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accession-icon GSE30318
Expression data from murine Fancc-deficient hematopoietic stem and progenitor cells
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

We used gene expression microarrays to identify genes whose expression was influenced differently by TNFa in Fancc-deficient mice compared to wild type (WT) mice. To identify genes whose expression was directly or indirectly influenced by Fancc, we looked in particular for genes either suppressed or induced by TNF in WT cells that were not affected by TNF in Fancc-deficient cells.

Publication Title

FANCL ubiquitinates β-catenin and enhances its nuclear function.

Sample Metadata Fields

Specimen part

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accession-icon GSE2535
Expression data in patients with chronic myelogenous leukemia for response to imatinib
  • organism-icon Homo sapiens
  • sample-icon 28 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U95 Version 2 Array (hgu95av2)

Description

This is a class prediction experiment, where the class is the response status to imatinib (also called Gleevec), a drug used to treat patients with chronic myelogenous leukemia (CML). There are two data sets, a training set (from Leipzig, 8 Responders and 5 Non-Responders) and a validation set (from Mannheim, 8 Responders and 7 Non-Responders). The objective is to identify differentially regulated genes between CML patients who respond and those who do not respond to imatinib and confirm the results in the validation data set. The samples from blood or bone marrow of CML patients were hybridized to Affymetrix HG-U95Av2 chip and RMA was used to generate the normalized signal values.

Publication Title

In chronic myeloid leukemia white cells from cytogenetic responders and non-responders to imatinib have very similar gene expression signatures.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE14671
EXPRESSION SIGNATURE TO PREDICT MAJOR CYTOGENETIC RESPONSE IN CHRONIC PHASE CML PATIENTS TREATED WITH IMATINIB
  • organism-icon Homo sapiens
  • sample-icon 58 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Newly diagnosed chronic phase chronic myeloid leukemia (CML) patients with a major cytogenetic response (MCyR) after 12 months of imatinib therapy have an excellent long-term outcome, while patients without MCyR have a high progression risk. Since patients with primary cytogenetic resistance may benefit from more intensive therapy up-front, we sought to identify biomarkers to predict MCyR.

Publication Title

A gene expression signature of CD34+ cells to predict major cytogenetic response in chronic-phase chronic myeloid leukemia patients treated with imatinib.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE24814
Role and function of STAT5 in BCR-ABL1 driven pre-B cells
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

In order to investigate the function of STAT5 in ALL, we isolated bone marrow cells from STAT5 fl/fl mice and transformed them with BCR-ABL1. In a second transduction the BCR-ABL1 driven pre-B cells were transformed either with CRE-GFP or empty vector control (GFP) and subjected to gene expression analysis.

Publication Title

BCL6-mediated repression of p53 is critical for leukemia stem cell survival in chronic myeloid leukemia.

Sample Metadata Fields

Age, Disease, Disease stage

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accession-icon SRP044124
BCR-ABL1 promotes leukemia by converting p27 into a cytoplasmic oncoprotein
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer

Description

Coordinated BCR-ABL1 kinase-dependent and -independent mechanisms convert p27 from a nuclear tumor suppressor to a cytoplasmic oncogene. Persistence of oncogenic p27 functions despite effective inhibition of BCR-ABL1 may contribute to resistance to tyrosine kinase inhibitors. Overall design: BCR-ABL1 induced p27 versus knockout, controlling with Empty vector p27 versus knock out

