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
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Philippe Dessen
PROVIDER: E-TABM-208 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Publications
Alpha E beta 7 integrin interaction with E-cadherin promotes antitumor CTL activity by triggering lytic granule polarization and exocytosis.
Le Floc'h Audrey A Jalil Abdelali A Vergnon Isabelle I Le Maux Chansac Béatrice B Lazar Vladimir V Bismuth Georges G Chouaib Salem S Mami-Chouaib Fathia F
The Journal of experimental medicine 20070226 3
Various T cell adhesion molecules and their cognate receptors on target cells promote T cell receptor (TCR)-mediated cell killing. In this report, we demonstrate that the interaction of epithelial cell marker E-cadherin with integrin alpha(E)(CD103)beta(7), often expressed by tumor-infiltrating lymphocytes (TILs), plays a major role in effective tumor cell lysis. Indeed, we found that although tumor-specific CD103(+) TIL-derived cytotoxic T lymphocyte (CTL) clones are able to kill E-cadherin(+)/ ...[more]
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2007-03-02 | E-TABM-207 | biostudies-arrayexpress
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2010-09-11 | E-TABM-792 | biostudies-arrayexpress
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2009-03-12 | E-TABM-611 | biostudies-arrayexpress
Project description:Goal of the experiment Recurrence is a frequent phenomenon in intracranial childhood ependymomas. To understand this process, we investigated whether the gene expression profiling of matched ependymomas at diagnosis and at relapse could reveal key molecular events involved in tumor progression. To gain new insight in this process and identify pathways associated with recurrence, we compared the gene expression profiles of local recurrences with the corresponding initial tumors. Brief description We analyzed 17 tumor samples at diagnosis and a total of 27 paired recurrences. Recurrences analyzed occurred after surgery only in 12 cases, surgery plus chemotherapy only in 9 cases and any treatment plus radiotherapy in 6 cases. We compared the level of gene expression for each tumor at recurrence relative to its expression at diagnosis using Agilent 44K dual color gene expression microarrays.
2010-12-31 | E-TABM-873 | biostudies-arrayexpress
Project description:Docetaxel is used as a standard treatment in patients with metastatic castration-resistant prostate cancer. However, a large subset of patients develops resistance by mechanisms that remain largely unknown. It is thus important to define the relevant pathways implicated in docetaxel-resistance and validate predictive biomarkers that will allow approaches of personalized treatment. In this aim, we established resistant IGR-CaP1 prostate cancer cell lines to different doses of docetaxel (IGR-CaP1-R cell lines) and investigated gene expression profiles by microarray analyses. We generated a signature of 112 genes potentially implicated in docetaxel-resistance whose expression is highly modified (Fold change M-bM-^IM-% 5). Among these genes, significant modification of expression was observed among cell cycle components in the resistant cells. Hence, we focused on the role of the cell cycle regulator LZTS1 located on chromosome 8p which was under-expressed in all our docetaxel-resistant models. LZTS1 extinction was confirmed at the RNA and protein levels. DNA methylation analysis revealed a stretch of 20 highly methylated CpGs in the region encompassing the exon 1 of LZTS1 promoter in the docetaxel-resistant cells suggesting the existence of an epigenetic regulation of LZTS1 expression in the resistant cells. By using siRNA strategy, we found evidence that LZTS1 plays an important role in the acquisition of the resistant phenotype. In addition, immunohistochemical staining showed that LZTS1 protein was absent or down-regulated in 33% of diagnostic biopsies obtained in patients with metastatic castration-resistant prostate cancer. This heterogeneous labeling suggests that LZTS1 might constitute a predictive biomarker of response to docetaxel chemotherapy. Furthermore, as Cdc25C is a LZTS1 partner in the mitosis regulation, we observed that targeting of Cdc25C with the pharmacological Cdc25C inhibitor NSC 663284 specifically killed the docetaxel-resistant cells. These results strongly suggest that Cdc25C plays a role in docetaxel resistance and that Cdc25C might be a therapeutic target to overcome docetaxel resistance. Altogether our findings identify an important role of LZTS1 in developing docetaxel resistance in prostate cancer through its role in regulating phosphatase Cdc25C. The set of gene expression with 4x44K Agilent ( design 014850) correspond to 6 doses of docetaxel 2?5 to 200 ug/ml) in dual color and dye-swap versus the IGR-Cap1 cell line without docetaxel.
