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accession-icon GSE47130
Vector-transduced neurons transcriptome profiles
  • organism-icon Homo sapiens
  • sample-icon 27 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

With the goal of specifically dissecting the toxicogenomic signatures of the helper-dependent (HD) human (HAd5) and canine (CAV-2) adenovirus, the VSV-G-pseudotyped SIN HIV-1 (LV) and the Adenoviral-associated vector 2/9 for human neurons (AAV2/9), we transduced a bona fide human neuronal system with HD-HAd5, HD-CAV-2, LV and AAV2/9, we analysed the transcriptional response of more than 47,000 transcripts using gene chips.

Publication Title

Differentiated neuroprogenitor cells incubated with human or canine adenovirus, or lentiviral vectors have distinct transcriptome profiles.

Sample Metadata Fields

Specimen part

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accession-icon GSE62687
CAV-2 vector-transduced human neurospheres transcriptome profiles
  • organism-icon Homo sapiens
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Brain gene transfer using viral vectors will likely become a therapeutic option for several disorders. Helper-dependent (HD) canine adenovirus type 2 vectors (CAV-2) are well suited for this goal. Indeed, these vectors are poorly immunogenic, efficiently transduce neurons, are retrogradely transported to afferent structures in the brain, and lead to long-term transgene expression. CAV-2 vectors have been exploited to unravel behavior, cognition, neural networks, axonal transport and therapy for orphan diseases. Here we describe the HD-CAV-2 vector induced transcriptional response of human dopaminergic neurospheres derived from midbrain progenitors. In this 3D model system, brain cell functions and dynamics mimic several aspects the dynamic nature of human brain. With the goal of better understanding and characterizing HD CAV-2 for brain therapy, we analyzed the transcriptomic modulation induced by HD-CAV-2 in this brain model system.

Publication Title

Transcriptional Response of Human Neurospheres to Helper-Dependent CAV-2 Vectors Involves the Modulation of DNA Damage Response, Microtubule and Centromere Gene Groups.

Sample Metadata Fields

Specimen part, Time

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accession-icon GSE13276
Candidate genes for the recurrence of glioblastoma multiforme identified by microarray
  • organism-icon Homo sapiens
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Background: Glioblastoma multiforme (GBM) is the most aggressive and most lethal primary malignant brain tumor, correlated with survival rates of less than one year from the time of diagnosis. Current surgical procedure attempts to remove the bulk of the tumor mass, whereas GBM frequently recurs within 1-3cm from the primary tumor resection site. Molecular mechanisms involved in the recurrence of the tumor are still poorly understood. The aim of the study was to define the molecular signature of GBM surrounding white matter (WM) in order to better understand the molecular mechanisms involved with tumor relapse.

Publication Title

Gene expression profile of glioblastoma peritumoral tissue: an ex vivo study.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE24747
NOVEL POTENTIAL MARKERS OF TUMOR-INITIATING CELLS IN COLON CANCER
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

BACKGROUND: Several in vitro assays have been used to identify cancer stem cells (CSC), including expression of cell surface markers and Hoechst dye efflux properties. However, each of these methods has potential pitfalls that complicate interpretation of the results. Focusing on colon cancers (CC), the CD133 antigen has been proposed as a marker of colon CSC. However, conflicting results have been reported in the literature indicating the need of a systematic analysis of CSC within CC and a complete validation of markers for the isolation of these cells.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE87865
AKR1C enzymes sustain therapy resistance in pediatric T-ALL
  • organism-icon Homo sapiens
  • sample-icon 54 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Although intensification of chemotherapy approaches considerably increased the outcome of pediatric T-cell Acute Lymphoblastic Leukemia (T-ALL) patients, a subgroup of them still experience treatment failure and relapse. In this context, we hypothesized that the Nrf2 signalling and its downstream effectors could be involved in sustain therapy resistance in T-ALL, as previously reported in other cancers. Indeed, in this study we identified the Aldo-Keto Reductase (AKR) enzymes AKR1C1-3, as over-expressed in T-ALL samples from therapy-resistant patients, demonstrating their fundamental role in the control of the response to vincristine (VCR) treatment. In particular, we evidence that the modulation of AKR1C1-3 gene expression and activity is sufficient to strongly affect the sensitivity of T-ALL cell lines and primary cells to VCR treatment, but not to daunorubicin, cytarabine or L-asparaginase. Moreover, we found a correlation between the degree of VCR response and the amount of AKR1Cs expression in patient-derived T-ALL xenografts. Interestingly, we show that daunorubicin and cytarabine are able to induce the over-activation of AKR1C enzymes, thus establishing a potential resistance loop generated by the combination of these drugs during T-ALL treatment.

Publication Title

AKR1C enzymes sustain therapy resistance in paediatric T-ALL.