Publication Title

BCR-ABL1 promotes leukemia by converting p27 into a cytoplasmic oncoprotein.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE44652
Gene expression profile of the human T-ALL cell line JURKAT after TYK2 and STAT1 knockdown
  • organism-icon Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Targeted molecular therapy has yielded remarkable outcomes in certain cancers, but specific therapeutic targets remain elusive for many others. As a result of two independent RNA interference (RNAi) screens, we identified pathway dependence on a member of the JAK tyrosine kinase family, TYK2, and its downstream effector STAT1 in T-cell acute lymphoblastic leukemia (T-ALL). Gene knockdown experiments consistently demonstrated TYK2 dependence in both T-ALL primary specimens and cell lines, and a small-molecule inhibitor of JAK kinase activity induced T-ALL cell death. Activation of this TYK2-STAT1 pathway in T-ALL cell lines occurs by gain-of-function TYK2 mutations or activation of IL-10 receptor signaling, and this pathway mediates T-ALL cell survival through upregulation of the anti-apoptotic protein BCL2. These findings indicate that in many T-ALL cases, the leukemic cells are dependent upon the TYK2-STAT1-BCL2 pathway for continued survival, supporting the development of molecular therapies targeting TYK2 and other components of this pathway.

Publication Title

TYK2-STAT1-BCL2 pathway dependence in T-cell acute lymphoblastic leukemia.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon E-TABM-112
Transcription profiling of barley embryo-derived tissue from Steptoe x Morex doubled-haploid lines and from the parental cultivars
  • organism-icon Hordeum vulgare
  • sample-icon 156 Downloadable Samples
  • Technology Badge Icon Affymetrix Barley Genome Array (barley1)

Description

We measured mRNA abundance in the embryogenic tissue of 150 recombinant Steptoe x Morex doubled-haploid lines (no replicates) and in parental genotypes, Steptoe and Morex, 3 replicates each, total 156 chips.

Publication Title

SFP genotyping from affymetrix arrays is robust but largely detects cis-acting expression regulators.

Sample Metadata Fields

Age, Specimen part, Time

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accession-icon GSE33394
Genetics of gene expression in barley
  • organism-icon Hordeum vulgare
  • sample-icon 41 Downloadable Samples
  • Technology Badge Icon Affymetrix Barley Genome Array (barley1)

Description

Comparison of mRNA accumulation in segregating doubled haploid barley lines ****[PLEXdb(http://www.plexdb.org) has submitted this series at GEO on behalf of the original contributor, . The equivalent experiment is BB21 at PLEXdb.]

Publication Title

SFP genotyping from affymetrix arrays is robust but largely detects cis-acting expression regulators.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE65402
Identification and Targeted Inhibition of a Fibroblast Lineage Responsible for Scarring and Cancer Stroma
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Dermal fibroblasts represent a heterogeneous population of cells with diverse features that remain largely undefined due to a lack of functional subclasses. Here we reveal the presence of multiple lineages of dermal fibroblasts within the dorsal back. Genetic lineage tracing and transplantation assays demonstrate that the bulk of connective tissue deposition during embryonic development, cutaneous wound healing, radiation fibrosis, and cancer stroma formation is carried out by a single, somitic-derived fibroblast lineage. Reciprocal transplantation of distinct fibroblast lineages between the dorsal back and oral cavity induced ectopic dermal architectures that mimic their placeof-origin. These studies demonstrate that intra and inter-site diversity of dermal architectures are set embryonically and maintained postnatally by distinct lineages of fibroblasts. Lineage-specific cell ablation using transgenic-mediated expression of the simian diphtheria toxin receptor in conjunction with localized administration of diphtheria toxin led to diminished connective tissue deposition in wounds and significantly reduced melanoma growth in the dorsal skin of mice. Using flow cytometry and in silico approaches, we identify CD26/DPP4 as a surface marker that allows for the isolation of this fibrogenic, scar-forming lineage. Small molecule-based inhibition of CD26/DPP4 enzymatic activity during wound healing results in diminished cutaneous scarring. The identification and prospective isolation of these lineages holds promise for translational medicine aimed at in vivo modulation of their fibrogenic behavior.

Publication Title

Skin fibrosis. Identification and isolation of a dermal lineage with intrinsic fibrogenic potential.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE12508
Transcription patterns during wheat development
  • organism-icon Triticum aestivum
  • sample-icon 39 Downloadable Samples
  • Technology Badge Icon Affymetrix Wheat Genome Array (wheat)

Description

The analysis of gene expression during wheat development:

Publication Title

Comparative transcriptomics in the Triticeae.

Sample Metadata Fields

No sample metadata fields

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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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