refine.bio
  • Search
      • Normalized Compendia
      • RNA-seq Sample Compendia
  • Docs
  • About
  • My Dataset
github link
Showing
of 138 results
Sort by

Filters

Technology

Platform

accession-icon GSE51044
Gamma-secretase inhibitor plus fludarabine in CLL
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U219 Array (hgu219)

Description

Combination of GSI with fludarabine has a synergistic antileukemic effect in primary NOTCH1-mutated CLL cells

Publication Title

The γ-secretase inhibitor PF-03084014 combined with fludarabine antagonizes migration, invasion and angiogenesis in NOTCH1-mutated CLL cells.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE100922
Expression data from whole blood in CD patients undergoing HSCT.
  • organism-icon Homo sapiens
  • sample-icon 42 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U219 Array (hgu219)

Description

Treatment of severely refractory Crohns disease (CD) patients remains a clinical challenge. Recent studies show efficacy of autologous hematopoietic stem cell transplant (HSCT) in these severely compromised patients. HSCT is thought to eliminate auto-reactive cells; however the mechanisms are incompletely understood. We followed a group of patients (n=18) receiving autologous HSCT, with 50% of them achieving endoscopic drug-free remission. To elucidate the mechanism driving efficacy we compared the immunological changes induced by HSCT in responders and non-responders.

Publication Title

Differences in peripheral and tissue immune cell populations following hematopoietic stem cell transplantation in Crohn's disease patients.

Sample Metadata Fields

Sex, Age, Specimen part, Disease, Time

View Samples
accession-icon SRP149847
Differences in tissue immune cell populations following hematopoietic stem cell transplantation in Crohn's disease patients
  • organism-icon Homo sapiens
  • sample-icon 80 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 4000

Description

Treatment of severely refractory Crohn's disease (CD) patients remains a clinical challenge. Recent studies show the efficacy of autologous hematopoietic stem cell transplant (HSCT) in these severely compromised patients. HSCT is thought to eliminate auto-reactive cells; however, no specific studies of immune reconstitution in CD patients are available. We studied a group of CD patients receiving autologous HSCT, with 50% of them achieving endoscopic drug-free remission. To elucidate the mechanism driving efficacy, we studied changes in the immune cell composition in tissue induced by HSCT. Overall design: Biopsy mRNA profiles of 14 CD patients undergoing HSCT were generated by deep sequencing, using HiSeq-4000 platform (Illumina, San Diego, CA).

Publication Title

Differences in Peripheral and Tissue Immune Cell Populations Following Haematopoietic Stem Cell Transplantation in Crohn's Disease Patients.

Sample Metadata Fields

Sex, Specimen part, Disease, Subject

View Samples
accession-icon SRP131004
RNA-Seq in human T-cell lymphoblastic lymphoma samples and control thymuses
  • organism-icon Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Precursor T-cell lymphoblastic neoplasms are aggressive haematological neoplasm that most often manifest with extensive marrow and blood affectation (T-cell acute lymphoblastic leukaemia or T-ALL) or less commonly as a thymic mass with limited bone marrow infiltration (T-cell lymphoblastic lymphoma or T-LBL). Here we show data from RNA-Seq in a sample series of T-LBL from Spanish patients.The goal was to determine the levels of expression of coding genes and microRNAs, and to identify all genetic variants including SNVs, indels, and fusion transcripts. Overall design: Expression data were determined by comparson of each tumour sample with two control thymuses (404 and 405). Genetic variants were determined by comparison of tumour sequences with canonical ENSEMBL normal-references of each gene.

Publication Title

RNA-Seq reveals the existence of a CDKN1C-E2F1-TP53 axis that is altered in human T-cell lymphoblastic lymphomas.

Sample Metadata Fields

Specimen part, Subject

View Samples
accession-icon SRP011435
High-thoughput Illumina RNA sequencing to identify downstream target genes of RABBIT EARS (RBE) in the flowers of Arabidopsis thaliana
  • organism-icon Arabidopsis thaliana
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

In order to identify putative downstream target genes of RBE, we sequenced mRNA from dexamethasone (DEX) and mock treated transgenic Arabidopsis line 35S:GR-RBE (RBE coding region fused to a glucocorticoid receptor domain driven by the constitutive 35S promoter) floral tissues. We compared the results from DEX and mock treatments and focused on the 832 genes whose expression was significantly reduced (P < 0.025) by 2-fold or more in DEX as compared to mock-treated plants. In this analysis, we identified MIR164c (EEP1) as a candidate target of RBE, which was further confirmed by other molecular and genetic analyses. Regulation of MIR164c by RBE is important for normal floral organ formation in Arabidopsis. Overall design: We used two biological replicates, each with two technical replicates for four hour DEX or mock treated floral tissues to produce 8 sequencing libraries.

Publication Title

RBE controls microRNA164 expression to effect floral organogenesis.

Sample Metadata Fields

Specimen part, Cell line, Subject

View Samples
accession-icon GSE44272
The Long-HER Study
  • organism-icon Homo sapiens
  • sample-icon 53 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U219 Array (hgu219)

Description

Trastuzumab improves survival outcomes in patients with HER2+ metastatic breast cancer. Some of these patients may become long-term survivors. The Long-Her study was designed to identify clinical and molecular markers that could differentiate long-term survivors from patients having early progression to trastuzumab.

