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accession-icon GSE15102
Targetting CD24 for treatment of colorectal and pancreatic cancer by monoclonal antibodies or siRNA
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

CD24 is a potential oncogene reported to be overexpressed in a large variety of human malignancies. We have shown that CD24 is overexpressed in 90% of colorectal tumors at a fairly early stage in the multistep process of carcinogenesis. Anti-CD24 monoclonal antibodies (mAb) induce a significant growth inhibition in colorectal and pancreatic cancer cell lines that express the protein. This study is designed to investigate further the effects of CD24 down-regulation using mAb or small interfering RNA in vitro and in vivo. Western blot analysis showed that anti-CD24 mAb induced CD24 protein down-regulation through lysosomal degradation. mAb augmented growth inhibition in combination with five classic chemotherapies. Xenograft models in vivo showed that tumor growth was significantly reduced in mAb-treated mice. Similarly, stable growth inhibition of cancer cell lines was achieved by down-regulation of CD24 expression using short hairpin RNA (shRNA). The produced clones proliferated more slowly, reached lower saturation densities, and showed impaired motility. Most importantly, down-regulation of CD24 retarded tumorigenicity of human cancer cell lines in nude mice. Microarray analysis revealed a similar pattern of gene expression alterations when cells were subjected to anti-CD24 mAb or shRNA. Genes in the Ras pathway, mitogenactivated protein kinase, or BCL-2 family and others of oncogenic association were frequently down-regulated. As a putative new oncogene that is overexpressed in gastrointestinal malignancies early in the carcinogenesis process, CD24 is a potential target for early intervention in the prevention and treatment of cancer.

Publication Title

Targeting CD24 for treatment of colorectal and pancreatic cancer by monoclonal antibodies or small interfering RNA.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE13313
Expression, ChIP-chip, and ChIP-Seq data from REH and SEM leukemia cell lines [Expression and ChIP-chip]
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

MLL-fusion proteins are potent inducers of cancer in hematopoietic cells, where they are known to cause changes in global gene expression. How MLL-fusion proteins interact with the genome has not been established, so we have limited understanding of the pathway by which these proteins generate aberrant gene expression programs. Here we describe how the MLL-AF4 protein occupies the genome in human leukemia cells and its striking effects on chromatin states. We find that the MLL-AF4 fusion protein selectively occupies regions of the genome that contain developmental regulatory genes important for hematopoietic stem cell identity and self-renewal. These MLL-AF4 bound regions have grossly altered chromatin structure, with histone modifications catalyzed by Trithorax Group (TrxG) proteins and Dot1 extending across unusually large domains. This indicates that a key feature of MLL-associated leukemogenesis is aberrant targeting of chromatin modifiers to regions of the genome controlling hematopoietic development. Our results define the direct targets of the MLL-fusion protein, reveal the global role of epigenetic misregulation in leukemia, and identify new targets for therapeutic intervention in human cancer.

Publication Title

Aberrant chromatin at genes encoding stem cell regulators in human mixed-lineage leukemia.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE20473
LEOPARD Syndrome iPS, BJ iPS and Fibroblasts
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

Expression data from LEOPARD Syndrome-iPS clones, BJ-iPS cells and parental Fibroblasts

Publication Title

Patient-specific induced pluripotent stem-cell-derived models of LEOPARD syndrome.

Sample Metadata Fields

Sex, Specimen part, Subject

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accession-icon E-MEXP-114
Transcription profiling of hypothalamus, liver, kidney, ovaries and testis from male and female humans and mice
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 71 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Expression 430A Array (moe430a), Affymetrix Human Genome U133A Array (hgu133a)

Description

Compared differentially express genes by sex in mouse for the following tissues: hypothalamus, liver, kidney, ovaries and testis (3 biological x 2 technical replicates for each tissues/sex). We used Affymetrix MOE430A Genechip arrays.

Publication Title

Major molecular differences between mammalian sexes are involved in drug metabolism and renal function.

Sample Metadata Fields

Sex, Specimen part

View Samples
accession-icon SRP007417
GSE30400: RNA-Seq in GM12878 (ENCODE Project)
  • organism-icon Homo sapiens
  • sample-icon 15 Downloadable Samples
  • Technology Badge IconIlluminaGenomeAnalyzerII

Description

.

Publication Title

AlleleSeq: analysis of allele-specific expression and binding in a network framework.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP002126
Human variation in PolII and NF-KappaB binding (RNA-seq study uninduced by TNF-alpha)
  • organism-icon Homo sapiens
  • sample-icon 14 Downloadable Samples
  • Technology Badge IconIlluminaGenomeAnalyzerII

Description

We examined genome-wide variation in transcription factor binding in different individuals and a chimpanzee using chromatin immunoprecipitation followed by massively-parallel sequencing (ChIP-Seq). The binding sites of RNA Polymerase II (Pol II) as well as a key regulator of immune responses, NFkB, were mapped in ten HapMap lymphoblastoid cell lines derived from individuals of African, European, and Asian ancestry, including a parent-offspring trio. We also mapped gene expression in all ten human cell lines for two treatment conditions: a) no treatment and b) following induction by TNF-alpha. Overall design: Genome-wide comparison of Pol II and NF-KappaB binding in ten individuals. RNA-seq study with no treatment.

Publication Title

Variation in transcription factor binding among humans.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP002128
Human variation in PolII and NF-KappaB binding (RNA-seq study with TNF-alpha induced)
  • organism-icon Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge IconIlluminaGenomeAnalyzerII

Description

We examined genome-wide variation in transcription factor binding in different individuals and a chimpanzee using chromatin immunoprecipitation followed by massively-parallel sequencing (ChIP-Seq). The binding sites of RNA Polymerase II (Pol II) as well as a key regulator of immune responses, NFkB, were mapped in ten HapMap lymphoblastoid cell lines derived from individuals of African, European, and Asian ancestry, including a parent-offspring trio. We also mapped gene expression in all ten human cell lines for two treatment conditions: a) no treatment and b) following induction by TNF-alpha. Overall design: Genome-wide comparison of Pol II and NF-KappaB binding in ten individuals. RNA-seq study with TNF-alpha treatment.

Publication Title

Variation in transcription factor binding among humans.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE34071
Expression data of Normal versus Mutant MPS VII C3H mouse
  • organism-icon Mus musculus
  • sample-icon 94 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

We used microarray to detect pathway differences in the various brain regions in a monogenic in mucopolysaccharidosis type VII ( MPS VII ), a mouse model of a lysosomal storage disease

Publication Title

Dysregulation of gene expression in a lysosomal storage disease varies between brain regions implicating unexpected mechanisms of neuropathology.

Sample Metadata Fields

Specimen part

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accession-icon GSE76283
Expression data of Normal versus Mutant MPS VII Bl6 mouse
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

We used microarray to detect pathway differences in the hippocampus in mucopolysaccharidosis type VII ( MPS VII ), a mouse model of a lysosomal storage disease

Publication Title

Integrated analysis of proteome and transcriptome changes in the mucopolysaccharidosis type VII mouse hippocampus.

Sample Metadata Fields

Sex, Age, Specimen part

View Samples
accession-icon GSE81225
Mouse myoblasts grown on Fibronectin or Collagen I for 72 hours
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The goal of this study was to investigate the transcriptional regulation in cells grown on Fibronectin when compared to Collagen I

Publication Title

Loss of fibronectin from the aged stem cell niche affects the regenerative capacity of skeletal muscle in mice.

Sample Metadata Fields

Sex, Age, Specimen part

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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