2013-06-30 | E-MTAB-1221 | biostudies-arrayexpress
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2013-08-13 | E-MTAB-993 | biostudies-arrayexpress
Project description:The OTT1-MAL fusion oncogene is specifically associated with human infant acute megakaryoblastic leukemia. In a murine model of OTT-MAL expression, leukemic cells expressing OTT-MAL present an aberrant activation of the Notch pathway target genes. IKZF1 was proposed to interact with the Notch signaling pathway during T-cell development and leukemogenesis. IKZF1-deficient animals present thrombocytosis with increased number of megkaryocytes indicating that it plays a role during megakaryocyte development. To assess the interaction betweeen the Notch signaling pathway and Ikaros in the context of acute megakaryoblastic leukemia, we expressed full-length IKZF1 in a cell line expressing the fusion OTT-MAL (6133 cells). To identify the target gene of IKZF1 we performed a global expression analysis as follow: i) 6133 cells were infected with the following retroviruses :1-empty retrovirus (MIE) 2-retrovirus allowing the expression of the full-length IKZF1 (IK1) and 3- a retrovirus allowing the expression of an alternatively spliced form of IKZF1 (IK7). Ii) Infected cells were sorted by flow cytometry 24 hours after infection and RNA was extracted with the Qiagen Rneasy kit with DNase treatment. After quantification biological replicates of RNA were hybridized on Agilent arrays with dye-swap as indicated below.
2013-08-08 | E-MTAB-897 | biostudies-arrayexpress
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2013-06-24 | E-MTAB-1452 | biostudies-arrayexpress
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2010-03-18 | E-TABM-899 | biostudies-arrayexpress
Project description:'Prostate cancer is the second cancer diagnosed among men worldwide. Beside approval of new therapies in the last five years, chemotherapeutic agents, docetaxel and cabazitaxel taxanes remain key treatments for metastatic castration resistant prostate cancers. However, primary and acquired resistance to taxanes still emerged in about half of patients. There is therefore an urgent need to discover and understand the taxane resistance mechanisms in order to identify new therapeutic targets. Indeed, targeted therapies that exploit the signaling pathways involved in prostate cancer are required to overcome chemoresistance and improve treatment outcomes. Molecular chaperones play a key role in the regulation of cellular homeostasis and the development of treatment resistance, and are promising therapeutic targets. Using high throughput siRNA functional screening based on a gene expression signature, we identified FKBP7, involved in acquired resistance to docetaxel and cabazitaxel. FKBP7 is a molecular chaperone that has not been studied in human so far. FKBP7 is overexpressed in prostate tumors and its expression is correlated with recurrence in patients who received docetaxel as neoadjuvant therapy. Moreover, FKBP7 is upregulated in taxane resistant prostate cancer cell lines and its expression sustains their growth in vitro and in a mice model of Docetaxel resistance. Using a high throughput proteomic approach, we identified the signaling pathway regulated by FKBP7 which is responsible for the survival of chemoresistant cells. Finally, we proposed a promising therapeutic strategy to overcome both docetaxel and cabazitaxel chemoresistance by targeting the downstream effector of FKBP7. Gene expression was profiled using a 4×44K Human Whole Genome (G4112F, id : 014850) expression array (Agilent Technologies, Santa Clara, Cal.) with a dual color dye-swap competitive hybridization procedure, according to the manufacturer''s instructions. Total RNA from untreated parental IGR-CaP1 cells was used as the RNA reference (NN1). Total RNA from IGR-CaP1 cells resistant to 5nM (NN2), 11.6nM (NN3), 25nM (NN4), 50nM (NN5), 100nM (NN6), and 200nM (NN7) of Docetaxel respectively, were used as samples. Two independent replicates of each samples (a and b) were used. Image analyses (quantification, normalization) were performed with Feature Extraction software (Agilent Technologies) and gene expression analysis was performed using Bioconductor.'
2018-11-07 | E-MTAB-4869 | biostudies-arrayexpress