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accession-icon GSE27947
Identification of differentially regulated genes in hematopoietic stem cells and URE leukemia cell line
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

H2.0-like homeobox regulates early hematopoiesis and promotes acute myeloid leukemia.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE27938
Identification of differentially regulated genes upon overexpression of HLX in wild-type hematopoietic stem cells
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

The goal was to study the role of Hlx in hematopoiesis.

Publication Title

H2.0-like homeobox regulates early hematopoiesis and promotes acute myeloid leukemia.

Sample Metadata Fields

Specimen part

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accession-icon GSE27939
Identification of differentially regulated genes upon shRNA-mediated knock-down of HLX in the URE leukemia cell line
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

To study the role of Hlx in hematopoietic differentiation and tumorigenesis, URE cells were infected with short-hairpin-containing pSIH1-H1-copGFP lentiviral vector (System Biosciences, Mountain View, CA) containing either nucleotide sequences targeting luciferase (shControl) or HLX (shHLX). After 24hrs incubation in Iscoves modified Dulbeccos medium (IMDM) containing FBS, mIL-3, mIL-6 and mSCF with lentiviral supernatants in the presence of 8ug/ml polybrene, cells were cultured in fresh medium for several days. Subsequently, GFP+ cells were sorted by FACS and RNA was prepared.

Publication Title

H2.0-like homeobox regulates early hematopoiesis and promotes acute myeloid leukemia.

Sample Metadata Fields

Cell line

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accession-icon GSE44107
Analysis of differentially expressed genes in murine Satb1-deficient hematopoietic stem cells (HSCs) compared to wild-type HSCs
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Gene expression analysis on purified murine hematopoietic stem cells (HSCs) deficient for Special AT-rich sequence-binding protein 1 (Satb1) compared to wild-type HSCs.

Publication Title

Satb1 regulates the self-renewal of hematopoietic stem cells by promoting quiescence and repressing differentiation commitment.

Sample Metadata Fields

Specimen part

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accession-icon GSE72253
Novel IDH1 Mutant Inhibitors for Treatment of Acute Myeloid Leukemia
  • organism-icon Homo sapiens
  • sample-icon 5 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000, Affymetrix Human Gene 2.0 ST Array (hugene20st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

New IDH1 mutant inhibitors for treatment of acute myeloid leukemia.

Sample Metadata Fields

Specimen part

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accession-icon GSE72152
Novel IDH1 Mutant Inhibitors for Treatment of Acute Myeloid Leukemia (expression)
  • organism-icon Homo sapiens
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.0 ST Array (hugene20st), Illumina HiSeq 2000

Description

Neomorphic mutations in isocitrate dehydrogenase 1 (IDH1) are driver mutations in acute myeloid leukemia (AML) and other cancers. We report the development of new allosteric inhibitors of mutant IDH1. Crystallographic and biochemical results demonstrated that compounds of this chemical series bind to an allosteric site and lock the enzyme in a catalytically inactive conformation, thereby enabling inhibition of different clinically relevant IDH1 mutants. Treatment of IDH1 mutant primary AML cells uniformly led to a decrease in intracellular 2-HG, abrogation of the myeloid differentiation block and induction of granulocytic differentiation at the level of leukemic blasts and more immature stem-like cells, in vitro and in vivo. Molecularly, treatment with the inhibitors led to a reversal of the DNA cytosine hypermethylation patterns caused by mutant IDH1 in AML patients cells. Our study provides proof-of-concept for the molecular and biological activity of novel allosteric inhibitors for targeting different mutant forms of IDH1 in leukemia. To obtain insight into the molecular mechanism for the induction of granulocytic differentiation and cell death following inhibition of IDH1 mutant protein in primary AML cells, we performed gene expression microarrays following treatment with either GSK321 IDH1 inhibitor or Controls (DMSO or GSK990 inactive inhibitor).

Publication Title

New IDH1 mutant inhibitors for treatment of acute myeloid leukemia.

Sample Metadata Fields

Specimen part

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accession-icon GSE60615
miRNAs in Treg-derived Exosomes
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Foxp3+ regulatory T (Treg) cells prevent inflammatory disease but the mechanistic basis of suppression is not understood completely . Gene silencing by RNA interference can act in a cell-autonomous and non-cell-autonomous manner, providing mechanisms of inter-cellular regulation. Here, we demonstrate that non-cell-autonomous gene silencing, mediated by miRNA-containing exosomes, is a mechanism employed by Treg cells to suppress T cell-mediated disease. Treg cells transferred microRNAs (miRNA) to various immune cells, including T helper 1 (Th1) cells, suppressing Th1 cell proliferation and cytokine secretion. Use of Dicer-deficient or Rab27a and Rab27b double-deficient Treg cells to disrupt miRNA-biogenesis or the exosomal pathway, respectively, established a requirement for miRNAs and exosomes for Treg cell-mediated suppression. Transcriptional analysis and miRNA inhibitor studies showed that exosome-mediated transfer of Let-7d from Treg cell to Th1 cells contributed to suppression and prevention of systemic disease. These studies reveal a mechanism of Treg cell-mediated suppression mediated by miRNA-containing exosomes.

Publication Title

MicroRNA-containing T-regulatory-cell-derived exosomes suppress pathogenic T helper 1 cells.

Sample Metadata Fields

Specimen part

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accession-icon GSE98518
Gene expression analysis of ex-Foxp3 Th2 cells during Heligmosomoides polygyrus infection
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Gene expression of Treg cells that have lost Foxp3 expression and acquired Il4 expression following adoptive transfer into T-cell deficient mice (HpTR-IL-4gfp+), cmpared to conventional Treg cells isolated from H. polygyrus-infected wild-type mice (HpTR) and Th2 cells generated from nave T cells following adoptive transfer into H. polygyrus-infected T-cell deficient mice (nT-IL-4gfp+).

Publication Title

Interleukin 4 promotes the development of ex-Foxp3 Th2 cells during immunity to intestinal helminths.

Sample Metadata Fields

Specimen part

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accession-icon GSE25990
Hodgkin lymphoma
  • organism-icon Homo sapiens
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

MHC class II transactivator CIITA is a recurrent gene fusion partner in lymphoid cancers.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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accession-icon GSE25986
Gene expression profiling of cell lines derived from classical Hodgkin lymphoma
  • organism-icon Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Hodgkin lymphoma is derived from germinal center / post-germinal center B cells.

Publication Title

MHC class II transactivator CIITA is a recurrent gene fusion partner in lymphoid cancers.

Sample Metadata Fields

Specimen part, Cell line

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

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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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