Publication Title

The Long-HER study: clinical and molecular analysis of patients with HER2+ advanced breast cancer who become long-term survivors with trastuzumab-based therapy.

Sample Metadata Fields

Age, Disease

View Samples
accession-icon GSE32609
Transcriptional profiling of liver samples from Lmna Gly609Gly knock-in mice
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Hutchinson-Gilford Progeria Syndrome (HGPS) is caused by a point mutation in the LMNA gene that activates a cryptic donor splice site and yields a truncated form of prelamin A called progerin. Small amounts of progerin are also produced during normal aging. Studies with mouse models of HGPS have allowed the recent development of the first therapeutic approaches for this disease. However, none of these earlier works have addressed the aberrant and pathogenic LMNA splicing observed in HGPS patients because of the lack of an appropriate mouse model. We report herein a genetically modified mouse strain that carries the HGPS mutation. These mice accumulate progerin, present histological and transcriptional alterations characteristic of progeroid models, and phenocopy the main clinical manifestations of human HGPS, including shortened life span and bone and cardiovascular aberrations. By using this animal model, we have developed an antisense morpholinobased therapy that prevents the pathogenic Lmna splicing, dramatically reducing the accumulation of progerin and its associated nuclear defects. Treatment of mutant mice with these morpholinos led to a marked amelioration of their progeroid phenotype and substantially extended their life span, supporting the effectiveness of antisense oligonucleotidebased therapies for treating human diseases of accelerated aging.

Publication Title

Splicing-directed therapy in a new mouse model of human accelerated aging.

Sample Metadata Fields

Sex, Age, Specimen part

View Samples
accession-icon SRP098816
Identification of intrinsic growth modulators for intact CNS neurons after injury
  • organism-icon Mus musculus
  • sample-icon 21 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Functional deficits persist after spinal cord injury (SCI) because axons in the adult mammalian central nervous system (CNS) fail to regenerate. However, modest levels of spontaneous functional recovery are typically observed after trauma, and are thought to be mediated by the plasticity of intact circuits. The mechanisms underlying intact circuit plasticity are not delineated. Here, we characterize the in vivo transcriptome of sprouting intact neurons from ngr1 null mice after partial SCI. We identify the lysophosphatidic acid signaling modulators Lppr1 and Lpar1 as intrinsic axon growth modulators for intact corticospinal motor neurons after adjacent injury. Furthermore, in vivo Lpar1 inhibition or Lppr1 overexpression enhances sprouting of intact corticospinal tract axons and yields greater functional recovery after unilateral brainstem lesion in wild type mice. Thus, the transcriptional profile of injury-induced sprouting of intact neurons reveals targets for therapeutic enhancement of axon growth initiation and new synapse formation. Overall design: GFP labeled Corticospinal motor neurons (CSMNs) were harvetsed via laser capture microdissection to assess gene expression between populations that were quiescent and those that initated a functional axon growth response.

Publication Title

Identification of Intrinsic Axon Growth Modulators for Intact CNS Neurons after Injury.

Sample Metadata Fields

Specimen part, Cell line, Subject

View Samples
accession-icon SRP167093
Distinct Adaptive Mechanisms Drive Recovery from Aneuploidy Caused by Loss of the Ulp2 SUMO Protease [RNA-seq]
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 49 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

In response to acute loss of the Ulp2 SUMO-specific protease, yeast become disomic for chromosome I (ChrI) and ChrXII. Here we report that ChrI disomy, which creates an adaptive advantage in part by increasing the dosage of the Ccr4 deadenylase, was eliminated by extended passaging. Loss of aneuploidy is often accompanied by mutations in essential SUMO-ligating enzymes, which reduced polySUMO-conjugate accumulation. The mRNA levels for almost all ribosomal proteins increases transiently upon initial loss of Ulp2, but elevated Ccr4 levels limit excess ribosome formation. Notably, extended passaging leads to increased levels of many small nucleolar RNAs (snoRNAs) involved in ribosome biogenesis, and higher dosage of three linked ChrXII snoRNA genes suppressed ChrXII disomy in ulp2? cells. Our data reveal that aneuploidy allows rapid adaptation to Ulp2 loss, but long-term adaptation restores euploidy. Cellular evolution restores homeostasis through countervailing mutations in SUMO-modification pathways and regulatory shifts in ribosome biogenesis. Overall design: In these comparisons, the ulp2? cells either carried a WT ULP2 plasmid or empty vector and were passaged for 50 or 500 generations. mRNA profiles of them were generated by sequencing, in triplicate, using Illumina HiSeq 2500 .

Publication Title

Distinct adaptive mechanisms drive recovery from aneuploidy caused by loss of the Ulp2 SUMO protease.

Sample Metadata Fields

Subject

View Samples
accession-icon GSE13771
The role of ERbeta2 in zebrafish neuromasts development
  • organism-icon Danio rerio
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Zebrafish Genome Array (zebrafish)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Estrogen receptor subtype beta2 is involved in neuromast development in zebrafish (Danio rerio) larvae.

Sample Metadata Fields

No sample metadata fields

View Samples
...

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)

fund-icon Fund the CCDL

Developed by the Childhood Cancer Data Lab

Powered by Alex's Lemonade Stand Foundation

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.

BSD 3-Clause LicensePrivacyTerms of UseContact