in FPD, this pathology represents a valuable model to understand how RUNX1 germ line mutations predispose to acquisition of additional genetic changes leading to leukemia transformation. To investigate how RUNX1 may predispose to leukemia, we performed a comparative study between two pedigrees harbouring different RUNX1 mutations, one associated with only thrombocytopenia (R139stop) and the other leading to thrombocytopenia and leukemic predisposition (R174Q).

2010-09-11 | E-TABM-792 | 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