Sample Metadata Fields

Specimen part, Disease stage

View Samples
accession-icon GSE71935
Gene expression profiling in 38 JMML patients and 9 healthy donors (Validation cohort)
  • organism-icon Homo sapiens
  • sample-icon 41 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Juvenile myelomonocytic leukemia (JMML) is a very rare and aggressive stem cell disease that mainly occurs in young children. RAS activation constitutes the core component of oncogenic signaling. In addition, the leukemic blasts of a quarter of JMML patients present with monosomy 7 (-7), whereas more than half of the patients show enhanced age-adjusted fetal hemoglobin (HbF) levels. Hematopoietic stem cell transplantation is the current standard of care. This results in an event-free survival of 50 - 60%, indicating that novel molecular driven therapeutic options are urgently needed. Using gene expression profiling in an extensive series of 82 patient samples, we aimed at understanding the molecular biology behind JMML and identified a previously unrecognized molecular subgroup characterized by high LIN28B expression.

Publication Title

LIN28B overexpression defines a novel fetal-like subgroup of juvenile myelomonocytic leukemia.

Sample Metadata Fields

Disease

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accession-icon GSE78513
NPM-ALK expression levels identify two distinct signatures in Anaplastic Large Cell Lymphoma of Childhood
  • organism-icon Homo sapiens
  • sample-icon 33 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Anaplastic large-cell lymphoma (ALCL) makes up approximately 15% of paediatric non-Hodgkin's lymphomas of childhood. The vast majority of them is associated with the t(2;5)(p23;q35) translocation that results in the expression of a hybrid oncogenic tyrosine kinase, NPM-ALK. In order to investigate ALCL biological characteristics we used transcriptional profiling approach. Genome-wide gene expression profiling, performed on 23 paediatric ALCL and 12 reactive lymph nodes specimens, showed two novel ALCL subgroups based on their NPM-ALK expression levels (named (ALK low and ALK high). Gene set enrichment analysis revealed, in ALK low samples, a positive enrichment of genes involved in the Interleukin signaling pathway, whereas we found increased expression of genes related to cell cycle progression and division in ALK high tumour samples, such as Aurora Kinase A (AURKA) and B (AURKB). Growth inhibition was observed upon administration of AURKA and AURKB inhibitors Alisertib and Barasertib and it was associated with perturbation of the cell cycle and induction of apoptosis. In conclusion we identified two novel ALCL subgroups, which display unique biological characteristics suggesting sensitivity to distinct targeted therapies.

Publication Title

NPM-ALK expression levels identify two distinct subtypes of paediatric anaplastic large cell lymphoma.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE72623
CRLF2 Over-expression is a Poor Prognostic Marker in Children With High Risk T-Cell Acute Lymphoblastic Leukemia
  • organism-icon Homo sapiens
  • sample-icon 28 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Seventeen T-ALL patients out of 120 (14.2%) presented CRLF2 expression 5 times higher than the median (CRLF2-high) with a significantly inferior 5-y EFS and an increased CIR compared to CRLF2-low patients.GEP of 15 T-ALL patients with (CRLF2-high) were compared to 15 CRLF2-low patients. GSEA identified cell cycle deregulating gene sets.

Publication Title

CRLF2 over-expression is a poor prognostic marker in children with high risk T-cell acute lymphoblastic leukemia.

Sample Metadata Fields

Disease

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accession-icon GSE29326
Gene expression profiling of pediatric myelodysplastic syndrome (MDS) characterizes disease subtype and time to progression into acute myeloid leukemia (AML)
  • organism-icon Homo sapiens
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Identification of relevant subgroups in childhood MDS patients by gene expression analysis and gene involve in progression into AML

Publication Title

Gene expression signatures of pediatric myelodysplastic syndromes are associated with risk of evolution into acute myeloid leukemia.

Sample Metadata Fields

Specimen part, Disease

View Samples
accession-icon GSE26701
Expression data from post mortem porcine skeletal muscle
  • organism-icon Sus scrofa
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Porcine Genome Array (porcine)

Description

We set up a pilot study using Affymetrix Gene Chip Porcine Genome Arrays to evaluate the impact of time lags from death on gene expression profiling of porcine skeletal muscle at four post mortem time points (up to 24 hrs) during the routine processing of fresh tights

Publication Title

Microarray gene expression analysis of porcine skeletal muscle sampled at several post mortem time points.

Sample Metadata Fields

Sex, Specimen part, Time

View Samples
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refine.bio is a repository of uniformly processed and normalized, ready-to-use transcriptome data from publicly available sources. refine.bio is a project of the Childhood Cancer Data Lab (CCDL)

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Cite refine.bio

Casey S. Greene, Dongbo Hu, Richard W. W. Jones, Stephanie Liu, David S. Mejia, Rob Patro, Stephen R. Piccolo, Ariel Rodriguez Romero, Hirak Sarkar, Candace L. Savonen, Jaclyn N. Taroni, William E. Vauclain, Deepashree Venkatesh Prasad, Kurt G. Wheeler. refine.bio: a resource of uniformly processed publicly available gene expression datasets.
URL: https://www.refine.bio

Note that the contributor list is in alphabetical order as we prepare a manuscript for submission.

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